PIAS1 Alleviates Hepatic Ischemia-Reperfusion Injury in Mice through a Mechanism Involving NFATc1 SUMOylation

Figure 5

IRF-1 promoted inflammatory response and apoptosis in H/R-exposed hepatocytes by activating p38 MAPK signaling pathway. (a) The phosphorylation levels of p38, JNK, and ERK1/2 in the liver tissues of sham-operated and HIRI mice determined by Western blot analysis (). (b) The phosphorylation level of p38 in AML12 cells treated with sh-IRF-1 or combined with SB203580 (p38 MAPK inhibitor) determined by western blot analysis (). (c) The phosphorylation level of p38 in AML12 cells treated with sh-IRF-1 or combined with SB203580 determined by immunocytochemical staining (). (d) The phosphorylation levels of p38, JNK, and ERK1/2 in AML12 cells treated with sh-IRF-1 or oe-IRF-1 detected by Western blot analysis ( vs. oe-NC, # vs. sh-NC). (e) The phosphorylation levels of p38, JNK, and ERK1/2 in AML12 cells treated with sh-IRF-1 or oe-IRF-1 detected by immunocytochemical staining ( vs. oe-NC, # vs. sh-NC). (f) The mRNA expression of inflammatory response and apoptosis-related proteins in AML12 cells treated with oe-IRF-1 or combined with SB203580 determined by RT-qPCR. (g) The protein expression of inflammatory response and apoptosis-related proteins in AML12 cells treated with oe-IRF-1 or combined with SB203580 determined by Western blot analysis. (h) AML12 cell apoptosis following treatment with oe-IRF-1 or combined with SB203580 determined by TUNEL staining. In (f)–(h), vs. oe-NC, # vs. oe-IRF-1. Cell experiments were all repeated 3 times.

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