anti endothelial nitric oxide synthase  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti endothelial nitric oxide synthase
    List of primers used for real-time RT-PCR.
    Anti Endothelial Nitric Oxide Synthase, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti endothelial nitric oxide synthase/product/Cell Signaling Technology Inc
    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti endothelial nitric oxide synthase - by Bioz Stars, 2023-02
    96/100 stars

    Images

    1) Product Images from "Metformin Protects against Oxidative Stress Injury Induced by Ischemia/Reperfusion via Regulation of the lncRNA-H19/miR-148a-3p/Rock2 Axis"

    Article Title: Metformin Protects against Oxidative Stress Injury Induced by Ischemia/Reperfusion via Regulation of the lncRNA-H19/miR-148a-3p/Rock2 Axis

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2019/8768327

    List of primers used for real-time RT-PCR.
    Figure Legend Snippet: List of primers used for real-time RT-PCR.

    Techniques Used: Sequencing

    Inhibition of lncRNA-H19 expression influenced the effect of metformin on oxidative stress following OGD/R in vitro via regulation of Rock2/HO-1/Nrf2. (a) Activities of SOD in the supernatant of cell culture medium. (b) Levels of MDA in the supernatant of cell culture medium. (c, d) The protein expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after transfection of pcDNA3.1-NC and pcDNA3.1-H19. (e) The mRNA expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after transfection of pcDNA3.1-NC and pcDNA3.1-H19. Data are represented as mean ± SD. ∗ p < 0.05 and ∗∗∗ p < 0.001 versus the normal group by 1-way analysis of variance with Tukey's multiple comparison test. # p < 0.05, ## p < 0.01, and ### p < 0.001 versus the OGD/R group by 1-way analysis of variance with Tukey's multiple comparison test. & p < 0.05, && p < 0.01, and &&& p < 0.001 versus the OGD/R+Met+pcDNA3.1-NC group by 1-way analysis of variance with Tukey's multiple comparison test.
    Figure Legend Snippet: Inhibition of lncRNA-H19 expression influenced the effect of metformin on oxidative stress following OGD/R in vitro via regulation of Rock2/HO-1/Nrf2. (a) Activities of SOD in the supernatant of cell culture medium. (b) Levels of MDA in the supernatant of cell culture medium. (c, d) The protein expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after transfection of pcDNA3.1-NC and pcDNA3.1-H19. (e) The mRNA expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after transfection of pcDNA3.1-NC and pcDNA3.1-H19. Data are represented as mean ± SD. ∗ p < 0.05 and ∗∗∗ p < 0.001 versus the normal group by 1-way analysis of variance with Tukey's multiple comparison test. # p < 0.05, ## p < 0.01, and ### p < 0.001 versus the OGD/R group by 1-way analysis of variance with Tukey's multiple comparison test. & p < 0.05, && p < 0.01, and &&& p < 0.001 versus the OGD/R+Met+pcDNA3.1-NC group by 1-way analysis of variance with Tukey's multiple comparison test.

    Techniques Used: Inhibition, Expressing, In Vitro, Cell Culture, Transfection

    Metformin protects against oxidative stress injury induced by I/R via regulation of the lncRNA-H19/miR-148a-3p/Rock2 axis. (a) The mRNA expressions of lncRNA-H19 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. (b) The level of miR-148a-3p. (c) Statistical analysis of the percentage of infarct volume was determined for each group. (d) Neurological scores after transient middle cerebral artery occlusion (tMCAO) in each groups. (e) Activities of SOD in the serum and the brain. (f) Levels of MDA in the serum and the brain. (g) The mRNA expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. (h, i) The protein expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. ∗ p < 0:05, ∗∗ p < 0:01, and ∗∗∗ p < 0:001 versus the sham group by 1-way analysis of variance with Tukey's multiple comparison test. # p < 0:05, ## p < 0:01, and ### p < 0:01 versus the MCAO/R group by 1-way analysis of variance with Tukey's multiple comparison test. & p < 0:05, && p < 0:01, and &&& p < 0:001 versus the MCAO/R+Met+NC group by 1-way analysis of variance with Tukey's multiple comparison test.
    Figure Legend Snippet: Metformin protects against oxidative stress injury induced by I/R via regulation of the lncRNA-H19/miR-148a-3p/Rock2 axis. (a) The mRNA expressions of lncRNA-H19 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. (b) The level of miR-148a-3p. (c) Statistical analysis of the percentage of infarct volume was determined for each group. (d) Neurological scores after transient middle cerebral artery occlusion (tMCAO) in each groups. (e) Activities of SOD in the serum and the brain. (f) Levels of MDA in the serum and the brain. (g) The mRNA expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. (h, i) The protein expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. ∗ p < 0:05, ∗∗ p < 0:01, and ∗∗∗ p < 0:001 versus the sham group by 1-way analysis of variance with Tukey's multiple comparison test. # p < 0:05, ## p < 0:01, and ### p < 0:01 versus the MCAO/R group by 1-way analysis of variance with Tukey's multiple comparison test. & p < 0:05, && p < 0:01, and &&& p < 0:001 versus the MCAO/R+Met+NC group by 1-way analysis of variance with Tukey's multiple comparison test.

    Techniques Used: Injection

    anti endothelial nitric oxide synthase  (Cell Signaling Technology Inc)


    Bioz Verified Symbol Cell Signaling Technology Inc is a verified supplier
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    Cell Signaling Technology Inc anti endothelial nitric oxide synthase
    List of primers used for real-time RT-PCR.
    Anti Endothelial Nitric Oxide Synthase, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti endothelial nitric oxide synthase/product/Cell Signaling Technology Inc
    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti endothelial nitric oxide synthase - by Bioz Stars, 2023-02
    96/100 stars

    Images

    1) Product Images from "Metformin Protects against Oxidative Stress Injury Induced by Ischemia/Reperfusion via Regulation of the lncRNA-H19/miR-148a-3p/Rock2 Axis"

    Article Title: Metformin Protects against Oxidative Stress Injury Induced by Ischemia/Reperfusion via Regulation of the lncRNA-H19/miR-148a-3p/Rock2 Axis

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2019/8768327

    List of primers used for real-time RT-PCR.
    Figure Legend Snippet: List of primers used for real-time RT-PCR.

