Curcumin(CUR),the main compound extracted from Curcuma longa,has various biological actions,including hepatoprotective,anti-infective,anti-inflammatory,antioxidant,and neurotrophic properties.But it has not yet been c...Curcumin(CUR),the main compound extracted from Curcuma longa,has various biological actions,including hepatoprotective,anti-infective,anti-inflammatory,antioxidant,and neurotrophic properties.But it has not yet been clarified how CUR affects the accumulation of fatty in hepatic cells.Our study uncovered that CUR decreased the lipid deposition in free fat acids(FFAs)-treated hepatocytes,which could be blocked by Compound C(an AMPK inhibitor).This result suggests that protective effect was associated with the AMPK pathway activation.MiR-3666 directly targets the AMPK gene,and overexpression of miR-3666 greatly weakens the hypolipidemic effect of CUR.Our results showed that CUR reduced FFAs-induced lipid deposition by targeting miR-3666.This boosted AMPK phosphorylation and inhibited its downstream targets,including ACC and SREBP1.These findings together confirm that CUR-mediated inhibition of miR-3666 to activate the AMPK pathway is a potential alternative for alleviation of hepatic lipid deposition.展开更多
基金supported by grants from Zhejiang Provincial Key R&D Program of China(2021C02018)National Natural Science Foundation of China(32172192).
文摘Curcumin(CUR),the main compound extracted from Curcuma longa,has various biological actions,including hepatoprotective,anti-infective,anti-inflammatory,antioxidant,and neurotrophic properties.But it has not yet been clarified how CUR affects the accumulation of fatty in hepatic cells.Our study uncovered that CUR decreased the lipid deposition in free fat acids(FFAs)-treated hepatocytes,which could be blocked by Compound C(an AMPK inhibitor).This result suggests that protective effect was associated with the AMPK pathway activation.MiR-3666 directly targets the AMPK gene,and overexpression of miR-3666 greatly weakens the hypolipidemic effect of CUR.Our results showed that CUR reduced FFAs-induced lipid deposition by targeting miR-3666.This boosted AMPK phosphorylation and inhibited its downstream targets,including ACC and SREBP1.These findings together confirm that CUR-mediated inhibition of miR-3666 to activate the AMPK pathway is a potential alternative for alleviation of hepatic lipid deposition.
