Renalase Attenuates Mouse Fatty Liver Ischemia/Reperfusion Injury through Mitigating Oxidative Stress and Mitochondrial Damage via Activating SIRT1

Figure 2

RNLS protects t-BHP-induced HepG2 cell oxidative stress injury in vitro. (a) Cell viability of HepG2 cells (Ctrl) and 200 μM OA-induced steatotic HepG2 cells (OA) treated with t-BHP at different concentrations. , t-BHP group vs. NC group; ^## Ctrl group vs. OA group. (b) Cell viability of HepG2 cells pretreated with RNLS at different concentrations, followed by 300 μM t-BHP treatment. (c) Cell viability of OA-induced steatotic HepG2 cells pretreated with or without 500 μM RNLS in an in vitro IR model induced by 300 μM t-BHP treatment. (d) The expression levels of apoptosis-related proteins of hepG2 cells were evaluated by western blotting. vs. NC group, ^#, ^## vs. t-BHP group; ^&, ^&& vs. Ctrl group. (e, f) RNLS protein levels and relative mRNA expression in HepG2 cells transfected with si-RNLS were evaluated by western blotting and RT-qPCR. (g) Cell viability of RNLS-knockdown HepG2 cells pretreated with or without 500 μg/L RNLS in an in vitro IR model. . Data are plotted as the from three independent experiments.

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