    Techniques Used: Sequencing

    Inhibition of lncRNA-H19 expression influenced the effect of metformin on oxidative stress following OGD/R in vitro via regulation of Rock2/HO-1/Nrf2. (a) Activities of SOD in the supernatant of cell culture medium. (b) Levels of MDA in the supernatant of cell culture medium. (c, d) The protein expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after transfection of pcDNA3.1-NC and pcDNA3.1-H19. (e) The mRNA expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after transfection of pcDNA3.1-NC and pcDNA3.1-H19. Data are represented as mean ± SD. ∗ p < 0.05 and ∗∗∗ p < 0.001 versus the normal group by 1-way analysis of variance with Tukey's multiple comparison test. # p < 0.05, ## p < 0.01, and ### p < 0.001 versus the OGD/R group by 1-way analysis of variance with Tukey's multiple comparison test. & p < 0.05, && p < 0.01, and &&& p < 0.001 versus the OGD/R+Met+pcDNA3.1-NC group by 1-way analysis of variance with Tukey's multiple comparison test.
    Figure Legend Snippet: Inhibition of lncRNA-H19 expression influenced the effect of metformin on oxidative stress following OGD/R in vitro via regulation of Rock2/HO-1/Nrf2. (a) Activities of SOD in the supernatant of cell culture medium. (b) Levels of MDA in the supernatant of cell culture medium. (c, d) The protein expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after transfection of pcDNA3.1-NC and pcDNA3.1-H19. (e) The mRNA expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after transfection of pcDNA3.1-NC and pcDNA3.1-H19. Data are represented as mean ± SD. ∗ p < 0.05 and ∗∗∗ p < 0.001 versus the normal group by 1-way analysis of variance with Tukey's multiple comparison test. # p < 0.05, ## p < 0.01, and ### p < 0.001 versus the OGD/R group by 1-way analysis of variance with Tukey's multiple comparison test. & p < 0.05, && p < 0.01, and &&& p < 0.001 versus the OGD/R+Met+pcDNA3.1-NC group by 1-way analysis of variance with Tukey's multiple comparison test.

    Techniques Used: Inhibition, Expressing, In Vitro, Cell Culture, Transfection

    Metformin protects against oxidative stress injury induced by I/R via regulation of the lncRNA-H19/miR-148a-3p/Rock2 axis. (a) The mRNA expressions of lncRNA-H19 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. (b) The level of miR-148a-3p. (c) Statistical analysis of the percentage of infarct volume was determined for each group. (d) Neurological scores after transient middle cerebral artery occlusion (tMCAO) in each groups. (e) Activities of SOD in the serum and the brain. (f) Levels of MDA in the serum and the brain. (g) The mRNA expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. (h, i) The protein expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. ∗ p < 0:05, ∗∗ p < 0:01, and ∗∗∗ p < 0:001 versus the sham group by 1-way analysis of variance with Tukey's multiple comparison test. # p < 0:05, ## p < 0:01, and ### p < 0:01 versus the MCAO/R group by 1-way analysis of variance with Tukey's multiple comparison test. & p < 0:05, && p < 0:01, and &&& p < 0:001 versus the MCAO/R+Met+NC group by 1-way analysis of variance with Tukey's multiple comparison test.
    Figure Legend Snippet: Metformin protects against oxidative stress injury induced by I/R via regulation of the lncRNA-H19/miR-148a-3p/Rock2 axis. (a) The mRNA expressions of lncRNA-H19 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. (b) The level of miR-148a-3p. (c) Statistical analysis of the percentage of infarct volume was determined for each group. (d) Neurological scores after transient middle cerebral artery occlusion (tMCAO) in each groups. (e) Activities of SOD in the serum and the brain. (f) Levels of MDA in the serum and the brain. (g) The mRNA expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. (h, i) The protein expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. ∗ p < 0:05, ∗∗ p < 0:01, and ∗∗∗ p < 0:001 versus the sham group by 1-way analysis of variance with Tukey's multiple comparison test. # p < 0:05, ## p < 0:01, and ### p < 0:01 versus the MCAO/R group by 1-way analysis of variance with Tukey's multiple comparison test. & p < 0:05, && p < 0:01, and &&& p < 0:001 versus the MCAO/R+Met+NC group by 1-way analysis of variance with Tukey's multiple comparison test.

    Techniques Used: Injection

    enos  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc enos
    Enos, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/enos/product/Cell Signaling Technology Inc
    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    enos - by Bioz Stars, 2023-02
    96/100 stars

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    enos  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc enos
    CAT alleviates oxidative stress in random skin flaps. (a) Immunohistochemical staining of <t>proteins</t> <t>SOD1</t> in random skin flaps (200 magnification; scan bar 25 μ m). (b) Quantification of integral absorbance of SOD1 in IHC. (c) Western blotting result of SOD1, <t>eNOS,</t> and HO1 in the control and CAT group. (d–f) Quantification of SOD1, eNOS, and HO1 expressions in each group. Significance: ∗∗ p < 0.01 vs. the control group. Data were expressed as means ± SEM, n = 6.
    Enos, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/enos/product/Cell Signaling Technology Inc
    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    enos - by Bioz Stars, 2023-02
    96/100 stars

    Images

    1) Product Images from "Catalpol Enhances Random-Pattern Skin Flap Survival by Activating SIRT1-Mediated Enhancement of Autophagy"

    Article Title: Catalpol Enhances Random-Pattern Skin Flap Survival by Activating SIRT1-Mediated Enhancement of Autophagy

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2022/5668226

    CAT alleviates oxidative stress in random skin flaps. (a) Immunohistochemical staining of proteins SOD1 in random skin flaps (200 magnification; scan bar 25 μ m). (b) Quantification of integral absorbance of SOD1 in IHC. (c) Western blotting result of SOD1, eNOS, and HO1 in the control and CAT group. (d–f) Quantification of SOD1, eNOS, and HO1 expressions in each group. Significance: ∗∗ p < 0.01 vs. the control group. Data were expressed as means ± SEM, n = 6.
    Figure Legend Snippet: CAT alleviates oxidative stress in random skin flaps. (a) Immunohistochemical staining of proteins SOD1 in random skin flaps (200 magnification; scan bar 25 μ m). (b) Quantification of integral absorbance of SOD1 in IHC. (c) Western blotting result of SOD1, eNOS, and HO1 in the control and CAT group. (d–f) Quantification of SOD1, eNOS, and HO1 expressions in each group. Significance: ∗∗ p < 0.01 vs. the control group. Data were expressed as means ± SEM, n = 6.

