Abstract:To explore the effect of Moringa isothiocyanate-4-[(α-L-rhamnosyloxy) benzyl] isothiocyanates (MIC-1) on the lipid accumulation in 3T3-L1 adipocytes and the possible regulatory mechanism, 3T3-L1 preadipocytes were induced in vitro to differentiate into mature adipocytes. After 48 h of intervention with MIC-1, lipid accumulation, triglyceride (TG), glycerol (Gly) and free fatty acid (FFA) contents were determined; qRT- PCR was used to detect the expression of the genes related to lipid metabolism; Western blot was used to determine the phosphorylation level of adenylate-activated protein kinase (AMPK) and the expression level of oxisome proliferation-activated receptor γ (PPARγ). The results show that MIC-1 has no effect on the survival rate of 3T3-L1 preadipocytes; compared with the control group, MIC-1 can reduce the distribution of lipid droplets in adipocytes and the degree of cell coloration, intracellular TG content, and FFA and glycerol overflow. When the concentration of MIC-1 reached 4 mol/L, the concentration of TG and FFA decreased by 64% and 75%, respectively. At the same time, the mRNA expression levels of PPARγ and stearoyl-CoA desaturase 1 (SCD1) in cells were significantly down-regulated (by 46.00% and 62.00%, respectively); the protein expression levels of AMPK protein phosphorylation and down-regulated PPARγ were significantly up-regulated (by 64.47% and 52.10%, respectively). The above results indicate that MIC-1 inhibits lipid accumulation by promoting the decomposition of TG and inhibiting the synthesis of TG. The mechanism may be related to the activation of AMPK.
