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Effect of Corilagin on the expression of ARG1 according to <t>ELISA.</t> Data shown are the mean ± SD from 3 independent experiments. # P< 0.05 vs . normal group; *P< 0.05 VS model group; as determined by Student’s t-test; ## P< 0.01 determined by One-way ANOVA.
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Effect of Corilagin on the expression of ARG1 according to <t>ELISA.</t> Data shown are the mean ± SD from 3 independent experiments. # P< 0.05 vs . normal group; *P< 0.05 VS model group; as determined by Student’s t-test; ## P< 0.01 determined by One-way ANOVA.
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Effect of Corilagin on the expression of ARG1 according to <t>ELISA.</t> Data shown are the mean ± SD from 3 independent experiments. # P< 0.05 vs . normal group; *P< 0.05 VS model group; as determined by Student’s t-test; ## P< 0.01 determined by One-way ANOVA.
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Effect of Corilagin on the expression of ARG1 according to <t>ELISA.</t> Data shown are the mean ± SD from 3 independent experiments. # P< 0.05 vs . normal group; *P< 0.05 VS model group; as determined by Student’s t-test; ## P< 0.01 determined by One-way ANOVA.
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Fig. 4. RIPreC attenuated the phosphorylation of PDGFRα in ischemic brain tissue by reducing the blood levels of PDGF-CC. (A-C) Western blot and quantification of phosphorylated and total PDGFRα in ischemic penumbra cortex at 24 h after intravenous thrombolysis (n = 6 rats per group). Three representative samples were shown. * ** P < 0.001, two-way ANOVA. Data represent mean ± SEM. (D) <t>ELISA</t> analysis of serum PDGF-CC at 24 h after intravenous thrombolysis. (n = 6–9 rats per group). Sham rats received only anesthesia without RIC procedure, while RIPreC rats received both procedures before stroke. * ** P < 0.001, two-way ANOVA. Data represent mean ± SEM. (E) The schematic protocol for healthy rats receiving RIC treatment. Serum samples were collected at day 0 (baseline), day 1, day 7 of RIC, and 24 h after the last RIC procedure (day 8). (F) ELISA analysis of serum PDGF-CC in non-stroke rats after RIC or sham-operation (n = 8 rats per group). Sham rats received only anesthesia without RIC procedure, while RIPreC rats received both procedures. ** P < 0.01, * ** P < 0.001, two-way ANOVA. Data represent mean ± SEM. (G) The schematic protocol for healthy humans receiving 7-day RIC treatment. (H-I) ELISA analysis of serum PDGF-CC levels in 30 healthy humans. One-way ANOVA. Data represent mean ± SEM.
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Fig. 4. RIPreC attenuated the phosphorylation of PDGFRα in ischemic brain tissue by reducing the blood levels of PDGF-CC. (A-C) Western blot and quantification of phosphorylated and total PDGFRα in ischemic penumbra cortex at 24 h after intravenous thrombolysis (n = 6 rats per group). Three representative samples were shown. * ** P < 0.001, two-way ANOVA. Data represent mean ± SEM. (D) <t>ELISA</t> analysis of serum PDGF-CC at 24 h after intravenous thrombolysis. (n = 6–9 rats per group). Sham rats received only anesthesia without RIC procedure, while RIPreC rats received both procedures before stroke. * ** P < 0.001, two-way ANOVA. Data represent mean ± SEM. (E) The schematic protocol for healthy rats receiving RIC treatment. Serum samples were collected at day 0 (baseline), day 1, day 7 of RIC, and 24 h after the last RIC procedure (day 8). (F) ELISA analysis of serum PDGF-CC in non-stroke rats after RIC or sham-operation (n = 8 rats per group). Sham rats received only anesthesia without RIC procedure, while RIPreC rats received both procedures. ** P < 0.01, * ** P < 0.001, two-way ANOVA. Data represent mean ± SEM. (G) The schematic protocol for healthy humans receiving 7-day RIC treatment. (H-I) ELISA analysis of serum PDGF-CC levels in 30 healthy humans. One-way ANOVA. Data represent mean ± SEM.
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Figure 1. Harmine increases the number of preosteoclasts and the production of PDGF-BB. (A-C) qRT-PCR analysis of Atp6v0d2, Ctsk and Pdgf-bb expression levels relative to Gapdh in RAW264.7 cells treated with vehicle (DMSO), RANKL and RANKL + harmine. n = 4 per group. (D) Representative images of TRAP staining showing osteoclast and preosteoclast formation from RAW264.7 cells treated with vehicle, RANKL and RANKL + harmine. Scale bar: 50 μm. (E-F) Quantification of TRAP+ osteoclasts (OCs) and preosteoclasts (POCs). n = 3 per group. (G) Detection of PDGF-BB concentration in conditioned media (CM) from RAW264.7 cells treated with vehicle, RANKL and RANKL + harmine by <t>ELISA.</t> n = 5 per group. *P < 0.05 vs. un-induced group (RAW264.7 cells treated with harmine vehicle DMSO), # P < 0.05 vs. RANKL group (RAW264.7 cells treated with RANKL + DMSO).
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Figure 1. Harmine increases the number of preosteoclasts and the production of PDGF-BB. (A-C) qRT-PCR analysis of Atp6v0d2, Ctsk and Pdgf-bb expression levels relative to Gapdh in RAW264.7 cells treated with vehicle (DMSO), RANKL and RANKL + harmine. n = 4 per group. (D) Representative images of TRAP staining showing osteoclast and preosteoclast formation from RAW264.7 cells treated with vehicle, RANKL and RANKL + harmine. Scale bar: 50 μm. (E-F) Quantification of TRAP+ osteoclasts (OCs) and preosteoclasts (POCs). n = 3 per group. (G) Detection of PDGF-BB concentration in conditioned media (CM) from RAW264.7 cells treated with vehicle, RANKL and RANKL + harmine by <t>ELISA.</t> n = 5 per group. *P < 0.05 vs. un-induced group (RAW264.7 cells treated with harmine vehicle DMSO), # P < 0.05 vs. RANKL group (RAW264.7 cells treated with RANKL + DMSO).
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Fig. 1. (a, b, c): H&E staining of groups. Yellow arrows show thickness of uterus. (d, e, f): <t>VEGF</t> and (g, h, i):PDGF immunostaining. Black arrows show immunopositive cells. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Fig. 1. (a, b, c): H&E staining of groups. Yellow arrows show thickness of uterus. (d, e, f): <t>VEGF</t> and (g, h, i):PDGF immunostaining. Black arrows show immunopositive cells. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Fig. 1. (a, b, c): H&E staining of groups. Yellow arrows show thickness of uterus. (d, e, f): <t>VEGF</t> and (g, h, i):PDGF immunostaining. Black arrows show immunopositive cells. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Image Search Results


