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背景:血管舒张在环孢素A所致肾毒性的发生过程中起重要的作用。目的:观察绿茶多酚对环孢素 A 抑制血管舒张的缓解作用及其机制。方法:SD 大鼠随机平均分为4组:环孢素A组、对照组、环孢素 A+绿茶多酚组和绿茶多酚组。经5周的药物处理之后,测定大鼠血尿素氮和肌酐水平。将各组大鼠的胸主动脉环放置于水浴系统上,以乙酰胆碱诱发血管舒张,并观察 L-NAME、吲哚美辛和去内皮细胞对血管舒张的作用。结果与结论:环孢素A组大鼠血尿素氮和肌酐水平显著高于对照组(P<0.05)。环孢素 A组中,乙酰胆碱诱发的血管舒张的最大反应率显著低于对照组和绿茶多酚组。以L-NAME 预处理后,环孢素A组,环孢素A+绿茶多酚组和绿茶多酚组中血管舒张显著低于对照组;以吲哚美辛预处理后,对照组,环孢素A+绿茶多酚组和绿茶多酚组的血管舒张显著高于环孢素A组。环孢素A组血管壁组织中一氧化氮代谢物水平显著低于其他组。提示环孢素A能减少血管壁组织中的一氧化氮水平,引起内皮细胞-依赖性的血管舒张反应发生异常变化。
BACKGROUND: Vasodilation plays an important role in the development of cyclosporine-induced nephrotoxicity. Objective: To observe the mitigating effect of green tea polyphenols on vasodilation induced by cyclosporin A and its mechanism. Methods: SD rats were randomly divided into 4 groups: cyclosporin A group, control group, cyclosporine A + green tea polyphenol group and green tea polyphenol group. After 5 weeks of drug treatment, blood urea nitrogen and creatinine levels were measured. The thoracic aorta rings of rats in each group were placed on a water bath system, and vasodilation was induced by acetylcholine. The effects of L-NAME, indomethacin and endotheliocyte on vasodilation were observed. RESULTS AND CONCLUSION: The levels of blood urea nitrogen and creatinine in cyclosporin A group were significantly higher than those in control group (P <0.05). In cyclosporine A group, the maximal response rate of acetylcholine-induced vasodilation was significantly lower than that of the control group and the green tea polyphenol group. After pretreatment with L-NAME, vasodilatation in cyclosporin A group, cyclosporin A + green tea polyphenol group and green tea polyphenol group was significantly lower than that in control group; after pretreatment with indomethacin, the control group, cyclosporine Vasodilatation in the A + green tea polyphenols and green tea polyphenols groups was significantly higher than that in the cyclosporine A group. Levels of nitric oxide metabolites in the cyclosporin A group were significantly lower than those in the other groups. This suggests that cyclosporin A can reduce nitric oxide level in the vascular wall tissue and cause abnormal changes of endothelial cell-dependent vasodilation.