血管钠肽促进小鼠3T3-L1脂肪细胞合成脂联素及其可能机制

Vasonatrin peptide promotes the synthesis of adiponectin in 3T3-L1 adipocytes of mouse and the underlying mechanism

目的探讨血管钠肽(VNP)对脂肪因子脂联素生成的影响及其机制。方法在3T3-L1细胞分化的脂肪细胞中加入不同浓度的VNP,分别用实时定量PCR法和Western blot法检测脂联素的mRNA水平和蛋白表达,放免法测定细胞内cGMP的水平。结果 VNP可显著增加脂联素mRNA水平和蛋白表达,同时提高细胞内cGMP,含量为(38±5)～(265±35)nmol/L,显著高于对照组的(10±2)nmol/L(P<0.01);该效应可用8-Br-cGMP诱导,可被cGMP依赖性蛋白激酶抑制剂KT-5823或钠尿肽受体NPR阻断剂HS-142-1抑制。结论 VNP可通过NPR/cGMP/PKG信号通路增加脂肪细胞脂联素的表达。

Objective To identify the roles of vasonatrin peptide （VNP） on adiponeetin ing mechanisms. Methods 3T3-L1 cells were differentiated into adipoeytes and exposed production and the underly- to various concentrations of VNP. Quantitative PCR and immunoassays were performed to determine the mRNA levels of adiponectin. Involved signaling pathway was identified by radioimmunoassay to detect the levels of intracellular cGMP[ （38 _ 5 ） - （265 ~ 35 ）nmol/L ]. Results VNP markedly enhanced adiponectin mRNA expression as well as protein secretion. In ad- dition, VNP significantly enhanced the intracellular level of cGMP. The effects of VNP were mimicked by 8-Br- cGMP, whereas inhibited by HS-142-1 or KT-5823. Conclusions VNP regulates adiponectin production in adipo- cytes via a guanylyl cyclase-coupled NPR/cGMP/PKG pathway.