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目的观察红豆杉多糖对Beagle犬心肌缺血再灌注导致的心肌细胞凋亡及单核细胞趋化蛋白-1(MCP-1)、NO表达的影响。方法将30只Beagle犬随机分为假手术组、模型组、红豆杉多糖(89.5、357mg/kg)组、卡维地洛(1mg/kg)对照组,每组6只,分别给药7d后,建立心肌缺血再灌注模型。TUNEL染色法标记缺血再灌注区凋亡心肌细胞,计算凋亡指数(AI);Western blotting法检测缺血再灌注区心肌MCP-1蛋白表达;硝酸还原酶法检测心肌组织中NO水平。结果模型组、红豆杉多糖低剂量组心肌细胞AI较假手术组显著升高(P<0.01);红豆杉多糖高剂量组、卡维地洛组心肌细胞AI显著低于模型组和红豆杉多糖低剂量组(P<0.05),与假手术组比较无显著差异(P>0.05)。模型组、红豆杉多糖低剂量组、卡维地洛组MCP-1蛋白表达较假手术组显著升高(P<0.05),红豆杉多糖低、高剂量组,卡维地洛组MCP-1蛋白表达较模型组显著下降(P<0.01),红豆杉多糖高剂量组MCP-1蛋白表达显著低于低剂量组和卡维地洛组(P<0.01)。模型组及各治疗组心肌组织NO水平较假手术组显著升高(P<0.01),红豆杉多糖高剂量组心肌NO显著低于模型组(P<0.05)及低剂量组(P<0.01)。结论红豆杉多糖可抑制缺血再灌注导致的心肌细胞凋亡,其机制可能与降低心肌组织MCP-1蛋白表达及NO水平、抑制心肌细胞凋亡有关。
Objective To observe the effects of Taxus chinensis polysaccharides on myocardial cell apoptosis and the expression of monocyte chemoattractant protein-1 (MCP-1) and nitric oxide synthase (NO) induced by myocardial ischemia-reperfusion in Beagle dogs. Methods Thirty Beagle dogs were randomly divided into sham operation group, model group, polysaccharides (89.5, 357mg / kg) group and carvedilol (1mg / kg) control group, , Establish myocardial ischemia-reperfusion model. Apoptotic index (AI) was measured by TUNEL staining. The protein expression of MCP-1 in myocardium was detected by Western blotting. Nitric oxide was used to detect the level of NO in myocardium. Results Compared with the sham-operation group, the AI in model group and low-dose group of polysaccharides of Taxus significantly increased (P <0.01), the AI of myocardial cells in high-dose group and carvedilol group was significantly lower than that of model group and polysaccharides Low dose group (P <0.05), no significant difference compared with sham operation group (P> 0.05). The expression of MCP-1 protein in model group, low dose polysaccharide group and carvedilol group was significantly higher than that in sham operation group (P <0.05) Compared with the model group, the protein expression of MCP-1 was significantly decreased (P <0.01). The MCP-1 protein expression of high dose polysaccharide group was significantly lower than that of low dose group and carvedilol group (P <0.01). Compared with sham operation group, NO level in model group and each treatment group was significantly higher than that in sham group (P <0.01); myocardial NO level in high dose polysaccharide group was significantly lower than that in model group and low dose group (P <0.01) . Conclusion Taxus polysaccharide can inhibit the apoptosis of myocardial cells induced by ischemia-reperfusion. Its mechanism may be related to the decrease of myocardial MCP-1 protein expression, NO level and the inhibition of cardiomyocyte apoptosis.