目的：探讨刺五加苷B／E（ ETS-B／E）对高糖环境大鼠肾小球系膜细胞HBZY-1增殖的影响及机制。方法：进行HBZY-1细胞传代、无菌培养，选生长良好的第4代HBZY-1细胞，测定高糖（25 mmol／L）环境下符合生长规律曲线图的细胞密度。然后接种6组，分成低糖组（ LG）、高糖组（ HG）、高糖ETS-B／E（低剂量、中剂量、高剂量）组和高糖洛沙坦组（ LTG）。予以相应药物干预后，测定在24 h、48 h和72 h时，其对HBZY-1细胞生长的抑制作用和抑制率，并用免疫细胞化学和Western blotting检测各组增殖过程中TGF-β1和PPARγ的表达情况。结果：HBZY-1细胞的接种浓度为每孔2000个时，符合细胞生长基本规律，高糖显著促进HBZY-1细胞的增殖。 ETS-B／E作用下，在各时点，对HBZY-1细胞的抑制作用和抑制率与HG有显著差异（ P＜0.05）；免疫细胞化学和West-ern blotting分析均显示，ETS-B／E能显著抑制TGF-β1表达和促进PPARγ表达（ P＜0.05），且ETS-E显著强于ETS-B（ P＜0.05），呈浓度和时间依赖性趋势。结论： ETS-B／E对高糖环境下HBZY-1细胞的增殖具有显著抑制作用，其作用机制与阻止TGF-β1的表达和促进PPARγ的表达相关。%[ ABSTRACT] AIM:To explore the effects and mechanism of eleutheroside ( ETS) B or E on the proliferation of HBZY-1 cells treated with high glucose.METHODS:The HBZY-1 cells were cultured under high glucose condition.The 4th generation of HBZY-1 cells was used for determining the optimal cell density, which was consistent with the growth reg-ulation curve of the cells.The cells were divided into 6 groups:low glucose ( LG) group, high glucose ( HG) group, high glucose plus ETS-B/E ( low dose, medium dose and high dose) groups, and high glucose plus losartan ( LTG) group.Af-ter all cells were treated with the corresponding drugs at 24 h, 48 h and 72 h, the inhibitory rate of the proliferation was measured, and the expression of TGF-β1 and PPARγwas detected by immunocytochemistry and Western blotting.RE-SULTS:The best cell density was 2 000 cells/well, which was complied with the basic rules of the cell growth, and high glucose significantly promoted the HBZY-1 cell proliferation.At each time point, the inhibitory effects of ETS-B/E were significantly different between HG group and LTG group on the proliferation of the HBZY-1 cells ( P<0.05) .The expres-sion of TGF-β1 was significantly inhibited, and the expression of PPARγwas significantly promoted by ETS-B/E ( P<0.05).ETS-E showed stronger effect than ETS-B (P<0.05) in a concentration-and time-dependent manner.CONCLU-SION:ETS-B/E significantly inhibits the proliferation of HBZY-1 cells under high glucose condition by decreasing TGF-β1 expression and promoting PPARγexpression.
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