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目的:在高糖刺激的肾小球系膜细胞MES13和HBZY-1中研究Apelin-13抑制高糖引起的细胞炎症。方法:在高糖诱导的MES13和HBZY-1细胞中给予不同剂量的Apelin-13,通过real time-PCR技术检测各实验组2种系膜细胞中Icam-1和Mcp-1基因的mRNA水平变化。结果:(1)与空白对照组细胞相比,高糖组MES13和HBZY-1细胞中Icam-1和Mcp-1基因的mRNA水平显著性上升(P<0.05);给药Apelin-13(300 pmol·L-1)能显著性抑制高糖刺激的MES13和HBZY-1细胞中Icam-1和Mcp-1基因的mRNA水平(P<0.05)。(2)与空白对照组细胞相比,通过免疫组化实验检测高糖组MES13和HBZY-1细胞中促炎蛋白p38的磷酸化水平上升(P<0.05);给药Apelin-13(300 pmol·L-1)能显著性抑制高糖引起MES13和HBZY-1细胞中促炎症蛋白p38的磷酸化(P<0.05)。结论:Apelin-13抑制高糖引起的MES13和HBZY-1细胞中p38的激活,从而抑制高糖所引起的炎症反应(Icam-1和Mcp-1基因水平)。
AIM: To investigate the effects of Apelin-13 on cellular inflammation induced by high glucose in high glucose-stimulated glomerular mesangial cells MES13 and HBZY-1. Methods: Different doses of Apelin-13 were administered to high glucose-induced MES13 and HBZY-1 cells, and the mRNA levels of Icam-1 and Mcp-1 in two mesangial cells of each experimental group were detected by real time-PCR . Results: (1) The mRNA levels of Icam-1 and Mcp-1 in MES13 and HBZY-1 cells were significantly increased compared with the blank control group (P <0.05) pmol·L-1) significantly inhibited the mRNA levels of Icam-1 and Mcp-1 in high glucose-stimulated MES13 and HBZY-1 cells (P <0.05). (2) The phosphorylation of proinflammatory protein p38 in MES13 and HBZY-1 cells in high glucose group was significantly higher than that in blank control group (P <0.05) by immunohistochemical staining; Apelin-13 · L-1) significantly inhibited phosphorylation of pro-inflammatory protein p38 in MES13 and HBZY-1 cells (P <0.05) by high glucose. CONCLUSION: Apelin-13 inhibits high glucose-induced activation of p38 in MES13 and HBZY-1 cells, thereby inhibiting the high glucose-induced inflammatory response (Icam-1 and Mcp-1 gene levels).