Fig. 5: MAPK13 deficiency alleviates oxidative stress-associated acute or chronic liver injury.

a Primary hepatocytes isolated from c57BL/6 J mice were transiently transfected with HA-Mapk13. Cells were then treated with 0.5 mM H₂O₂ for 0 h, 4 h or 8 h. HA-Mapk13 was immunoprecipitated and phosphorylation of Mapk13 was detected. b‒d WT and Mapk13 KO mice were intraperitoneally injected with normal saline (control) or 300 mg/kg APAP. After 24 h treatment, serum ALT and AST levels in these mice were detected by kit (b). Positive liver cells in TUNEL-stained sections were quantified (c). Liver necrosis area in H&E-stained sections were circled and quantified (d). Representative images of H&E staining or TUNEL staining were shown on the left panel and statistical analysis were shown on the right panel (n = 5 per group). e Survival during 72 h of WT and Mapk13 KO mice intraperitoneally injected with normal saline (control) or 800 mg/kg APAP (n = 13 per group). f‒h WT and Mapk13 KO mice were fed with irradiated diet with or without 0.1% DDC for 2 weeks. Serum ALT and AST levels were detected in these mice (f). Mouse livers were dissected and subjected to Sirius Red staining (g) and TUNEL staining (h) (n = 5 per group). i WT and Mapk13 KO mice were intraperitoneally injected with normal saline (control) or 300 mg/kg APAP. Livers were collected at 16 h after treatment. Immunoblotting analysis was performed (n = 2 per group). j WT and Mapk13 KO mice were intraperitoneally injected with normal saline or 300 mg/kg APAP. The GSH level in mouse livers was measured (n = 5 per group). Immunoblots are representative of three independent experiments. Survival data are based on Long-rank test (e). Other data are means ± SD. Each point or lane represents an individual mouse. P values were determined by two-tailed Student’s t-test.