探究辣木异硫氰酸酯-4-[(α-L-rhamnosyloxy) benzyl] Isothiocyanates（MIC-1）抑制3T3-L1脂肪细胞脂质积累的作用及可能的调控机制。体外诱导3T3-L1前脂肪细胞分化为成熟脂肪细胞，用MIC-1干预48 h后检测细胞脂质积累情况，甘油三酯（TG）、甘油（Gly）和游离脂肪酸（FFA）含量；qRT-PCR检测脂代谢相关基因的表达；Western blot法测定腺苷酸活化蛋白激酶（AMPK）蛋白磷酸化水平和氧化物酶体增殖激活受体γ（PPARγ）蛋白表达水平。结果表明，MIC-1对3T3-L1前脂肪细胞存活率无影响；与对照组相比，MIC-1可降低脂肪细胞内脂滴分布及细胞着色程度，降低细胞内TG含量，减少FFA及甘油的溢出。MIC-1处理浓度达4 mol/L时，TG和FFA浓度分别下降64.00%和75.00%。同时，显著下调细胞中PPARγ（46.00%）、硬脂酰辅酶A去饱和酶1（SCD1）（62.00%）的mRNA表达水平；显著上调AMPK蛋白磷酸化水平（64.47%）和下调PPARγ（52.10%）蛋白表达水平。以上结果表明，MIC-1通过促进TG分解和抑制TG的合成，从而抑制脂质积累，其机制可能与AMPK的活化有关。

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.

云南省科技厅重大专项（202002AA100005）；云南省重大科技专项-绿色食品国际合作研究中心项目(2019ZG009)；云南省科技厅科技计划项目（202201AT070262）