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mouse s1p k 1900 echelon  (Echelon Biosciences)


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    Structured Review

    Echelon Biosciences mouse s1p k 1900 echelon
    A CD45.1 + and irradiated CD45.2 + mice were surgically jointed from olecranon to knee joint and recovered for 4 weeks to establish blood chimerism. Subsequently, CD45.1 + mice were treated with HDM as Fig. . B The percentages and the numbers of ST2 – KLRG1 + IL-17RB + ml-ILC2s in siLP of CD45.1 + and CD45.2 + were analyzed on day 30. Cells were gated on CD45.1 + lineage – CD90.2 + NK1.1 – NKp46 – GATA3 + . For in vivo imaging experiments, mice were treated with HDM to establish the asthma relapse model as portrayed in Fig. . C On day 30 (remission), ST2 – KLRG1 + IL-17RB + ILC2s were sorted from siLP and stained with 5 mM Xenolight DiR, and then injected intravenously (5 × 10 5 cells/each) into various groups of mice. Specifically, mice in DiR- group were injected with unstained cells. For the remission + CCX282-B group, recipient mice resting from asthma symptoms were treated with the CCR9 antagonist CCX282-B at 50 mg/kg (daily injection subcutaneously) from day 24 to day 30. For the remission + Etrolizumab group, recipient mice resting from asthma symptoms were treated with the anti-α4β7 monoclonal antibody Etrolizumab at 5 mg/kg (injection intravenously) on day 24, 26, 28 and 30. For the relapse group, mice in remission were injected with DiR-stained cells, followed with treatment of HDM at 50 μg intranasally for 2 times once per hour. Mice in the relapse + FTY720 group received intravenous injection of FTY720 along with 2-time intranasal administration of HDM. Mice in all groups were imaged 2 hours post cell injection, and organs including lungs, spleen, liver, SI and large intestine were then rapidly harvested and imaged. D <t>S1P</t> expression in plasma collected from mice post asthma relapse (D34, D37 and D40) was measured by ELISA. The S1P signaling antagonist FTY720 was administered intraperitoneally to asthmatic mice on days 31 to 33 for 3 times. E The percentages and the numbers of ST2 – KLRG1 + IL-17RB + ILC2s in lungs were detected on D34. F Histological examination of lungs by hematoxylin-eosin staining. Magnification: ×200, scale bar = 100 μm. G Protein levels of IL-13 in lungs was detected by ELISA. Results are representative of three independent experiments. Means ± SD from 6 mice for each group. Statistical comparison was conducted using unpaired, two-sided Welch’s t test for B and unpaired one-way ANOVA with Dunnett’s test for the rest. p values are shown on the graphs. Source data are provided as a Source Data file. Fig. 3A Created with BioRender.com released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International license https://creativecommons.org/licenses/by-nc-nd/4.0/deed.en .
    Mouse S1p K 1900 Echelon, supplied by Echelon Biosciences, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "TCF-1 and TOX regulate the memory formation of intestinal group 2 innate lymphoid cells in asthma"

    Article Title: TCF-1 and TOX regulate the memory formation of intestinal group 2 innate lymphoid cells in asthma