    Techniques Used: Immunohistochemical staining, Staining, Western Blot

    32027s  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc 32027s
    32027s, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/32027s/product/Cell Signaling Technology Inc
    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    32027s - by Bioz Stars, 2023-02
    96/100 stars

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    endothelial nitric oxide synthase  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc endothelial nitric oxide synthase
    Docking results of core components and core targets.
    Endothelial Nitric Oxide Synthase, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/endothelial nitric oxide synthase/product/Cell Signaling Technology Inc
    Average 96 stars, based on 1 article reviews
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    endothelial nitric oxide synthase - by Bioz Stars, 2023-02
    96/100 stars

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    1) Product Images from "Network Pharmacology Prediction and Pharmacological Verification Mechanism of Yeju Jiangya Decoction on Hypertension"

    Article Title: Network Pharmacology Prediction and Pharmacological Verification Mechanism of Yeju Jiangya Decoction on Hypertension

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    doi: 10.1155/2021/5579129

    Docking results of core components and core targets.
    Figure Legend Snippet: Docking results of core components and core targets.

    Techniques Used:

    Interaction diagram of chemical composition and protein. (a) NOS2 and luteolin; (b) NOS3 and luteolin; (c) NOS2 and quercetin; (d) NOS3 and quercetin.
    Figure Legend Snippet: Interaction diagram of chemical composition and protein. (a) NOS2 and luteolin; (b) NOS3 and luteolin; (c) NOS2 and quercetin; (d) NOS3 and quercetin.

    Techniques Used:

    Effect of CIF on NOS3/GC α 1/cGMP/PRKG1. (a) Representative results of NOS3/sGC/PRKG1 in Western blot; (b) cGMP in the aortic homogenate for ELISA; (c–f) protein level of NOS3, GC- α 1, NOS3, GC- α 2, and PRKG1. The data were expressed as mean ± SD. # P < 0.05 and ## P < 0.01 compared with the normal control group; ∗ , P < 0.05 and ∗ , ∗ , P < 0.01 compared with the model control group.
    Figure Legend Snippet: Effect of CIF on NOS3/GC α 1/cGMP/PRKG1. (a) Representative results of NOS3/sGC/PRKG1 in Western blot; (b) cGMP in the aortic homogenate for ELISA; (c–f) protein level of NOS3, GC- α 1, NOS3, GC- α 2, and PRKG1. The data were expressed as mean ± SD. # P < 0.05 and ## P < 0.01 compared with the normal control group; ∗ , P < 0.05 and ∗ , ∗ , P < 0.01 compared with the model control group.

    Techniques Used: Western Blot, Enzyme-linked Immunosorbent Assay

    CIF on the protein expressions of NOS3GC- α /cGMP/PRKG1 in immunohistochemical IHC to observe myocardial histopathological changes of aorta (×200 magnification). (a) NOS3; (b) GCal; (c) GCa2; (d) PRKG1.
    Figure Legend Snippet: CIF on the protein expressions of NOS3GC- α /cGMP/PRKG1 in immunohistochemical IHC to observe myocardial histopathological changes of aorta (×200 magnification). (a) NOS3; (b) GCal; (c) GCa2; (d) PRKG1.

    Techniques Used: Immunohistochemical staining

    anti enos  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti enos
    S1pr2 <t>inhibits</t> <t>AKT/eNOS/NO</t> signaling pathway, and thus reduces EC migration, proliferation, and angiogenic activity. A-C. Western blotting of AKT or eNOS activation status in HUVECs and quantification in the indicated groups (n = 3). D. S1PR2 inhibits the NO production of HUVECs through AKT/eNOS signaling pathway (n = 8). E. S1PR2 inhibits the ability of proliferation of HUVECs through AKT/eNOS signaling pathway, as shown by MTT assay (n = 5). F-I, S1PR2 inhibits the ability of migration of HUVECs through AKT/eNOS signaling pathway, as shown by transwell chemotactic assay (F-G) and scratch wound healing assay (H-I) (n = 6). J-K , S1PR2 inhibits the ability of angiogenic sprouting of HUVECs through AKT/eNOS signaling pathway, as shown by fibrin gel bead sprouting assay (n = 5). L and M , S1PR2 inhibits the ability of tube formation of HUVECs through AKT/eNOS signaling pathway, as shown by tube formation assay (n = 5). LY294002 (LY), AKT inhibitor. L-NAME (LN), eNOS antagonist. O/E, overexpression. SH, shRNA. Scale Bars, 200 μm. Data are mean ± SEM. n.s indicates not significant. *P < 0.05; **P < 0.01.
    Anti Enos, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti enos - by Bioz Stars, 2023-02
    96/100 stars

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    1) Product Images from "Endothelial S1pr2 regulates post-ischemic angiogenesis via AKT/eNOS signaling pathway"

    Article Title: Endothelial S1pr2 regulates post-ischemic angiogenesis via AKT/eNOS signaling pathway

    Journal: Theranostics

    doi: 10.7150/thno.71585

    S1pr2 inhibits AKT/eNOS/NO signaling pathway, and thus reduces EC migration, proliferation, and angiogenic activity. A-C. Western blotting of AKT or eNOS activation status in HUVECs and quantification in the indicated groups (n = 3). D. S1PR2 inhibits the NO production of HUVECs through AKT/eNOS signaling pathway (n = 8). E. S1PR2 inhibits the ability of proliferation of HUVECs through AKT/eNOS signaling pathway, as shown by MTT assay (n = 5). F-I, S1PR2 inhibits the ability of migration of HUVECs through AKT/eNOS signaling pathway, as shown by transwell chemotactic assay (F-G) and scratch wound healing assay (H-I) (n = 6). J-K , S1PR2 inhibits the ability of angiogenic sprouting of HUVECs through AKT/eNOS signaling pathway, as shown by fibrin gel bead sprouting assay (n = 5). L and M , S1PR2 inhibits the ability of tube formation of HUVECs through AKT/eNOS signaling pathway, as shown by tube formation assay (n = 5). LY294002 (LY), AKT inhibitor. L-NAME (LN), eNOS antagonist. O/E, overexpression. SH, shRNA. Scale Bars, 200 μm. Data are mean ± SEM. n.s indicates not significant. *P < 0.05; **P < 0.01.
    Figure Legend Snippet: S1pr2 inhibits AKT/eNOS/NO signaling pathway, and thus reduces EC migration, proliferation, and angiogenic activity. A-C. Western blotting of AKT or eNOS activation status in HUVECs and quantification in the indicated groups (n = 3). D. S1PR2 inhibits the NO production of HUVECs through AKT/eNOS signaling pathway (n = 8). E. S1PR2 inhibits the ability of proliferation of HUVECs through AKT/eNOS signaling pathway, as shown by MTT assay (n = 5). F-I, S1PR2 inhibits the ability of migration of HUVECs through AKT/eNOS signaling pathway, as shown by transwell chemotactic assay (F-G) and scratch wound healing assay (H-I) (n = 6). J-K , S1PR2 inhibits the ability of angiogenic sprouting of HUVECs through AKT/eNOS signaling pathway, as shown by fibrin gel bead sprouting assay (n = 5). L and M , S1PR2 inhibits the ability of tube formation of HUVECs through AKT/eNOS signaling pathway, as shown by tube formation assay (n = 5). LY294002 (LY), AKT inhibitor. L-NAME (LN), eNOS antagonist. O/E, overexpression. SH, shRNA. Scale Bars, 200 μm. Data are mean ± SEM. n.s indicates not significant. *P < 0.05; **P < 0.01.

