RÉSUMÉ
OBJECTIVE: To investigate the effect of two amide alkaloid derivatives (LCAA and LCAB) from Lycii Cortex on lipid metabolism in HepG2 cells and explore their possible mechanisms. METHODS: The lipid accumulation model of HepG2 cells induced by sodium oleate was established. The cells were pretreated with different concentrations of LCAA and LCAB, and the lipid accumulation was observed by oil red O staining. The content of TC in HepG2 cells was measured by oxidizing enzyme method, and the content of TG in HepG2 cells was measured by GPO-PAP method. The expression of lipid metabolism related proteins, such as SIRT1, FOXO1, AMPK and phospho-AMPK (p-AMPK), was detected by Western blot. The mRNA expression of AMPK, SIRT1, ACC2, COXII and COXIII were detected by RT-qPCR. RESULTS: Both LCAA and LCAB could significantly decrease the lipid accumulation in HepG2 cells induced by sodium oleate (200 μmol•L-1) (P<0.01) and the TC and TG levels (P<0.05 or P<0.01). At the same time, the sodium oleate-induced high expression of p-AMPK protein, the low expression of SIRT1, FOXO1 (P<0.01), and the low expression of AMPK, SIRT1, ACC2, COXII and COXIII mRNA (P<0 05 or P<0 01) were all improved by LCAA and LCAB. CONCLUSION: Both LCAA and LCAB can significantly improve lipid metabolism in HepG2 cells, and regulate lipid metabolism by regulating lipid metabolism-related proteins p-AMPK, SIRT1, FOXO1 and mitochondrial oxidation-related factors COXII and COXIII.