    Journal: Nature Communications

    doi: 10.1038/s41467-024-52252-2

    A CD45.1 + and irradiated CD45.2 + mice were surgically jointed from olecranon to knee joint and recovered for 4 weeks to establish blood chimerism. Subsequently, CD45.1 + mice were treated with HDM as Fig. . B The percentages and the numbers of ST2 – KLRG1 + IL-17RB + ml-ILC2s in siLP of CD45.1 + and CD45.2 + were analyzed on day 30. Cells were gated on CD45.1 + lineage – CD90.2 + NK1.1 – NKp46 – GATA3 + . For in vivo imaging experiments, mice were treated with HDM to establish the asthma relapse model as portrayed in Fig. . C On day 30 (remission), ST2 – KLRG1 + IL-17RB + ILC2s were sorted from siLP and stained with 5 mM Xenolight DiR, and then injected intravenously (5 × 10 5 cells/each) into various groups of mice. Specifically, mice in DiR- group were injected with unstained cells. For the remission + CCX282-B group, recipient mice resting from asthma symptoms were treated with the CCR9 antagonist CCX282-B at 50 mg/kg (daily injection subcutaneously) from day 24 to day 30. For the remission + Etrolizumab group, recipient mice resting from asthma symptoms were treated with the anti-α4β7 monoclonal antibody Etrolizumab at 5 mg/kg (injection intravenously) on day 24, 26, 28 and 30. For the relapse group, mice in remission were injected with DiR-stained cells, followed with treatment of HDM at 50 μg intranasally for 2 times once per hour. Mice in the relapse + FTY720 group received intravenous injection of FTY720 along with 2-time intranasal administration of HDM. Mice in all groups were imaged 2 hours post cell injection, and organs including lungs, spleen, liver, SI and large intestine were then rapidly harvested and imaged. D S1P expression in plasma collected from mice post asthma relapse (D34, D37 and D40) was measured by ELISA. The S1P signaling antagonist FTY720 was administered intraperitoneally to asthmatic mice on days 31 to 33 for 3 times. E The percentages and the numbers of ST2 – KLRG1 + IL-17RB + ILC2s in lungs were detected on D34. F Histological examination of lungs by hematoxylin-eosin staining. Magnification: ×200, scale bar = 100 μm. G Protein levels of IL-13 in lungs was detected by ELISA. Results are representative of three independent experiments. Means ± SD from 6 mice for each group. Statistical comparison was conducted using unpaired, two-sided Welch’s t test for B and unpaired one-way ANOVA with Dunnett’s test for the rest. p values are shown on the graphs. Source data are provided as a Source Data file. Fig. 3A Created with BioRender.com released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International license https://creativecommons.org/licenses/by-nc-nd/4.0/deed.en .
    Figure Legend Snippet: A CD45.1 + and irradiated CD45.2 + mice were surgically jointed from olecranon to knee joint and recovered for 4 weeks to establish blood chimerism. Subsequently, CD45.1 + mice were treated with HDM as Fig. . B The percentages and the numbers of ST2 – KLRG1 + IL-17RB + ml-ILC2s in siLP of CD45.1 + and CD45.2 + were analyzed on day 30. Cells were gated on CD45.1 + lineage – CD90.2 + NK1.1 – NKp46 – GATA3 + . For in vivo imaging experiments, mice were treated with HDM to establish the asthma relapse model as portrayed in Fig. . C On day 30 (remission), ST2 – KLRG1 + IL-17RB + ILC2s were sorted from siLP and stained with 5 mM Xenolight DiR, and then injected intravenously (5 × 10 5 cells/each) into various groups of mice. Specifically, mice in DiR- group were injected with unstained cells. For the remission + CCX282-B group, recipient mice resting from asthma symptoms were treated with the CCR9 antagonist CCX282-B at 50 mg/kg (daily injection subcutaneously) from day 24 to day 30. For the remission + Etrolizumab group, recipient mice resting from asthma symptoms were treated with the anti-α4β7 monoclonal antibody Etrolizumab at 5 mg/kg (injection intravenously) on day 24, 26, 28 and 30. For the relapse group, mice in remission were injected with DiR-stained cells, followed with treatment of HDM at 50 μg intranasally for 2 times once per hour. Mice in the relapse + FTY720 group received intravenous injection of FTY720 along with 2-time intranasal administration of HDM. Mice in all groups were imaged 2 hours post cell injection, and organs including lungs, spleen, liver, SI and large intestine were then rapidly harvested and imaged. D S1P expression in plasma collected from mice post asthma relapse (D34, D37 and D40) was measured by ELISA. The S1P signaling antagonist FTY720 was administered intraperitoneally to asthmatic mice on days 31 to 33 for 3 times. E The percentages and the numbers of ST2 – KLRG1 + IL-17RB + ILC2s in lungs were detected on D34. F Histological examination of lungs by hematoxylin-eosin staining. Magnification: ×200, scale bar = 100 μm. G Protein levels of IL-13 in lungs was detected by ELISA. Results are representative of three independent experiments. Means ± SD from 6 mice for each group. Statistical comparison was conducted using unpaired, two-sided Welch’s t test for B and unpaired one-way ANOVA with Dunnett’s test for the rest. p values are shown on the graphs. Source data are provided as a Source Data file. Fig. 3A Created with BioRender.com released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International license https://creativecommons.org/licenses/by-nc-nd/4.0/deed.en .