    Techniques Used: Migration, Activity Assay, Western Blot, Activation Assay, MTT Assay, Chemotaxis Assay, Wound Healing Assay, Tube Formation Assay, Over Expression, shRNA

    Pharmacological inhibition of S1pr2 by JTE013 improves post-ischemic angiogenesis and enhances blood flow perfusion in hindlimbs. A , Representative laser Doppler images show improved blood flow perfusion in JTE013-treated mice compared with control mice. B, Cumulative results for control mice (n = 6) and JTE-treated mice (n = 6) are shown graphically as the ratio of blood flow in the ischemic limb to that in the non-ischemic limb at each time point. C-D, Representative images of isolectin-B4 staining of gastrocnemius muscles in control mice and JTE013-treated mice, with quantification of capillary density in gastrocnemius muscles after sham or HLI operation (n = 5). E-F, Representative images of α-SMA staining of gastrocnemius muscles in control mice and JTE013-treated mice (E) , with quantification of arteriole density in gastrocnemius muscles after sham or HLI operation (F) (n = 5). G-H, Representative images of H&E staining of gastrocnemius muscles in control mice and JTE013-treated mice (G) , with quantification of muscle fiber area after sham or HLI operation (H) (n = 5). I-J, Representative images of Sirius red-stained of gastrocnemius muscles in control mice and JTE013-treated mice (I) , with quantification of the percentage of fibrotic tissue in muscle (J) (n = 5). K-M, Functional assessment of ischemic muscle over follow-up. Cumulative results for control mice and JTE013-treated mice are shown graphically as Tarlov score (K) , ischemia score (L) , and ambulatory impairment score (M) (n = 6). N-P, Western blotting of AKT or eNOS activation status in hindlimbs of mice treated with JTE013 or DMSO and quantification in the indicated groups (n = 4). Scale Bars: C and E , 50 μm; G and I ,100 μm. Data are mean ± SEM. n.s indicates not significant. *P < 0.05; **P < 0.01.
    Figure Legend Snippet: Pharmacological inhibition of S1pr2 by JTE013 improves post-ischemic angiogenesis and enhances blood flow perfusion in hindlimbs. A , Representative laser Doppler images show improved blood flow perfusion in JTE013-treated mice compared with control mice. B, Cumulative results for control mice (n = 6) and JTE-treated mice (n = 6) are shown graphically as the ratio of blood flow in the ischemic limb to that in the non-ischemic limb at each time point. C-D, Representative images of isolectin-B4 staining of gastrocnemius muscles in control mice and JTE013-treated mice, with quantification of capillary density in gastrocnemius muscles after sham or HLI operation (n = 5). E-F, Representative images of α-SMA staining of gastrocnemius muscles in control mice and JTE013-treated mice (E) , with quantification of arteriole density in gastrocnemius muscles after sham or HLI operation (F) (n = 5). G-H, Representative images of H&E staining of gastrocnemius muscles in control mice and JTE013-treated mice (G) , with quantification of muscle fiber area after sham or HLI operation (H) (n = 5). I-J, Representative images of Sirius red-stained of gastrocnemius muscles in control mice and JTE013-treated mice (I) , with quantification of the percentage of fibrotic tissue in muscle (J) (n = 5). K-M, Functional assessment of ischemic muscle over follow-up. Cumulative results for control mice and JTE013-treated mice are shown graphically as Tarlov score (K) , ischemia score (L) , and ambulatory impairment score (M) (n = 6). N-P, Western blotting of AKT or eNOS activation status in hindlimbs of mice treated with JTE013 or DMSO and quantification in the indicated groups (n = 4). Scale Bars: C and E , 50 μm; G and I ,100 μm. Data are mean ± SEM. n.s indicates not significant. *P < 0.05; **P < 0.01.

    Techniques Used: Inhibition, Staining, Functional Assay, Western Blot, Activation Assay

    Graphic abstract shows that endothelial cell-expressing S1pr2 plays an important role in post-ischemic angiogenesis and blood flow recovery via AKT/eNOS signaling pathway in peripheral artery disease, and that EC-targeted therapy against S1pr2 might be a potential and novel intervention for patients with peripheral artery disease.
    Figure Legend Snippet: Graphic abstract shows that endothelial cell-expressing S1pr2 plays an important role in post-ischemic angiogenesis and blood flow recovery via AKT/eNOS signaling pathway in peripheral artery disease, and that EC-targeted therapy against S1pr2 might be a potential and novel intervention for patients with peripheral artery disease.

    Techniques Used: Expressing

    anti enos  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti enos
    S1pr2 <t>inhibits</t> <t>AKT/eNOS/NO</t> signaling pathway, and thus reduces EC migration, proliferation, and angiogenic activity. A-C. Western blotting of AKT or eNOS activation status in HUVECs and quantification in the indicated groups (n = 3). D. S1PR2 inhibits the NO production of HUVECs through AKT/eNOS signaling pathway (n = 8). E. S1PR2 inhibits the ability of proliferation of HUVECs through AKT/eNOS signaling pathway, as shown by MTT assay (n = 5). F-I, S1PR2 inhibits the ability of migration of HUVECs through AKT/eNOS signaling pathway, as shown by transwell chemotactic assay (F-G) and scratch wound healing assay (H-I) (n = 6). J-K , S1PR2 inhibits the ability of angiogenic sprouting of HUVECs through AKT/eNOS signaling pathway, as shown by fibrin gel bead sprouting assay (n = 5). L and M , S1PR2 inhibits the ability of tube formation of HUVECs through AKT/eNOS signaling pathway, as shown by tube formation assay (n = 5). LY294002 (LY), AKT inhibitor. L-NAME (LN), eNOS antagonist. O/E, overexpression. SH, shRNA. Scale Bars, 200 μm. Data are mean ± SEM. n.s indicates not significant. *P < 0.05; **P < 0.01.
    Anti Enos, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Endothelial S1pr2 regulates post-ischemic angiogenesis via AKT/eNOS signaling pathway"

    Article Title: Endothelial S1pr2 regulates post-ischemic angiogenesis via AKT/eNOS signaling pathway

