Fig. 6

Oleic acid abrogated pyroptosis in HepG2 cells through inhibiting ER stress. The ER stress in cells were inhibited by chemical chaperones 4-phenylbutyric acid (4-PBA) or tauroursodeoxycholic acid (TUDCA) for 24 h against ER stress. a. and b. Cell viability of HepG2 cells was assessed using CCK8 assay. c. The mRNA expression of key genes governing pyroptosis were detected after 24 h treatment, and β-ACTIN was used as an internal control. d. Representative western blots of NLRP3 and GSDMD-N after 24 h treatment, and β-ACTIN was used as a protein-loading control. e. HepG2 cells were exposed to PA or plus OA, TUDCA or 4-PBA followed by labeling with anti-GSDMD (red) antibody and DAPI staining, and were visualized under a microscope at 100× magnification after 24 h treatment. f. and g. Cell supernatants were analyzed for IL-1β and TNF-α secretion by HepG2 cells by ELISA. The data are presented as means ± SD for 3–5 biological replicates; *P < 0.05, **P < 0.01, and ***P < 0.001vs. BSA;#P < 0.05, ##P < 0.01vs.PA;ns no significant differences between two connected groups