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目的 :明确缺氧对心肌细胞表达血管内皮生长因子 (VEGF)的影响及蛋白激酶C(PKC)信号传导通路在其中的作用。方法 :将原代培养大鼠心肌细胞模型分组 :①正常缺氧 4组 :A组正常对照 ;B组缺氧 6h ;C组缺氧 12h ;D组缺氧 2 4h。②PKC激动剂 4组 :A组缺氧 2 4h对照 ;B组加入PMA 10ng/ml缺氧 2 4h ;C组加入PMA 10 0ng/ml缺氧 2 4h ;D组加入PMA 10 0 0ng/ml缺氧 2 4h。③PKC抑制剂 2组 :A组缺氧 2 4h对照 ;B组加入Chelerythrine 10mmol/L缺氧 2 4h。免疫组化方法检测各组心肌细胞中VEGF的表达 ,经计算机图像处理 ,定量分析。结果 :缺氧刺激心肌细胞VEGF表达上调 ,PMA与Chelerythrine分别增强及减弱VEGF在缺氧心肌细胞中的表达。结论 :缺氧是心肌细胞表达VEGF的强烈刺激因素之一。缺氧诱导VEGF在心肌细胞中的表达 ,其信号传导途径部分是通过PKC通路实现的。
Objective: To clarify the effect of hypoxia on the expression of vascular endothelial growth factor (VEGF) and the role of protein kinase C (PKC) signal transduction pathway in cardiomyocytes. Methods: Primary cultured rat cardiomyocytes were divided into groups: ① normal hypoxia group 4: group A normal control; group B hypoxia 6h; group C hypoxia 12h; group D hypoxia 24h. PKC agonist group 4: group A 24 h hypoxia control; group B added PMA 10ng / ml hypoxia 24 h; group C PMA 10 0ng / ml hypoxia 24 h; group D added PMA 10 0ng / ml hypoxia 2 4h. ③ PKC inhibitor group 2: A group 24 h hypoxia control; B group Chelerythrine 10mmol / L hypoxia 24 h. Immunohistochemical method was used to detect the expression of VEGF in each group of cardiomyocytes. After computer image processing, quantitative analysis. Results: Hypoxia stimulated the expression of VEGF in cardiomyocytes, and PMA and Chelerythrine enhanced and decreased the expression of VEGF in hypoxic cardiomyocytes, respectively. Conclusion: Hypoxia is one of the strong stimulators of VEGF expression in cardiomyocytes. Hypoxia induces the expression of VEGF in cardiomyocytes, and part of its signaling pathway is through the PKC pathway.