    Techniques Used: Irradiation, In Vivo Imaging, Staining, Injection, Expressing, Enzyme-linked Immunosorbent Assay, Comparison



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    A CD45.1 + and irradiated CD45.2 + mice were surgically jointed from olecranon to knee joint and recovered for 4 weeks to establish blood chimerism. Subsequently, CD45.1 + mice were treated with HDM as Fig. . B The percentages and the numbers of ST2 – KLRG1 + IL-17RB + ml-ILC2s in siLP of CD45.1 + and CD45.2 + were analyzed on day 30. Cells were gated on CD45.1 + lineage – CD90.2 + NK1.1 – NKp46 – GATA3 + . For in vivo imaging experiments, mice were treated with HDM to establish the asthma relapse model as portrayed in Fig. . C On day 30 (remission), ST2 – KLRG1 + IL-17RB + ILC2s were sorted from siLP and stained with 5 mM Xenolight DiR, and then injected intravenously (5 × 10 5 cells/each) into various groups of mice. Specifically, mice in DiR- group were injected with unstained cells. For the remission + CCX282-B group, recipient mice resting from asthma symptoms were treated with the CCR9 antagonist CCX282-B at 50 mg/kg (daily injection subcutaneously) from day 24 to day 30. For the remission + Etrolizumab group, recipient mice resting from asthma symptoms were treated with the anti-α4β7 monoclonal antibody Etrolizumab at 5 mg/kg (injection intravenously) on day 24, 26, 28 and 30. For the relapse group, mice in remission were injected with DiR-stained cells, followed with treatment of HDM at 50 μg intranasally for 2 times once per hour. Mice in the relapse + FTY720 group received intravenous injection of FTY720 along with 2-time intranasal administration of HDM. Mice in all groups were imaged 2 hours post cell injection, and organs including lungs, spleen, liver, SI and large intestine were then rapidly harvested and imaged. D <t>S1P</t> expression in plasma collected from mice post asthma relapse (D34, D37 and D40) was measured by ELISA. The S1P signaling antagonist FTY720 was administered intraperitoneally to asthmatic mice on days 31 to 33 for 3 times. E The percentages and the numbers of ST2 – KLRG1 + IL-17RB + ILC2s in lungs were detected on D34. F Histological examination of lungs by hematoxylin-eosin staining. Magnification: ×200, scale bar = 100 μm. G Protein levels of IL-13 in lungs was detected by ELISA. Results are representative of three independent experiments. Means ± SD from 6 mice for each group. Statistical comparison was conducted using unpaired, two-sided Welch’s t test for B and unpaired one-way ANOVA with Dunnett’s test for the rest. p values are shown on the graphs. Source data are provided as a Source Data file. Fig. 3A Created with BioRender.com released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International license https://creativecommons.org/licenses/by-nc-nd/4.0/deed.en .
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    <t>S1P</t> is involved in the process of heart ischemia/reperfusion injury. a Dot plot showed the individual lipids in the plasma of mice after cardiac ischemia-reperfusion (I/R) injury (45 min of ischemia/6 h of reperfusion) expressed as log 2 (fold change) versus the plasma of the control mice after sham operations (n = 3 per group). The dashed red box highlights sphingosine lipids that are down-regulated after cardiac I/R. b-c Sphingosine 1-Phosphate (S1P) concentrations in the plasma of the mice after cardiac I/R injury (45 min of ischemia/6 h of reperfusion) compared to the mice after sham operations by <t>ELISA</t> (n = 8 per group) ( b ), and the S1P concentrations in the plasma of patients diagnosed with coronary heart disease (CHD) at 24 h after coronary angiography procedures (CAG-24h, n = 17 per group) or percutaneous coronary intervention (PCI-24h, n = 28 per group) by ELISA ( c ). d The plasma S1P concentration in the mice after S1P lyase inhibitor 2-Acetyl-5-tetrahydroxybutyl Imidazole (THI) treatment compared to control mice by ELISA (n = 6 per