    Journal: Theranostics

    doi: 10.7150/thno.71585

    S1pr2 inhibits AKT/eNOS/NO signaling pathway, and thus reduces EC migration, proliferation, and angiogenic activity. A-C. Western blotting of AKT or eNOS activation status in HUVECs and quantification in the indicated groups (n = 3). D. S1PR2 inhibits the NO production of HUVECs through AKT/eNOS signaling pathway (n = 8). E. S1PR2 inhibits the ability of proliferation of HUVECs through AKT/eNOS signaling pathway, as shown by MTT assay (n = 5). F-I, S1PR2 inhibits the ability of migration of HUVECs through AKT/eNOS signaling pathway, as shown by transwell chemotactic assay (F-G) and scratch wound healing assay (H-I) (n = 6). J-K , S1PR2 inhibits the ability of angiogenic sprouting of HUVECs through AKT/eNOS signaling pathway, as shown by fibrin gel bead sprouting assay (n = 5). L and M , S1PR2 inhibits the ability of tube formation of HUVECs through AKT/eNOS signaling pathway, as shown by tube formation assay (n = 5). LY294002 (LY), AKT inhibitor. L-NAME (LN), eNOS antagonist. O/E, overexpression. SH, shRNA. Scale Bars, 200 μm. Data are mean ± SEM. n.s indicates not significant. *P < 0.05; **P < 0.01.
    Figure Legend Snippet: S1pr2 inhibits AKT/eNOS/NO signaling pathway, and thus reduces EC migration, proliferation, and angiogenic activity. A-C. Western blotting of AKT or eNOS activation status in HUVECs and quantification in the indicated groups (n = 3). D. S1PR2 inhibits the NO production of HUVECs through AKT/eNOS signaling pathway (n = 8). E. S1PR2 inhibits the ability of proliferation of HUVECs through AKT/eNOS signaling pathway, as shown by MTT assay (n = 5). F-I, S1PR2 inhibits the ability of migration of HUVECs through AKT/eNOS signaling pathway, as shown by transwell chemotactic assay (F-G) and scratch wound healing assay (H-I) (n = 6). J-K , S1PR2 inhibits the ability of angiogenic sprouting of HUVECs through AKT/eNOS signaling pathway, as shown by fibrin gel bead sprouting assay (n = 5). L and M , S1PR2 inhibits the ability of tube formation of HUVECs through AKT/eNOS signaling pathway, as shown by tube formation assay (n = 5). LY294002 (LY), AKT inhibitor. L-NAME (LN), eNOS antagonist. O/E, overexpression. SH, shRNA. Scale Bars, 200 μm. Data are mean ± SEM. n.s indicates not significant. *P < 0.05; **P < 0.01.

    Techniques Used: Migration, Activity Assay, Western Blot, Activation Assay, MTT Assay, Chemotaxis Assay, Wound Healing Assay, Tube Formation Assay, Over Expression, shRNA

    Pharmacological inhibition of S1pr2 by JTE013 improves post-ischemic angiogenesis and enhances blood flow perfusion in hindlimbs. A , Representative laser Doppler images show improved blood flow perfusion in JTE013-treated mice compared with control mice. B, Cumulative results for control mice (n = 6) and JTE-treated mice (n = 6) are shown graphically as the ratio of blood flow in the ischemic limb to that in the non-ischemic limb at each time point. C-D, Representative images of isolectin-B4 staining of gastrocnemius muscles in control mice and JTE013-treated mice, with quantification of capillary density in gastrocnemius muscles after sham or HLI operation (n = 5). E-F, Representative images of α-SMA staining of gastrocnemius muscles in control mice and JTE013-treated mice (E) , with quantification of arteriole density in gastrocnemius muscles after sham or HLI operation (F) (n = 5). G-H, Representative images of H&E staining of gastrocnemius muscles in control mice and JTE013-treated mice (G) , with quantification of muscle fiber area after sham or HLI operation (H) (n = 5). I-J, Representative images of Sirius red-stained of gastrocnemius muscles in control mice and JTE013-treated mice (I) , with quantification of the percentage of fibrotic tissue in muscle (J) (n = 5). K-M, Functional assessment of ischemic muscle over follow-up. Cumulative results for control mice and JTE013-treated mice are shown graphically as Tarlov score (K) , ischemia score (L) , and ambulatory impairment score (M) (n = 6). N-P, Western blotting of AKT or eNOS activation status in hindlimbs of mice treated with JTE013 or DMSO and quantification in the indicated groups (n = 4). Scale Bars: C and E , 50 μm; G and I ,100 μm. Data are mean ± SEM. n.s indicates not significant. *P < 0.05; **P < 0.01.
    Figure Legend Snippet: Pharmacological inhibition of S1pr2 by JTE013 improves post-ischemic angiogenesis and enhances blood flow perfusion in hindlimbs. A , Representative laser Doppler images show improved blood flow perfusion in JTE013-treated mice compared with control mice. B, Cumulative results for control mice (n = 6) and JTE-treated mice (n = 6) are shown graphically as the ratio of blood flow in the ischemic limb to that in the non-ischemic limb at each time point. C-D, Representative images of isolectin-B4 staining of gastrocnemius muscles in control mice and JTE013-treated mice, with quantification of capillary density in gastrocnemius muscles after sham or HLI operation (n = 5). E-F, Representative images of α-SMA staining of gastrocnemius muscles in control mice and JTE013-treated mice (E) , with quantification of arteriole density in gastrocnemius muscles after sham or HLI operation (F) (n = 5). G-H, Representative images of H&E staining of gastrocnemius muscles in control mice and JTE013-treated mice (G) , with quantification of muscle fiber area after sham or HLI operation (H) (n = 5). I-J, Representative images of Sirius red-stained of gastrocnemius muscles in control mice and JTE013-treated mice (I) , with quantification of the percentage of fibrotic tissue in muscle (J) (n = 5). K-M, Functional assessment of ischemic muscle over follow-up. Cumulative results for control mice and JTE013-treated mice are shown graphically as Tarlov score (K) , ischemia score (L) , and ambulatory impairment score (M) (n = 6). N-P, Western blotting of AKT or eNOS activation status in hindlimbs of mice treated with JTE013 or DMSO and quantification in the indicated groups (n = 4). Scale Bars: C and E , 50 μm; G and I ,100 μm. Data are mean ± SEM. n.s indicates not significant. *P < 0.05; **P < 0.01.

    Techniques Used: Inhibition, Staining, Functional Assay, Western Blot, Activation Assay

    Graphic abstract shows that endothelial cell-expressing S1pr2 plays an important role in post-ischemic angiogenesis and blood flow recovery via AKT/eNOS signaling pathway in peripheral artery disease, and that EC-targeted therapy against S1pr2 might be a potential and novel intervention for patients with peripheral artery disease.
    Figure Legend Snippet: Graphic abstract shows that endothelial cell-expressing S1pr2 plays an important role in post-ischemic angiogenesis and blood flow recovery via AKT/eNOS signaling pathway in peripheral artery disease, and that EC-targeted therapy against S1pr2 might be a potential and novel intervention for patients with peripheral artery disease.