Effect of Corilagin on the expression of ARG1 according to ELISA. Data shown are the mean ± SD from 3 independent experiments. # P< 0.05 vs . normal group; *P< 0.05 VS model group; as determined by Student’s t-test; ## P< 0.01 determined by One-way ANOVA.

Journal: bioRxiv

Article Title: Corilagin controls post-parasiticide schistosome egg-induced liver fibrosis by inhibiting Stat6 signalling pathway

doi: 10.1101/340299

Figure Lengend Snippet: Effect of Corilagin on the expression of ARG1 according to ELISA. Data shown are the mean ± SD from 3 independent experiments. # P< 0.05 vs . normal group; *P< 0.05 VS model group; as determined by Student’s t-test; ## P< 0.01 determined by One-way ANOVA.

Article Snippet: The Mouse ARG1, Fizz1, Ym1, TGFβ and PDGF ELISA kits were purchased from Elabscience Biotechnology Co., Ltd (Wuhan, China).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay

Effect of Corilagin on expression of PDGF, Fizz1, Ym1, and TGFβ according to ELISA. Data shown are the mean ± SD from 6 experiment mice. # P< 0.05, ## P< 0.01 vs . normal group; *P< 0.05, ** P< 0.01 VS model group; As determined by Student’s t-test; ### P< 0.01 determined by One-way ANOVA.

Journal: bioRxiv

Article Title: Corilagin controls post-parasiticide schistosome egg-induced liver fibrosis by inhibiting Stat6 signalling pathway

doi: 10.1101/340299

Figure Lengend Snippet: Effect of Corilagin on expression of PDGF, Fizz1, Ym1, and TGFβ according to ELISA. Data shown are the mean ± SD from 6 experiment mice. # P< 0.05, ## P< 0.01 vs . normal group; *P< 0.05, ** P< 0.01 VS model group; As determined by Student’s t-test; ### P< 0.01 determined by One-way ANOVA.

Article Snippet: The Mouse ARG1, Fizz1, Ym1, TGFβ and PDGF ELISA kits were purchased from Elabscience Biotechnology Co., Ltd (Wuhan, China).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay

Fig. 4. RIPreC attenuated the phosphorylation of PDGFRα in ischemic brain tissue by reducing the blood levels of PDGF-CC. (A-C) Western blot and quantification of phosphorylated and total PDGFRα in ischemic penumbra cortex at 24 h after intravenous thrombolysis (n = 6 rats per group). Three representative samples were shown. * ** P < 0.001, two-way ANOVA. Data represent mean ± SEM. (D) ELISA analysis of serum PDGF-CC at 24 h after intravenous thrombolysis. (n = 6–9 rats per group). Sham rats received only anesthesia without RIC procedure, while RIPreC rats received both procedures before stroke. * ** P < 0.001, two-way ANOVA. Data represent mean ± SEM. (E) The schematic protocol for healthy rats receiving RIC treatment. Serum samples were collected at day 0 (baseline), day 1, day 7 of RIC, and 24 h after the last RIC procedure (day 8). (F) ELISA analysis of serum PDGF-CC in non-stroke rats after RIC or sham-operation (n = 8 rats per group). Sham rats received only anesthesia without RIC procedure, while RIPreC rats received both procedures. ** P < 0.01, * ** P < 0.001, two-way ANOVA. Data represent mean ± SEM. (G) The schematic protocol for healthy humans receiving 7-day RIC treatment. (H-I) ELISA analysis of serum PDGF-CC levels in 30 healthy humans. One-way ANOVA. Data represent mean ± SEM.

Journal: Pharmacological research

Article Title: Remote ischemic conditioning attenuates blood-brain barrier disruption after recombinant tissue plasminogen activator treatment via reducing PDGF-CC.

doi: 10.1016/j.phrs.2022.106641

Figure Lengend Snippet: Fig. 4. RIPreC attenuated the phosphorylation of PDGFRα in ischemic brain tissue by reducing the blood levels of PDGF-CC. (A-C) Western blot and quantification of phosphorylated and total PDGFRα in ischemic penumbra cortex at 24 h after intravenous thrombolysis (n = 6 rats per group). Three representative samples were shown. * ** P < 0.001, two-way ANOVA. Data represent mean ± SEM. (D) ELISA analysis of serum PDGF-CC at 24 h after intravenous thrombolysis. (n = 6–9 rats per group). Sham rats received only anesthesia without RIC procedure, while RIPreC rats received both procedures before stroke. * ** P < 0.001, two-way ANOVA. Data represent mean ± SEM. (E) The schematic protocol for healthy rats receiving RIC treatment. Serum samples were collected at day 0 (baseline), day 1, day 7 of RIC, and 24 h after the last RIC procedure (day 8). (F) ELISA analysis of serum PDGF-CC in non-stroke rats after RIC or sham-operation (n = 8 rats per group). Sham rats received only anesthesia without RIC procedure, while RIPreC rats received both procedures. ** P < 0.01, * ** P < 0.001, two-way ANOVA. Data represent mean ± SEM. (G) The schematic protocol for healthy humans receiving 7-day RIC treatment. (H-I) ELISA analysis of serum PDGF-CC levels in 30 healthy humans. One-way ANOVA. Data represent mean ± SEM.

