Skip to main content
. 2021 Feb 3;13:640215. doi: 10.3389/fnagi.2021.640215

Figure 8.

Figure 8

Inhibition of UCP-2 pathway reversed the beneficial effects of irisin on apoptosis, mitochondrial function, and oxidative stress after SAH. (A,B) TUNEL-positive neurons were significantly increased after genipin administration in the irisin treatment group. Scale bar = 50 μm, n = 3 for each group (The area of observation was circled in red). (C–I) Representative western blotting images and relative density analysis of proteins related to mitochondrial biogenesis (TFAM, PGC-1α), oxidative stress (SOD2), and apoptotic markers (Cleaved caspase-3, Bax, Bcl-2) at 24 h after SAH. As an exogenous UCP-2 inhibitor, genipin significantly blunted the expressions of PGC-1α, TFAM, SOD2, and Bcl-2 (D,E,F,I) and resulted in an increased level of cleaved caspase-3 and Bax (G,H), n = 6 for each group. All data were presented as mean ± SD. The one-way ANOVA was used followed by the Tukey's HSD post-hoc test and the Holm–Bonferroni correction method. *P < 0.05, **P < 0.01, ***P < 0.001 vs. Sham group; ##P < 0.01, ###P < 0.001 vs. SAH + Vehicle group. &P < 0.05, &&P < 0.01, &&&P < 0.001 vs. SAH + irisin + Vehicle group. Vehicle group, sterile 0.9% of NaCl; TUNEL, TdT-UTP nick end labeling; SOD, Superoxide Dismutase; UCP-2, Uncoupling Protein-2.