group). e Representative images of evans blue/triphenyl-2H-tetrazolium chloride (TTC) staining of heart tissue sections collected from mice treated with PBS or THI after I/R injury (45 min of ischemia/24 h of reperfusion), with their quantification of the infarct area (IF), at-risk area (AAR), and left ventricle (LV) (n = 6 per group). f Serum LDH (lactate dehydrogenase) levels of mice treated with PBS or THI after cardiac I/R injury (45 min of ischemia/24 h of reperfusion) were measured (n = 6 per group). g The plasma S1P concentration of mice in the indicated groups by ELISA (n = 6 per group). h Representative images of evans blue/TTC-staining of heart tissue sections collected from WT or S1pr1 ECKO mice treated with PBS or THI after cardiac I/R injury (45 min of ischemia/24 h of reperfusion), with their quantification of the infarct area (IF), at-risk area (AAR), and left ventricle (LV) area (n = 5–6 per group). i Serum LDH levels of WT or S1pr1 ECKO mice treated with PBS or THI after cardiac I/R injury (45 min of ischemia/24 h of reperfusion) were measured (n = 6 per group). Data were shown as mean ± SEM. n.s. indicated not significant. Scale bars: e and h , 2 mm. Unpaired Student's t-test ( b , c , d , e and f ). One-way ANOVA ( g , h and i ).
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    A CD45.1 + and irradiated CD45.2 + mice were surgically jointed from olecranon to knee joint and recovered for 4 weeks to establish blood chimerism. Subsequently, CD45.1 + mice were treated with HDM as Fig. . B The percentages and the numbers of ST2 – KLRG1 + IL-17RB + ml-ILC2s in siLP of CD45.1 + and CD45.2 + were analyzed on day 30. Cells were gated on CD45.1 + lineage – CD90.2 + NK1.1 – NKp46 – GATA3 + . For in vivo imaging experiments, mice were treated with HDM to establish the asthma relapse model as portrayed in Fig. . C On day 30 (remission), ST2 – KLRG1 + IL-17RB + ILC2s were sorted from siLP and stained with 5 mM Xenolight DiR, and then injected intravenously (5 × 10 5 cells/each) into various groups of mice. Specifically, mice in DiR- group were injected with unstained cells. For the remission + CCX282-B group, recipient mice resting from asthma symptoms were treated with the CCR9 antagonist CCX282-B at 50 mg/kg (daily injection subcutaneously) from day 24 to day 30. For the remission + Etrolizumab group, recipient mice resting from asthma symptoms were treated with the anti-α4β7 monoclonal antibody Etrolizumab at 5 mg/kg (injection intravenously) on day 24, 26, 28 and 30. For the relapse group, mice in remission were injected with DiR-stained cells, followed with treatment of HDM at 50 μg intranasally for 2 times once per hour. Mice in the relapse + FTY720 group received intravenous injection of FTY720 along with 2-time intranasal administration of HDM. Mice in all groups were imaged 2 hours post cell injection, and organs including lungs, spleen, liver, SI and large intestine were then rapidly harvested and imaged. D S1P expression in plasma collected from mice post asthma relapse (D34, D37 and D40) was measured by ELISA. The S1P signaling antagonist FTY720 was administered intraperitoneally to asthmatic mice on days 31 to 33 for 3 times. E The percentages and the numbers of ST2 – KLRG1 + IL-17RB + ILC2s in lungs were detected on D34. F Histological examination of lungs by hematoxylin-eosin staining. Magnification: ×200, scale bar = 100 μm. G Protein levels of IL-13 in lungs was detected by ELISA. Results are representative of three independent experiments. Means ± SD from 6 mice for each group. Statistical comparison was conducted using unpaired, two-sided Welch’s t test for B and unpaired one-way ANOVA with Dunnett’s test for the rest. p values are shown on the graphs. Source data are provided as a Source Data file. Fig. 3A Created with BioRender.com released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International license https://creativecommons.org/licenses/by-nc-nd/4.0/deed.en .

