ABSTRACT
Objective To observe the fatty deposition in thapsigargin-induced endoplasmic reticulum stress model in hepatocytes and to discuss the possible mechanism. Methods Hepatocytes (L02 cell and HepG2 cell line) were divided into control group and experimental group (treated with 1 μmol/L thapsigargin). Fatty deposition in the hepatocytes was observed by biochemical assay and oil red O staining. Real-time PCR was used to test the expression of SREBP-1c and LXRs mRNA. And Western blotting analysis was used to examine the expression of protein of GRP78, SREBP-1c and LXRs. Results Western blotting analysis showed that GRP78 protein expression in the experimental group was remarkably higher than that inthe control group (P<0. 05), indicating the successful establishment of the endoplasmic reticulum stress model in hepatocytes. The hepatocyte fatty deposition in the experimental group was significantly more than that in the control group 48 h after thapsigargin exposure(P<0. 01). The expression of SREBP-1c mRNA and protein in the experimental group was significantly higher than that in the control group (P<0. 05), and the expression of LXRs mRNA and proteinwas not significantly between the two groups. Conclusion Endoplasmic reticulum stress may induce hepatocyte fatty deposition throuth up-regulating SREBP-1c, and LXRs is not involved in the process.
ABSTRACT
Objective To observe the fatty deposition in thapsigargin-induced endoplasmic reticulum stress model in hepatocytes and to discuss the possible mechanism. Methods Hepatocytes (L02 cell and HepG2 cell line) were divided into control group and experimental group (treated with 1 μmol/L thapsigargin). Fatty deposition in the hepatocytes was observed by biochemical assay and oil red O staining. Real-time PCR was used to test the expression of SREBP-1c and LXRs mRNA. And Western blotting analysis was used to examine the expression of protein of GRP78, SREBP-1c and LXRs. Results Western blotting analysis showed that GRP78 protein expression in the experimental group was remarkably higher than that inthe control group (P<0. 05), indicating the successful establishment of the endoplasmic reticulum stress model in hepatocytes. The hepatocyte fatty deposition in the experimental group was significantly more than that in the control group 48 h after thapsigargin exposure(P<0. 01). The expression of SREBP-1c mRNA and protein in the experimental group was significantly higher than that in the control group (P<0. 05), and the expression of LXRs mRNA and proteinwas not significantly between the two groups. Conclusion Endoplasmic reticulum stress may induce hepatocyte fatty deposition throuth up-regulating SREBP-1c, and LXRs is not involved in the process.