Sulforaphane inhibits hepatic steatosis in rats by down-regulating DGAT2 and ACAT1 expression

Abstract

Objective To study the effects of sulforaphane (SFN) on the deposition of lipid droplets and the expression of their peripheral proteins in the liver and elucidate the mechanism by which SFN inhibits non-alcoholic fatty liver caused by high-fat diet. Methods Sixty male Wistar rats were randomized into 6 equal groups (n=10), includinganormal food group, ahigh-fat diet group, 3 high-fat diet groups treated with high (20 mg/kg), moderate (10 mg/kg) and low (5 mg/kg) doses of SFN, andahigh-fat diet group treated withapositive drug (30 mg/kg). Triglyceride and total cholesterol contents were examined and the deposition of lipid droplets in the liver was detected with oil redOstaining in all the rats. The protein expression of DGAT2 and ACAT1 (the key synthases of triglyceride and cholesterol, respectively) in the liver tissues were detected with Western blotting; immunohistochemistry and real-time PCR were performed to examine the expression of the PAT proteins (PLIN1, PLIN2, PLIN3 and PLIN5) at both the protein and mRNA levels in the liver. Results SFN treatment obviously reduced high-fat diet-induced bodyweight gain in the rats, lowered the levels of triglyceride and total cholesterol, lessened lipid droplet deposition in the liver and reduced the volume of the lipid droplets. Treatment with SFN at all the 3 doses significantly down-regulated the expression of ACAT1 and DGAT2 in the liver of the rats (P < 0.01). SFN at the high doses significantly down-regulated the expression of PLIN2 and PLIN5 in liver tissue at both the mRNA and protein levels (P < 0.01, P < 0.05). Conclusion SFN can inhibit the formation of lipid droplets by reducing the expressions of DGAT2, ACAT1, PLIN2 and PLIN5 in the liver of rats.

Keywords

• sulforaphane
• triglyceride
• cholesterol
• lipid droplets
• dgat2
• acat1
• plin2
• plin5