    Techniques Used: Expressing

    col1a1  (Cell Signaling Technology Inc)


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    S1pr2 <t>inhibits</t> <t>AKT/eNOS/NO</t> signaling pathway, and thus reduces EC migration, proliferation, and angiogenic activity. A-C. Western blotting of AKT or eNOS activation status in HUVECs and quantification in the indicated groups (n = 3). D. S1PR2 inhibits the NO production of HUVECs through AKT/eNOS signaling pathway (n = 8). E. S1PR2 inhibits the ability of proliferation of HUVECs through AKT/eNOS signaling pathway, as shown by MTT assay (n = 5). F-I, S1PR2 inhibits the ability of migration of HUVECs through AKT/eNOS signaling pathway, as shown by transwell chemotactic assay (F-G) and scratch wound healing assay (H-I) (n = 6). J-K , S1PR2 inhibits the ability of angiogenic sprouting of HUVECs through AKT/eNOS signaling pathway, as shown by fibrin gel bead sprouting assay (n = 5). L and M , S1PR2 inhibits the ability of tube formation of HUVECs through AKT/eNOS signaling pathway, as shown by tube formation assay (n = 5). LY294002 (LY), AKT inhibitor. L-NAME (LN), eNOS antagonist. O/E, overexpression. SH, shRNA. Scale Bars, 200 μm. Data are mean ± SEM. n.s indicates not significant. *P < 0.05; **P < 0.01.
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    List of primers used for real-time RT-PCR.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Metformin Protects against Oxidative Stress Injury Induced by Ischemia/Reperfusion via Regulation of the lncRNA-H19/miR-148a-3p/Rock2 Axis

    doi: 10.1155/2019/8768327

    Figure Lengend Snippet: List of primers used for real-time RT-PCR.

    Article Snippet: Membranes were probed with the primary antibodies including anti-Rock2 (9029; Cell Signaling Technology), anti-endothelial nitric oxide synthase (eNOS; 32027; Cell Signaling Technology), anti-HO-1 (43966; Cell Signaling Technology), anti-Nrf2 (ab89443; Abcam), anti-glyceraldehyde 3-phosphate dehydrogenase (GAPDH; ab181602, Abcam) antibodies.

    Techniques: Sequencing

    Inhibition of lncRNA-H19 expression influenced the effect of metformin on oxidative stress following OGD/R in vitro via regulation of Rock2/HO-1/Nrf2. (a) Activities of SOD in the supernatant of cell culture medium. (b) Levels of MDA in the supernatant of cell culture medium. (c, d) The protein expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after transfection of pcDNA3.1-NC and pcDNA3.1-H19. (e) The mRNA expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after transfection of pcDNA3.1-NC and pcDNA3.1-H19. Data are represented as mean ± SD. ∗ p < 0.05 and ∗∗∗ p < 0.001 versus the normal group by 1-way analysis of variance with Tukey's multiple comparison test. # p < 0.05, ## p < 0.01, and ### p < 0.001 versus the OGD/R group by 1-way analysis of variance with Tukey's multiple comparison test. & p < 0.05, && p < 0.01, and &&& p < 0.001 versus the OGD/R+Met+pcDNA3.1-NC group by 1-way analysis of variance with Tukey's multiple comparison test.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Metformin Protects against Oxidative Stress Injury Induced by Ischemia/Reperfusion via Regulation of the lncRNA-H19/miR-148a-3p/Rock2 Axis

    doi: 10.1155/2019/8768327

    Figure Lengend Snippet: Inhibition of lncRNA-H19 expression influenced the effect of metformin on oxidative stress following OGD/R in vitro via regulation of Rock2/HO-1/Nrf2. (a) Activities of SOD in the supernatant of cell culture medium. (b) Levels of MDA in the supernatant of cell culture medium. (c, d) The protein expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after transfection of pcDNA3.1-NC and pcDNA3.1-H19. (e) The mRNA expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after transfection of pcDNA3.1-NC and pcDNA3.1-H19. Data are represented as mean ± SD. ∗ p < 0.05 and ∗∗∗ p < 0.001 versus the normal group by 1-way analysis of variance with Tukey's multiple comparison test. # p < 0.05, ## p < 0.01, and ### p < 0.001 versus the OGD/R group by 1-way analysis of variance with Tukey's multiple comparison test. & p < 0.05, && p < 0.01, and &&& p < 0.001 versus the OGD/R+Met+pcDNA3.1-NC group by 1-way analysis of variance with Tukey's multiple comparison test.

    Article Snippet: Membranes were probed with the primary antibodies including anti-Rock2 (9029; Cell Signaling Technology), anti-endothelial nitric oxide synthase (eNOS; 32027; Cell Signaling Technology), anti-HO-1 (43966; Cell Signaling Technology), anti-Nrf2 (ab89443; Abcam), anti-glyceraldehyde 3-phosphate dehydrogenase (GAPDH; ab181602, Abcam) antibodies.

    Techniques: Inhibition, Expressing, In Vitro, Cell Culture, Transfection

    Metformin protects against oxidative stress injury induced by I/R via regulation of the lncRNA-H19/miR-148a-3p/Rock2 axis. (a) The mRNA expressions of lncRNA-H19 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. (b) The level of miR-148a-3p. (c) Statistical analysis of the percentage of infarct volume was determined for each group. (d) Neurological scores after transient middle cerebral artery occlusion (tMCAO) in each groups. (e) Activities of SOD in the serum and the brain. (f) Levels of MDA in the serum and the brain. (g) The mRNA expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. (h, i) The protein expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. ∗ p < 0:05, ∗∗ p < 0:01, and ∗∗∗ p < 0:001 versus the sham group by 1-way analysis of variance with Tukey's multiple comparison test. # p < 0:05, ## p < 0:01, and ### p < 0:01 versus the MCAO/R group by 1-way analysis of variance with Tukey's multiple comparison test. & p < 0:05, && p < 0:01, and &&& p < 0:001 versus the MCAO/R+Met+NC group by 1-way analysis of variance with Tukey's multiple comparison test.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Metformin Protects against Oxidative Stress Injury Induced by Ischemia/Reperfusion via Regulation of the lncRNA-H19/miR-148a-3p/Rock2 Axis

