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目的观察肝X受体(liver X receptors,LXRs)激动剂T0901317对人脐静脉内皮细胞(human umbilical veinendothelial cell,HUVEC)增殖活性的影响。方法体外分离和培养原代HUVEC,不同浓度的T0901317(0、0.5、2、5μmol/L)干预HUVEC 48 h后,采用MTS法检测HUVEC增殖情况;Western blot检测磷酸化Akt(Ser473)及总Akt的表达。结果T0901317(0～5μmol/L)呈浓度依赖性的促进HUVEC的增殖(P<0.01)和上调HUVEC中p-Akt-Ser473的表达(P<0.01),PI3K抑制剂LY294002(10μmol/L)和基因转录抑制剂放线菌素-D(actinomycin D,Act-D,5μg/ml)可以阻断T0901317(5μmol/L)上调p-Akt-Ser473的作用(P<0.01),提示T0901317通过基因转录调节的方式激活PI3K/Akt信号,此外,PI3K抑制剂LY294002(10μmol/L)预处理可以逆转T0901317(5μmol/L)促HUVEC增殖作用(P<0.01)。结论 LXRs激动剂T0901317可通过激活PI3K/Akt信号通路增强HUVEC的增殖能力。
Objective To observe the effect of T0901317, a liver X receptor (LXRs) agonist, on the proliferation of human umbilical veinendothelial cell (HUVEC). Methods HUVECs were isolated and cultured in vitro. HUVECs were treated with different concentrations of T0901317 (0, 0.5, 2, 5μmol / L) for 48 h. MTS was used to detect the proliferation of HUVECs. Western blot was used to detect phosphorylated Akt (Ser473) expression. Results T0901317 (0-5 μmol / L) promoted the proliferation of HUVEC in a concentration-dependent manner (P <0.01) and up-regulated the expression of p-Akt-Ser473 in HUVEC (P <0.01) and PI3K inhibitor LY294002 Actinomycin D (Act-D, 5μg / ml) could block the up-regulation of p-Akt-Ser473 by T0901317 (5μmol / L) (P <0.01), suggesting that T0901317 gene transcription PI3K / Akt signaling was activated by PI3K inhibitor LY294002 (10μmol / L), which could reverse the proliferation of HUVEC induced by T0901317 (5μmol / L) (P <0.01). Conclusion LXRs agonist T0901317 can enhance the proliferation of HUVEC by activating the PI3K / Akt signaling pathway.