Bletilla striata polysaccharides alleviate metabolic dysfunction-associated steatotic liver disease through enhancing hepatocyte RelA/ HNF1α signaling

Figure 10 RELA silencing alters endoplasmic reticulum and oxidative responses in mouse liver induced by high-fat-diet. A: Intracellular malondialdehyde levels; B: Reduced glutathione levels; C: Transmission electron microscopy analysis of liver tissue ultrastructure; D: Western blot analysis of the relative levels of hepatic nuclear factor kappa B p65, and hepatocyte nuclear factor-1 alpha protein expression; E: Western blot analysis of the relative levels of hepatic endoplasmic reticulum stress-related protein expression; F: Western blot analysis of the relative levels of hepatic lipid metabolism-related protein expression. Data are representative images or expressed as the mean ± SD of each group of mice from three separate experiments. ^bP < 0.01. ¹P < 0.01 vs the high-fat-diet group. ²P < 0.01 vs the RELA-knockdown + high-fat-diet group. BSP: Bletilla striata polysaccharides; KD: Knockdown; HFD: High-fat-diet; MDA: Malondialdehyde; GSH: Glutathione; ER: Endoplasmic reticulum; L: Lipid droplet; M: Mitochondria; N: Nucleus; HNF1α: Hepatocyte nuclear factor-1 alpha; GRP78: 78-kDa glucose-regulated protein; CHOP: CCAAT-enhancer-binding protein homologous protein; HRD1: 3-hydroxy-3-methyl glutaryl coenzyme A reductase degradation 1 homolog; SREBP1c: Cleaved sterol regulatory element-binding protein 1; MTP: Microsomal triglyceride transfer protein; MCAD: Medium-chain acyl-CoA dehydrogenase; GPX4: Glutathione peroxidase 4; ATF4: Activating transcription factor 4; RelA: Nuclear factor kappa B p65.