Article Snippet: The rat PDGF-CC protein level was measured using a rat PDGF-CC ELISA kit (CSB-EL017710RA; Cusabio, Houston, TX, USA).

Techniques: Phospho-proteomics, Western Blot, Enzyme-linked Immunosorbent Assay

Fig. 6. RIC reduces circulating PDGF-CC levels by reducing the PDGF-CC level in the skeletal muscle from RIC-treated hindlimbs and blood platelets. (A-C) Western blot and qRT-PCR analysis of Hif-1α levels in the hindlimbs skeletal muscles receiving RIC or sham procedure. Healthy rats received RIC or sham operation for 7 days and the skeletal muscles from the treated hindlimbs were harvested 24 h after the last round of RIC. Three representative samples were shown (n = 6 rats per group). * P < 0.05, unpaired t-test. Data represent mean ± SEM. (D-F) Western blot analysis of PDGF-CC levels in the skeletal muscles of the hindlimbs receiving RIC or sham procedure (n = 8 rats per group). Three representative samples were shown. Unpaired t-test, * ** P < 0.001. Data represent mean ± SEM. (G-H) ELISA and qRT-PCR analysis of PDGF-CC protein and Pdgfc mRNA levels in the hindlimbs skeletal muscles receiving RIC or sham procedure (n = 8 rats per group) * P < 0.05, * * P < 0.01, unpaired t-test. Data represent mean ± SEM. (I-J) Platelets analysis from blood routine examination in rats received RIC or sham procedure. The blood samples were obtained via inferior vena cava of rats which received a 7-day RIC or sham operation (n = 9 rats per group). Unpaired t-test, * P < 0.05. Data represent mean ± SEM. (K-L) ELISA analysis of PDGF-CC level from platelets or plasma in healthy rats after RIC or sham operation (n = 10 rats per group). Unpaired t-test, * P < 0⋅05. Data represent mean ± SEM. (M) ELISA analysis of PDGF-CC level from indicated tissues harvested from healthy rats after RIC or sham operation (n = 6 rats per group). * ** P < 0.001, Unpaired t-test. Data represent mean ± SEM.

Journal: Pharmacological research

Article Title: Remote ischemic conditioning attenuates blood-brain barrier disruption after recombinant tissue plasminogen activator treatment via reducing PDGF-CC.

doi: 10.1016/j.phrs.2022.106641

Figure Lengend Snippet: Fig. 6. RIC reduces circulating PDGF-CC levels by reducing the PDGF-CC level in the skeletal muscle from RIC-treated hindlimbs and blood platelets. (A-C) Western blot and qRT-PCR analysis of Hif-1α levels in the hindlimbs skeletal muscles receiving RIC or sham procedure. Healthy rats received RIC or sham operation for 7 days and the skeletal muscles from the treated hindlimbs were harvested 24 h after the last round of RIC. Three representative samples were shown (n = 6 rats per group). * P < 0.05, unpaired t-test. Data represent mean ± SEM. (D-F) Western blot analysis of PDGF-CC levels in the skeletal muscles of the hindlimbs receiving RIC or sham procedure (n = 8 rats per group). Three representative samples were shown. Unpaired t-test, * ** P < 0.001. Data represent mean ± SEM. (G-H) ELISA and qRT-PCR analysis of PDGF-CC protein and Pdgfc mRNA levels in the hindlimbs skeletal muscles receiving RIC or sham procedure (n = 8 rats per group) * P < 0.05, * * P < 0.01, unpaired t-test. Data represent mean ± SEM. (I-J) Platelets analysis from blood routine examination in rats received RIC or sham procedure. The blood samples were obtained via inferior vena cava of rats which received a 7-day RIC or sham operation (n = 9 rats per group). Unpaired t-test, * P < 0.05. Data represent mean ± SEM. (K-L) ELISA analysis of PDGF-CC level from platelets or plasma in healthy rats after RIC or sham operation (n = 10 rats per group). Unpaired t-test, * P < 0⋅05. Data represent mean ± SEM. (M) ELISA analysis of PDGF-CC level from indicated tissues harvested from healthy rats after RIC or sham operation (n = 6 rats per group). * ** P < 0.001, Unpaired t-test. Data represent mean ± SEM.

