[Steatosis and inflammation of L02 hepatocytes induced by sodium oleate].

Abstract

Objective: To observe the steatosis and inflammatory effects of L02 hepatocytes induced by different concentrations of sodium oleate.

Methods: L02 cells were incubated with sodium oleate in different concentration for 24 h, and the cell viability was detected. L02 cells were respectively cultured with 75, 150, 300 μmol/L sodium oleate for 24 h. The lipid accumulation of the cells was observed by oil red staining. The content of triglyceride in the cells was detected, the IL-6 content in the cell supernatant was detected. The expression of SIRT1 and nuclear factor-κB(NF-κB) was detected by Western Blot. The expression of Toll-like receptor 2 and Toll-like receptor 4(TLR2 and TLR4) on the cell surface was detected by flow cytometry.

Results: With the increase of sodium oleate concentration, the cell viability decreased, the cell growth inhibition rate increased. The content of triglyceride in L02 cells treated with 75, 150 and 300 μmol/L sodium oleate was significantly higher than that in the control group(P<0. 01, P<0. 001, P<0. 001), the IL-6 in the supernate was significantly higher than that in the control group(P<0. 05, P<0. 01, P<0. 001). The result of oil red staining showed that the lipids in the cells were obviously accumulated after sodium oleate treatment. The expression of TLR2 in L02 cells treated with 150 and 300 μmol/L sodium oleate was significantly higher than that in the control group(P<0. 05, P<0. 001). There was no significant increase in TLR4 expression after sodium oleate intervention in L02 cells. The expression of SIRT1 protein in the sodium oleate group was lower than that in the control group, and the expression of NF-κB p65 was higher than that in the control group through Western Blot result.

Conclusion: L02 hepatocyte steatosis caused by sodium oleate may be associated with TLR2/NF-κB mediated inflammatory pathway.