    doi: 10.1155/2019/8768327

    Figure Lengend Snippet: Metformin protects against oxidative stress injury induced by I/R via regulation of the lncRNA-H19/miR-148a-3p/Rock2 axis. (a) The mRNA expressions of lncRNA-H19 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. (b) The level of miR-148a-3p. (c) Statistical analysis of the percentage of infarct volume was determined for each group. (d) Neurological scores after transient middle cerebral artery occlusion (tMCAO) in each groups. (e) Activities of SOD in the serum and the brain. (f) Levels of MDA in the serum and the brain. (g) The mRNA expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. (h, i) The protein expressions of Rock2, eNOS, HO-1, and Nrf2 were determined after lateral ventricular injection of pcDNA3.1-NC and pcDNA3.1-H19. ∗ p < 0:05, ∗∗ p < 0:01, and ∗∗∗ p < 0:001 versus the sham group by 1-way analysis of variance with Tukey's multiple comparison test. # p < 0:05, ## p < 0:01, and ### p < 0:01 versus the MCAO/R group by 1-way analysis of variance with Tukey's multiple comparison test. & p < 0:05, && p < 0:01, and &&& p < 0:001 versus the MCAO/R+Met+NC group by 1-way analysis of variance with Tukey's multiple comparison test.

    Article Snippet: Membranes were probed with the primary antibodies including anti-Rock2 (9029; Cell Signaling Technology), anti-endothelial nitric oxide synthase (eNOS; 32027; Cell Signaling Technology), anti-HO-1 (43966; Cell Signaling Technology), anti-Nrf2 (ab89443; Abcam), anti-glyceraldehyde 3-phosphate dehydrogenase (GAPDH; ab181602, Abcam) antibodies.

    Techniques: Injection

    Docking results of core components and core targets.

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Network Pharmacology Prediction and Pharmacological Verification Mechanism of Yeju Jiangya Decoction on Hypertension

    doi: 10.1155/2021/5579129

    Figure Lengend Snippet: Docking results of core components and core targets.

    Article Snippet: Endothelial nitric oxide synthase (eNOS/NOS3, 32027) was purchased from Cell Signaling Technology (Danvers, USA).

    Techniques:

    Interaction diagram of chemical composition and protein. (a) NOS2 and luteolin; (b) NOS3 and luteolin; (c) NOS2 and quercetin; (d) NOS3 and quercetin.

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Network Pharmacology Prediction and Pharmacological Verification Mechanism of Yeju Jiangya Decoction on Hypertension

    doi: 10.1155/2021/5579129

    Figure Lengend Snippet: Interaction diagram of chemical composition and protein. (a) NOS2 and luteolin; (b) NOS3 and luteolin; (c) NOS2 and quercetin; (d) NOS3 and quercetin.

    Article Snippet: Endothelial nitric oxide synthase (eNOS/NOS3, 32027) was purchased from Cell Signaling Technology (Danvers, USA).

    Techniques:

    Effect of CIF on NOS3/GC α 1/cGMP/PRKG1. (a) Representative results of NOS3/sGC/PRKG1 in Western blot; (b) cGMP in the aortic homogenate for ELISA; (c–f) protein level of NOS3, GC- α 1, NOS3, GC- α 2, and PRKG1. The data were expressed as mean ± SD. # P < 0.05 and ## P < 0.01 compared with the normal control group; ∗ , P < 0.05 and ∗ , ∗ , P < 0.01 compared with the model control group.

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Network Pharmacology Prediction and Pharmacological Verification Mechanism of Yeju Jiangya Decoction on Hypertension

    doi: 10.1155/2021/5579129

    Figure Lengend Snippet: Effect of CIF on NOS3/GC α 1/cGMP/PRKG1. (a) Representative results of NOS3/sGC/PRKG1 in Western blot; (b) cGMP in the aortic homogenate for ELISA; (c–f) protein level of NOS3, GC- α 1, NOS3, GC- α 2, and PRKG1. The data were expressed as mean ± SD. # P < 0.05 and ## P < 0.01 compared with the normal control group; ∗ , P < 0.05 and ∗ , ∗ , P < 0.01 compared with the model control group.

    Article Snippet: Endothelial nitric oxide synthase (eNOS/NOS3, 32027) was purchased from Cell Signaling Technology (Danvers, USA).

    Techniques: Western Blot, Enzyme-linked Immunosorbent Assay

    CIF on the protein expressions of NOS3GC- α /cGMP/PRKG1 in immunohistochemical IHC to observe myocardial histopathological changes of aorta (×200 magnification). (a) NOS3; (b) GCal; (c) GCa2; (d) PRKG1.

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Network Pharmacology Prediction and Pharmacological Verification Mechanism of Yeju Jiangya Decoction on Hypertension

    doi: 10.1155/2021/5579129

    Figure Lengend Snippet: CIF on the protein expressions of NOS3GC- α /cGMP/PRKG1 in immunohistochemical IHC to observe myocardial histopathological changes of aorta (×200 magnification). (a) NOS3; (b) GCal; (c) GCa2; (d) PRKG1.

    Article Snippet: Endothelial nitric oxide synthase (eNOS/NOS3, 32027) was purchased from Cell Signaling Technology (Danvers, USA).

    Techniques: Immunohistochemical staining

    S1pr2 inhibits AKT/eNOS/NO signaling pathway, and thus reduces EC migration, proliferation, and angiogenic activity. A-C. Western blotting of AKT or eNOS activation status in HUVECs and quantification in the indicated groups (n = 3). D. S1PR2 inhibits the NO production of HUVECs through AKT/eNOS signaling pathway (n = 8). E. S1PR2 inhibits the ability of proliferation of HUVECs through AKT/eNOS signaling pathway, as shown by MTT assay (n = 5). F-I, S1PR2 inhibits the ability of migration of HUVECs through AKT/eNOS signaling pathway, as shown by transwell chemotactic assay (F-G) and scratch wound healing assay (H-I) (n = 6). J-K , S1PR2 inhibits the ability of angiogenic sprouting of HUVECs through AKT/eNOS signaling pathway, as shown by fibrin gel bead sprouting assay (n = 5). L and M , S1PR2 inhibits the ability of tube formation of HUVECs through AKT/eNOS signaling pathway, as shown by tube formation assay (n = 5). LY294002 (LY), AKT inhibitor. L-NAME (LN), eNOS antagonist. O/E, overexpression. SH, shRNA. Scale Bars, 200 μm. Data are mean ± SEM. n.s indicates not significant. *P < 0.05; **P < 0.01.