Article Snippet: The rat PDGF-CC protein level was measured using a rat PDGF-CC ELISA kit (CSB-EL017710RA; Cusabio, Houston, TX, USA).

Techniques: Western Blot, Quantitative RT-PCR, Muscles, Enzyme-linked Immunosorbent Assay, Clinical Proteomics

Fig. 7. The protective effect of RIPostC on BBB integrity was also dependent on reduction of the blood PDGF-CC levels. (A) The schematic protocol for RIPostC intervention in rats with embolic stroke. (B-C) Representative images of TTC staining at 72 h after intravenous thrombolysis (n = 8 rats per group). Sham rats received only anesthesia without RIC procedure, while RIPostC rats received both procedures after thrombolysis. * P < 0.05, unpaired t-test. Data represent mean ± SEM. (D) Neurological deficit score at 1 and 3 days after intravenous thrombolysis (n = 10 rats per group). * P < 0.05, two-way ANOVA. Data represent mean ± SEM. (E) qRT-PCR analysis of IL-1β, IL-6, and TNF-α mRNA levels. (n = 8 rats per group). * * P < 0.01, * ** P < 0.001, unpaired t-test. Data represent mean ± SEM. (F) ELISA analysis of serum PDGF-CC (n = 10 rats per group). * * P < 0.01, two-way ANOVA. Data represent mean ± SEM. (G-H) Evans blue leakage at 72 h post intravenous thrombolysis. Recombinant PDGF-CC or normal saline were intravenously injected before and at 24 h and 48 h after thrombolysis (n = 9 rats per group). * P < 0.05, * * P < 0.01, one-way ANOVA. Data represent mean ± SEM. (I-J) The schematic protocol and ELISA analysis for RIPostC intervention in AIS patients with intravenous thrombolysis. Participants received two administrations of RIPostC (22 patients) or sham (20 patients) treatment at 6 h for the first round and 18 h for the second round after intravenous thrombolysis. Unpaired t-test. Data represent mean ± SEM.

Journal: Pharmacological research

Article Title: Remote ischemic conditioning attenuates blood-brain barrier disruption after recombinant tissue plasminogen activator treatment via reducing PDGF-CC.

doi: 10.1016/j.phrs.2022.106641

Figure Lengend Snippet: Fig. 7. The protective effect of RIPostC on BBB integrity was also dependent on reduction of the blood PDGF-CC levels. (A) The schematic protocol for RIPostC intervention in rats with embolic stroke. (B-C) Representative images of TTC staining at 72 h after intravenous thrombolysis (n = 8 rats per group). Sham rats received only anesthesia without RIC procedure, while RIPostC rats received both procedures after thrombolysis. * P < 0.05, unpaired t-test. Data represent mean ± SEM. (D) Neurological deficit score at 1 and 3 days after intravenous thrombolysis (n = 10 rats per group). * P < 0.05, two-way ANOVA. Data represent mean ± SEM. (E) qRT-PCR analysis of IL-1β, IL-6, and TNF-α mRNA levels. (n = 8 rats per group). * * P < 0.01, * ** P < 0.001, unpaired t-test. Data represent mean ± SEM. (F) ELISA analysis of serum PDGF-CC (n = 10 rats per group). * * P < 0.01, two-way ANOVA. Data represent mean ± SEM. (G-H) Evans blue leakage at 72 h post intravenous thrombolysis. Recombinant PDGF-CC or normal saline were intravenously injected before and at 24 h and 48 h after thrombolysis (n = 9 rats per group). * P < 0.05, * * P < 0.01, one-way ANOVA. Data represent mean ± SEM. (I-J) The schematic protocol and ELISA analysis for RIPostC intervention in AIS patients with intravenous thrombolysis. Participants received two administrations of RIPostC (22 patients) or sham (20 patients) treatment at 6 h for the first round and 18 h for the second round after intravenous thrombolysis. Unpaired t-test. Data represent mean ± SEM.