    Journal: Nature Communications

    Article Title: TCF-1 and TOX regulate the memory formation of intestinal group 2 innate lymphoid cells in asthma

    doi: 10.1038/s41467-024-52252-2

    Figure Lengend Snippet: A CD45.1 + and irradiated CD45.2 + mice were surgically jointed from olecranon to knee joint and recovered for 4 weeks to establish blood chimerism. Subsequently, CD45.1 + mice were treated with HDM as Fig. . B The percentages and the numbers of ST2 – KLRG1 + IL-17RB + ml-ILC2s in siLP of CD45.1 + and CD45.2 + were analyzed on day 30. Cells were gated on CD45.1 + lineage – CD90.2 + NK1.1 – NKp46 – GATA3 + . For in vivo imaging experiments, mice were treated with HDM to establish the asthma relapse model as portrayed in Fig. . C On day 30 (remission), ST2 – KLRG1 + IL-17RB + ILC2s were sorted from siLP and stained with 5 mM Xenolight DiR, and then injected intravenously (5 × 10 5 cells/each) into various groups of mice. Specifically, mice in DiR- group were injected with unstained cells. For the remission + CCX282-B group, recipient mice resting from asthma symptoms were treated with the CCR9 antagonist CCX282-B at 50 mg/kg (daily injection subcutaneously) from day 24 to day 30. For the remission + Etrolizumab group, recipient mice resting from asthma symptoms were treated with the anti-α4β7 monoclonal antibody Etrolizumab at 5 mg/kg (injection intravenously) on day 24, 26, 28 and 30. For the relapse group, mice in remission were injected with DiR-stained cells, followed with treatment of HDM at 50 μg intranasally for 2 times once per hour. Mice in the relapse + FTY720 group received intravenous injection of FTY720 along with 2-time intranasal administration of HDM. Mice in all groups were imaged 2 hours post cell injection, and organs including lungs, spleen, liver, SI and large intestine were then rapidly harvested and imaged. D S1P expression in plasma collected from mice post asthma relapse (D34, D37 and D40) was measured by ELISA. The S1P signaling antagonist FTY720 was administered intraperitoneally to asthmatic mice on days 31 to 33 for 3 times. E The percentages and the numbers of ST2 – KLRG1 + IL-17RB + ILC2s in lungs were detected on D34. F Histological examination of lungs by hematoxylin-eosin staining. Magnification: ×200, scale bar = 100 μm. G Protein levels of IL-13 in lungs was detected by ELISA. Results are representative of three independent experiments. Means ± SD from 6 mice for each group. Statistical comparison was conducted using unpaired, two-sided Welch’s t test for B and unpaired one-way ANOVA with Dunnett’s test for the rest. p values are shown on the graphs. Source data are provided as a Source Data file. Fig. 3A Created with BioRender.com released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International license https://creativecommons.org/licenses/by-nc-nd/4.0/deed.en .

    Article Snippet: Mouse IL-4, IL-5, IL-13, IL-17A, IgE, CCL25, MAdCAM-1 and S1P concentrations in indicated samples were detected by performing ELISA assays according to the manufacturers’ instructions (mouse IL-4, IL-5, IL-13, IL-17A and IgE: #88-7044-86, #88-7054-86, #88-7137-88, # 88-7371-86 and #88-50460-88; Invitrogen, mouse CCL25 and MAdCAM-1: #DY481 and #DY2768; R&D systems and mouse S1P: #K-1900, Echelon).

    Techniques: Irradiation, In Vivo Imaging, Staining, Injection, Expressing, Enzyme-linked Immunosorbent Assay, Comparison

