Objective To study the effect of BRL37344 on 3T3-L1 preadipocyte differentiation and the role of ERK1/ 2 phosphorylation in this process. Methods 3T3-L1 preadipocytes were cultured in vitro with different drugs, Western blot analysis for PPARγ, phospho- and total ERK1/2 was performed by using cell lysates. Results 10-7 mol/L BRL37344 could significantly increase ERK1/2 molecule phosphorylation levels in 3T3-L1 preadipocyte and down-regulate the expression of PPARγ; partial blockade of phosphorylation of ERK1/2 induced by BRL37344 could restore PPAR7 expression. Conclusion The long time and high level phosphorylation of ERK1/2 signaling pathway trigged by BRL37344 plays an important role in the process of inhibition of 3T3-L1 preadipocyte differentiation.%目的 探讨选择性β3受体激动剂BRL37344对3T3-L1前体脂肪细胞分化的影响及ERK1/2分子磷酸化在此过程中的作用.方法 体外培养3T3-L1前体脂肪细胞,不同药物干预一定时间后裂解细胞收集蛋白,应用Western blot法检测PPARγ、ERK1/2及pERK1/2蛋白表达.结果 10-7 mol/L BRL37344可以显著提高3T3-L1前体脂肪细胞内ERK1/2分子的磷酸化水平,下调PPARγ表达.部分阻断BRL37344引起的ERK1/2磷酸化可以恢复PPARγ表达.结论 10-7 mol/L BRL37344引起的ERK1/2长时间高水平磷酸化在抑制3T3-L1细胞分化过程中起着十分重要的作用.
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