Article Snippet: The rat PDGF-CC protein level was measured using a rat PDGF-CC ELISA kit (CSB-EL017710RA; Cusabio, Houston, TX, USA).

Techniques: Staining, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Recombinant, Saline, Injection

Figure 1. Harmine increases the number of preosteoclasts and the production of PDGF-BB. (A-C) qRT-PCR analysis of Atp6v0d2, Ctsk and Pdgf-bb expression levels relative to Gapdh in RAW264.7 cells treated with vehicle (DMSO), RANKL and RANKL + harmine. n = 4 per group. (D) Representative images of TRAP staining showing osteoclast and preosteoclast formation from RAW264.7 cells treated with vehicle, RANKL and RANKL + harmine. Scale bar: 50 μm. (E-F) Quantification of TRAP+ osteoclasts (OCs) and preosteoclasts (POCs). n = 3 per group. (G) Detection of PDGF-BB concentration in conditioned media (CM) from RAW264.7 cells treated with vehicle, RANKL and RANKL + harmine by ELISA. n = 5 per group. *P < 0.05 vs. un-induced group (RAW264.7 cells treated with harmine vehicle DMSO), # P < 0.05 vs. RANKL group (RAW264.7 cells treated with RANKL + DMSO).

Journal: Theranostics

Article Title: Harmine enhances type H vessel formation and prevents bone loss in ovariectomized mice.

doi: 10.7150/thno.22144

Figure Lengend Snippet: Figure 1. Harmine increases the number of preosteoclasts and the production of PDGF-BB. (A-C) qRT-PCR analysis of Atp6v0d2, Ctsk and Pdgf-bb expression levels relative to Gapdh in RAW264.7 cells treated with vehicle (DMSO), RANKL and RANKL + harmine. n = 4 per group. (D) Representative images of TRAP staining showing osteoclast and preosteoclast formation from RAW264.7 cells treated with vehicle, RANKL and RANKL + harmine. Scale bar: 50 μm. (E-F) Quantification of TRAP+ osteoclasts (OCs) and preosteoclasts (POCs). n = 3 per group. (G) Detection of PDGF-BB concentration in conditioned media (CM) from RAW264.7 cells treated with vehicle, RANKL and RANKL + harmine by ELISA. n = 5 per group. *P < 0.05 vs. un-induced group (RAW264.7 cells treated with harmine vehicle DMSO), # P < 0.05 vs. RANKL group (RAW264.7 cells treated with RANKL + DMSO).

Article Snippet: The concentrations of PDGF-BB and VEGF in the supernatant of bone marrow or in the CM were measured using a commercial Mouse PDGF-BB ELISA Kit (Cusabio, Wuhan, China) and a Mouse VEGF ELISA Kit (Multi Sciences LTD., Hangzhou, China) according to the protocol provided by the manufacturer.

Techniques: Quantitative RT-PCR, Expressing, Staining, Concentration Assay, Enzyme-linked Immunosorbent Assay

Figure 6. Harmine emulsion induces type H vessel formation and PDGF-BB production in OVX mice. (A) Representative images of CD31 (red) and Emcn (green) immunostaining in femora from sham, OVX and OVX + harmine mice. BM: bone marrow; GP: growth plate; TB: trabecular bone. Scale bar: 100 µm. (B) Quantification of the ratio of type H vessel (HV; yellow) in different treatment groups. n = 4 per group. TV: total vessels. (C-D) Bone marrow concentrations of PDGF-BB and VEGF from sham, OVX and OVX + harmine mice were detected by ELISA. n = 4 per group. *P < 0.05 vs. sham group, # P < 0.05 vs. OVX group.