    Journal: Theranostics

    Article Title: Endothelial S1pr2 regulates post-ischemic angiogenesis via AKT/eNOS signaling pathway

    doi: 10.7150/thno.71585

    Figure Lengend Snippet: S1pr2 inhibits AKT/eNOS/NO signaling pathway, and thus reduces EC migration, proliferation, and angiogenic activity. A-C. Western blotting of AKT or eNOS activation status in HUVECs and quantification in the indicated groups (n = 3). D. S1PR2 inhibits the NO production of HUVECs through AKT/eNOS signaling pathway (n = 8). E. S1PR2 inhibits the ability of proliferation of HUVECs through AKT/eNOS signaling pathway, as shown by MTT assay (n = 5). F-I, S1PR2 inhibits the ability of migration of HUVECs through AKT/eNOS signaling pathway, as shown by transwell chemotactic assay (F-G) and scratch wound healing assay (H-I) (n = 6). J-K , S1PR2 inhibits the ability of angiogenic sprouting of HUVECs through AKT/eNOS signaling pathway, as shown by fibrin gel bead sprouting assay (n = 5). L and M , S1PR2 inhibits the ability of tube formation of HUVECs through AKT/eNOS signaling pathway, as shown by tube formation assay (n = 5). LY294002 (LY), AKT inhibitor. L-NAME (LN), eNOS antagonist. O/E, overexpression. SH, shRNA. Scale Bars, 200 μm. Data are mean ± SEM. n.s indicates not significant. *P < 0.05; **P < 0.01.

    Article Snippet: The primary antibodies included Anti-Phospho-AKT (CST, #4060), Anti-AKT (CST, #9272), Anti-eNOS (CST, #32027) and phospho-eNOS (Abcam, #ab184154).

    Techniques: Migration, Activity Assay, Western Blot, Activation Assay, MTT Assay, Chemotaxis Assay, Wound Healing Assay, Tube Formation Assay, Over Expression, shRNA

    Pharmacological inhibition of S1pr2 by JTE013 improves post-ischemic angiogenesis and enhances blood flow perfusion in hindlimbs. A , Representative laser Doppler images show improved blood flow perfusion in JTE013-treated mice compared with control mice. B, Cumulative results for control mice (n = 6) and JTE-treated mice (n = 6) are shown graphically as the ratio of blood flow in the ischemic limb to that in the non-ischemic limb at each time point. C-D, Representative images of isolectin-B4 staining of gastrocnemius muscles in control mice and JTE013-treated mice, with quantification of capillary density in gastrocnemius muscles after sham or HLI operation (n = 5). E-F, Representative images of α-SMA staining of gastrocnemius muscles in control mice and JTE013-treated mice (E) , with quantification of arteriole density in gastrocnemius muscles after sham or HLI operation (F) (n = 5). G-H, Representative images of H&E staining of gastrocnemius muscles in control mice and JTE013-treated mice (G) , with quantification of muscle fiber area after sham or HLI operation (H) (n = 5). I-J, Representative images of Sirius red-stained of gastrocnemius muscles in control mice and JTE013-treated mice (I) , with quantification of the percentage of fibrotic tissue in muscle (J) (n = 5). K-M, Functional assessment of ischemic muscle over follow-up. Cumulative results for control mice and JTE013-treated mice are shown graphically as Tarlov score (K) , ischemia score (L) , and ambulatory impairment score (M) (n = 6). N-P, Western blotting of AKT or eNOS activation status in hindlimbs of mice treated with JTE013 or DMSO and quantification in the indicated groups (n = 4). Scale Bars: C and E , 50 μm; G and I ,100 μm. Data are mean ± SEM. n.s indicates not significant. *P < 0.05; **P < 0.01.

    Journal: Theranostics

    Article Title: Endothelial S1pr2 regulates post-ischemic angiogenesis via AKT/eNOS signaling pathway

    doi: 10.7150/thno.71585

    Figure Lengend Snippet: Pharmacological inhibition of S1pr2 by JTE013 improves post-ischemic angiogenesis and enhances blood flow perfusion in hindlimbs. A , Representative laser Doppler images show improved blood flow perfusion in JTE013-treated mice compared with control mice. B, Cumulative results for control mice (n = 6) and JTE-treated mice (n = 6) are shown graphically as the ratio of blood flow in the ischemic limb to that in the non-ischemic limb at each time point. C-D, Representative images of isolectin-B4 staining of gastrocnemius muscles in control mice and JTE013-treated mice, with quantification of capillary density in gastrocnemius muscles after sham or HLI operation (n = 5). E-F, Representative images of α-SMA staining of gastrocnemius muscles in control mice and JTE013-treated mice (E) , with quantification of arteriole density in gastrocnemius muscles after sham or HLI operation (F) (n = 5). G-H, Representative images of H&E staining of gastrocnemius muscles in control mice and JTE013-treated mice (G) , with quantification of muscle fiber area after sham or HLI operation (H) (n = 5). I-J, Representative images of Sirius red-stained of gastrocnemius muscles in control mice and JTE013-treated mice (I) , with quantification of the percentage of fibrotic tissue in muscle (J) (n = 5). K-M, Functional assessment of ischemic muscle over follow-up. Cumulative results for control mice and JTE013-treated mice are shown graphically as Tarlov score (K) , ischemia score (L) , and ambulatory impairment score (M) (n = 6). N-P, Western blotting of AKT or eNOS activation status in hindlimbs of mice treated with JTE013 or DMSO and quantification in the indicated groups (n = 4). Scale Bars: C and E , 50 μm; G and I ,100 μm. Data are mean ± SEM. n.s indicates not significant. *P < 0.05; **P < 0.01.

    Article Snippet: The primary antibodies included Anti-Phospho-AKT (CST, #4060), Anti-AKT (CST, #9272), Anti-eNOS (CST, #32027) and phospho-eNOS (Abcam, #ab184154).

    Techniques: Inhibition, Staining, Functional Assay, Western Blot, Activation Assay

    Graphic abstract shows that endothelial cell-expressing S1pr2 plays an important role in post-ischemic angiogenesis and blood flow recovery via AKT/eNOS signaling pathway in peripheral artery disease, and that EC-targeted therapy against S1pr2 might be a potential and novel intervention for patients with peripheral artery disease.

    Journal: Theranostics

    Article Title: Endothelial S1pr2 regulates post-ischemic angiogenesis via AKT/eNOS signaling pathway

    doi: 10.7150/thno.71585

    Figure Lengend Snippet: Graphic abstract shows that endothelial cell-expressing S1pr2 plays an important role in post-ischemic angiogenesis and blood flow recovery via AKT/eNOS signaling pathway in peripheral artery disease, and that EC-targeted therapy against S1pr2 might be a potential and novel intervention for patients with peripheral artery disease.

    Article Snippet: The primary antibodies included Anti-Phospho-AKT (CST, #4060), Anti-AKT (CST, #9272), Anti-eNOS (CST, #32027) and phospho-eNOS (Abcam, #ab184154).

    Techniques: Expressing