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. Author manuscript; available in PMC: 2022 Nov 1.
Published in final edited form as: Life Sci. 2021 Sep 1;284:119925. doi: 10.1016/j.lfs.2021.119925

Figure 2. Mitochondrial function is improved in endothelial cells from type 2 diabetic mice by interfering with 12(S)-HETE/TRPV1 interaction.

Figure 2.

Mitochondrial reserve capacity (A, K, One-way ANOVA/Bonferroni, D, G Kruskal-Wallis test) and mitochondrial oxygen consumption rate (OCR, B, E, H, L, Two-way ANOVA/Bonferroni) in endothelial cells isolated from diabetic vs. non-diabetic mice, 5–8 mice/group. Maximum mitochondrial respiration was assessed after addition of oligomycin (Oligo) and FCCP indicated by arrows. Mitochondrial reserve capacity calculated by subtracting basal mitochondrial OCR from maximum OCR. Data is presented as mean±SEM, *P<0.05, **P<0.01, ***P<0.001 WT vs. LepRdb/db and #P<0.05, ##P<0.01, ###P<0.001 LepRdb/db+treatment vs. LepRdb/db. Illustrations indicate the application of the 12/15LO inhibitor baicalein to isolated endothelial cells in vitro (C), i.p. application in vivo of the 12/15LO inhibitor ML351 with consecutive endothelial cell isolation for mitochondrial functional analysis in vitro (F), the TRPV1 inhibitor BCTC to isolated endothelial cells in vitro (J) and the intravenous application of the V1-cal or V1-scr peptide in vivo with consecutive endothelial cell isolation for mitochondrial functional analysis in vitro (M). WT-wild type, Rot/AA – rotenone/antimycin A.