Journal: Theranostics

Article Title: Harmine enhances type H vessel formation and prevents bone loss in ovariectomized mice.

doi: 10.7150/thno.22144

Figure Lengend Snippet: Figure 6. Harmine emulsion induces type H vessel formation and PDGF-BB production in OVX mice. (A) Representative images of CD31 (red) and Emcn (green) immunostaining in femora from sham, OVX and OVX + harmine mice. BM: bone marrow; GP: growth plate; TB: trabecular bone. Scale bar: 100 µm. (B) Quantification of the ratio of type H vessel (HV; yellow) in different treatment groups. n = 4 per group. TV: total vessels. (C-D) Bone marrow concentrations of PDGF-BB and VEGF from sham, OVX and OVX + harmine mice were detected by ELISA. n = 4 per group. *P < 0.05 vs. sham group, # P < 0.05 vs. OVX group.

Article Snippet: The concentrations of PDGF-BB and VEGF in the supernatant of bone marrow or in the CM were measured using a commercial Mouse PDGF-BB ELISA Kit (Cusabio, Wuhan, China) and a Mouse VEGF ELISA Kit (Multi Sciences LTD., Hangzhou, China) according to the protocol provided by the manufacturer.

Techniques: Emulsion, Immunostaining, Enzyme-linked Immunosorbent Assay

Fig. 1. (a, b, c): H&E staining of groups. Yellow arrows show thickness of uterus. (d, e, f): VEGF and (g, h, i):PDGF immunostaining. Black arrows show immunopositive cells. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: Taiwanese journal of obstetrics & gynecology

Article Title: The role of resveratrol on full - Thickness uterine wound healing in rats.

doi: 10.1016/j.tjog.2017.08.015

Figure Lengend Snippet: Fig. 1. (a, b, c): H&E staining of groups. Yellow arrows show thickness of uterus. (d, e, f): VEGF and (g, h, i):PDGF immunostaining. Black arrows show immunopositive cells. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: Enzyme-linked immunosorbent assay (ELISA) kits were used to evaluate vascular endothelial growth factor (CUSABIO, CSBE04757r, limit determination 3.9 pg/mle250 pg/ml) and plateletderived growth factor (CUSABIO, CSB-E14313r, limit determination 0.312 pg/mle20 pg/ml) levels in homogenized tissue.

Techniques: Staining, Immunostaining

Fig. 3. (A) VEGF level and (B) PDGF level of groups. Data are means ± SD; VEGF level *p < 0.05 compared to Control group, #p < 0.05 compared to Injury group. PDGF level *p < 0.05 compared to Control group, #p < 0.05 compared to Injury group.

Journal: Taiwanese journal of obstetrics & gynecology

Article Title: The role of resveratrol on full - Thickness uterine wound healing in rats.

doi: 10.1016/j.tjog.2017.08.015

Figure Lengend Snippet: Fig. 3. (A) VEGF level and (B) PDGF level of groups. Data are means ± SD; VEGF level *p < 0.05 compared to Control group, #p < 0.05 compared to Injury group. PDGF level *p < 0.05 compared to Control group, #p < 0.05 compared to Injury group.

Article Snippet: Enzyme-linked immunosorbent assay (ELISA) kits were used to evaluate vascular endothelial growth factor (CUSABIO, CSBE04757r, limit determination 3.9 pg/mle250 pg/ml) and plateletderived growth factor (CUSABIO, CSB-E14313r, limit determination 0.312 pg/mle20 pg/ml) levels in homogenized tissue.

Techniques: Control