Abstract

Objective To explore the role of caveolin1 in palmitic acid (PA)-induced hepatic steatosis. Methods Stable caveolin1 (CAV1) overexpressing HepG2 cells were developed by transfection with lentiviral particles containing human CAV1 protein (Lenti-CAV1). Lenti-Control served as a negative control. After 24 hours fatty acid free bovine serum albumin (BSA) and PA incubation, lipid deposition was determined by Oil red staining and cellular triglyceride was measured. Real time PCR was used to detect the mRNA expression of PGC1α and sirt3. Results Compared with BSA treatment, PA treatment for 24 hours increased the lipid droplets and triglyceride content (P<0.01). Compared with negative control, overexpression of caveolin1 attenuated the accumulation of lipid droplets and triglyceride content in HepG2 cells (P<0.05) . At the same time , the mRNA expression of PGC1α and sirt3 were increased in CAV1 overexpressing cells (P<0.05). Conclusions Caveolin1 may improve PA-induced hepatic steatosis through up-regulating PGC1α-sirt3 axis. Key words: NAFLD; Caveolin1; PGC1α; Sirt3

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