Fig. 5

HSF2BP deficiency exacerbates I/R-induced liver injury, inflammatory response and ER stress. Liver is induced by 1-hour ischemia followed by 24-hour reperfusion in HSF2BP-KO and WT mice. Sham mice received all procedures except for hepatic ischemia. ER stress was induced by intraperitoneal injection of tunicamycin (0.5 µg/g body weight, 500 µl) for 48 h in HSF2BP-TG and NTG mice. Sham mice treated with 500 µl normal saline. A, Liver H&E staining after hepatic I/R in HSF2BP-KO and WT mice. Original magnification, x100 and x200. Liver necrosis area (B) and histological score (C) after hepatic I/R in HSF2BP-KO and WT mice. Serum AST (D) and ALT (E) after hepatic I/R in HSF2BP-KO and WT mice. Liver CD3 and Ly6G staining (H) and their quantitative results (F and G) after hepatic I/R in HSF2BP-KO and WT mice. Original magnification, x400. I, Transmission electron microscope of liver endoplasmic reticulum (ER) after hepatic I/R in HSF2BP-KO and WT mice. Original magnification, x1.5k and x5.0k. Results are expressed as mean ± SE (n = 4–6/group) and compared by one-way ANOVA. * p < 0.05 versus sham mice, # p < 0.05 versus NTG mice