    S1P is involved in the process of heart ischemia/reperfusion injury. a Dot plot showed the individual lipids in the plasma of mice after cardiac ischemia-reperfusion (I/R) injury (45 min of ischemia/6 h of reperfusion) expressed as log 2 (fold change) versus the plasma of the control mice after sham operations (n = 3 per group). The dashed red box highlights sphingosine lipids that are down-regulated after cardiac I/R. b-c Sphingosine 1-Phosphate (S1P) concentrations in the plasma of the mice after cardiac I/R injury (45 min of ischemia/6 h of reperfusion) compared to the mice after sham operations by ELISA (n = 8 per group) ( b ), and the S1P concentrations in the plasma of patients diagnosed with coronary heart disease (CHD) at 24 h after coronary angiography procedures (CAG-24h, n = 17 per group) or percutaneous coronary intervention (PCI-24h, n = 28 per group) by ELISA ( c ). d The plasma S1P concentration in the mice after S1P lyase inhibitor 2-Acetyl-5-tetrahydroxybutyl Imidazole (THI) treatment compared to control mice by ELISA (n = 6 per group). e Representative images of evans blue/triphenyl-2H-tetrazolium chloride (TTC) staining of heart tissue sections collected from mice treated with PBS or THI after I/R injury (45 min of ischemia/24 h of reperfusion), with their quantification of the infarct area (IF), at-risk area (AAR), and left ventricle (LV) (n = 6 per group). f Serum LDH (lactate dehydrogenase) levels of mice treated with PBS or THI after cardiac I/R injury (45 min of ischemia/24 h of reperfusion) were measured (n = 6 per group). g The plasma S1P concentration of mice in the indicated groups by ELISA (n = 6 per group). h Representative images of evans blue/TTC-staining of heart tissue sections collected from WT or S1pr1 ECKO mice treated with PBS or THI after cardiac I/R injury (45 min of ischemia/24 h of reperfusion), with their quantification of the infarct area (IF), at-risk area (AAR), and left ventricle (LV) area (n = 5–6 per group). i Serum LDH levels of WT or S1pr1 ECKO mice treated with PBS or THI after cardiac I/R injury (45 min of ischemia/24 h of reperfusion) were measured (n = 6 per group). Data were shown as mean ± SEM. n.s. indicated not significant. Scale bars: e and h , 2 mm. Unpaired Student's t-test ( b , c , d , e and f ). One-way ANOVA ( g , h and i ).

    Journal: Redox Biology

    Article Title: A detrimental role of endothelial S1PR2 in cardiac ischemia-reperfusion injury via modulating mitochondrial dysfunction, NLRP3 inflammasome activation, and pyroptosis

    doi: 10.1016/j.redox.2024.103244

    Figure Lengend Snippet: S1P is involved in the process of heart ischemia/reperfusion injury. a Dot plot showed the individual lipids in the plasma of mice after cardiac ischemia-reperfusion (I/R) injury (45 min of ischemia/6 h of reperfusion) expressed as log 2 (fold change) versus the plasma of the control mice after sham operations (n = 3 per group). The dashed red box highlights sphingosine lipids that are down-regulated after cardiac I/R. b-c Sphingosine 1-Phosphate (S1P) concentrations in the plasma of the mice after cardiac I/R injury (45 min of ischemia/6 h of reperfusion) compared to the mice after sham operations by ELISA (n = 8 per group) ( b ), and the S1P concentrations in the plasma of patients diagnosed with coronary heart disease (CHD) at 24 h after coronary angiography procedures (CAG-24h, n = 17 per group) or percutaneous coronary intervention (PCI-24h, n = 28 per group) by ELISA ( c ). d The plasma S1P concentration in the mice after S1P lyase inhibitor 2-Acetyl-5-tetrahydroxybutyl Imidazole (THI) treatment compared to control mice by ELISA (n = 6 per group). e Representative images of evans blue/triphenyl-2H-tetrazolium chloride (TTC) staining of heart tissue sections collected from mice treated with PBS or THI after I/R injury (45 min of ischemia/24 h of reperfusion), with their quantification of the infarct area (IF), at-risk area (AAR), and left ventricle (LV) (n = 6 per group). f Serum LDH (lactate dehydrogenase) levels of mice treated with PBS or THI after cardiac I/R injury (45 min of ischemia/24 h of reperfusion) were measured (n = 6 per group). g The plasma S1P concentration of mice in the indicated groups by ELISA (n = 6 per group). h Representative images of evans blue/TTC-staining of heart tissue sections collected from WT or S1pr1 ECKO mice treated with PBS or THI after cardiac I/R injury (45 min of ischemia/24 h of reperfusion), with their quantification of the infarct area (IF), at-risk area (AAR), and left ventricle (LV) area (n = 5–6 per group). i Serum LDH levels of WT or S1pr1 ECKO mice treated with PBS or THI after cardiac I/R injury (45 min of ischemia/24 h of reperfusion) were measured (n = 6 per group). Data were shown as mean ± SEM. n.s. indicated not significant. Scale bars: e and h , 2 mm. Unpaired Student's t-test ( b , c , d , e and f ). One-way ANOVA ( g , h and i ).

    Article Snippet: The S1P concentrations in plasma were measured by S1P ELISA kit (#K-1900, Echelon Biosciences, USA).

    Techniques: Control, Enzyme-linked Immunosorbent Assay, Concentration Assay, Staining