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目的探讨坎地沙坦(Cand esartan,CAN)是否具有不依赖血管紧张素1型受体(anti-inflammation viaindependent,AT1R)的抗炎作用及其可能的机制。方法以人肾小管上皮细胞为研究对象,观察CAN对肿瘤坏死因子(TNF-α)诱导炎症趋化因子的影响及CAN对TNF-α所诱导ROS的作用。采用RT-PCR方法测定相关分子mRNA表达,Western blotting和ELISA方法测定相关分子蛋白含量。结果 CAN能有效抑制TNF-α诱导炎症趋化因子MCP-1、RANTES mRNA和蛋白表达,且能抑制TNF-α诱导的NF-αB磷酸化。CAN还具有类是抗氧化应激物N乙酰半胱氨酸(NCA)的作用,抑制TNF-α诱导的ROS产生。结论 CAN能抑制TNF-α诱导肾小管上皮细胞发生炎症反应,其机制与CAN的直接抗氧化作用有关。
Objective To investigate the anti-inflammatory effect of Candidaartan (CAN) on angiotensin-1-type 1 receptor (AT1R) and its possible mechanism. Methods Human renal tubular epithelial cells were used as experimental subjects. The effects of CAN on tumor necrosis factor (TNF-α) -induced inflammatory chemokines and the effect of CAN on TNF-α-induced ROS were observed. The mRNA expression of related molecules was determined by RT-PCR, and the protein content of related molecules was determined by Western blotting and ELISA. Results CAN effectively inhibited TNF-α-induced inflammatory MCP-1, RANTES mRNA and protein expression, and inhibited TNF-α-induced NF-αB phosphorylation. CAN also has the effect that the class is an antioxidant stress regulator, N-acetylcysteine (NCA), that inhibits TNF-α-induced ROS production. Conclusion CAN can inhibit TNF-α-induced tubular epithelial cell inflammatory reaction, the mechanism of which is directly related to the anti-oxidative effect of CAN.