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出 处:《中药药理与临床》2014年第4期1-5,共5页Pharmacology and Clinics of Chinese Materia Medica
基 金:国家自然科学基金(81274111)
摘 要:目的:研究三黄泻心汤(简称泻心汤)对全脑缺血再灌注(Ischemia Reperfusion,I/R)损伤后大鼠脑组织中氧化损伤及炎性损伤的保护作用。方法:连续给药7天后,采用两侧颈总动脉夹闭结合低血压方法制备全脑缺血再灌注损伤大鼠模型,再灌注后继续给药2d,末次给药0.5h后处死大鼠,测定脑指数、脑组织含水量、脑组织中H2O2、MDA的含量和Na+-K+-ATP、Ca2+-ATP、SOD、CAT、GSH-Px的活力,血清中IL-1β、IL-6、TNF-α的含量,脑组织中NFκB p65蛋白亚基及其磷酸化表达情况,及IL-1β、IL-6、TNF-α等mRNA表达情况。结果:泻心汤8.74 g/kg剂量能降低全脑缺血再灌注模型大鼠的脑指数及脑组织含水量,减少脑内H2O2及MDA含量,提高CAT、SOD、GSH-Px、Na+-K+-ATP、Ca2+-ATP等酶的活力,降低IL-1β、IL-6、TNF-α含量,抑制NFκB p65亚基磷酸化及IL-1β、TNF-αmRNA表达。结论:泻心汤可通过提高模型大鼠脑内Na+-K+-ATP、Ca2+-ATP酶及抗氧化酶活力,减轻受损组织中的水肿及氧化应激损伤,且抑制转核因子的激活及炎性因子的转录,发挥对全脑缺血再灌注大鼠脑组织损伤的保护作用。To investigate the Protective effect of Sanhuangxiexin Decoction (Xiexin Decoction) on oxidative and inflammation damage induced by global cerebral ischemia reperfusion injury in rats. Methods: Xiexin Decoction( 8.74g/( kg · d) ,3.74g/( kg · d) ) was intragas- tric administrated for 7 days before the operation, the rat model of global cerebral ischemia reperfusion injury by bilateral common carotid ar- teries occlusion combined with hemorrhagic hypotension. The rats were continued administrated,then sacrificed at 48h after reperfusion. The content of H2 02 and MDA, the activity of Na + -K + -ATP, Ca2 + -ATP, SOD, CAT and GSH-Px, the phosphorylation NFKB 1)65 subunit and the expression of IL-1β, IL-6, TNF-α mRNA in brain tissue were measured. And the content of IL-1β, IL-6, TNF-α in serum also been test. Results: Xiexin Decoction (8.74g/( kg · d) ) can significantly strengthen the activity of Na + -K + -ATP, Ca2 + -ATP to ease Cerebral e- dema, reduce the content of H2O2 and MDA, strengthen notably the activity of CAT, SOD and GSH-Px, reduce the content of IL-1β, IL-6 and TNF-α, inhibited apparently the expression of IL-113 mRNA, IL-6 mRNA and TNF-α mRNA, Suppress evidently the phosphorylation of NFKB p65 subunit. Conclusion: Xiexin Decoction can play a protective role against cerebral ischemia-reperfusion injury by increasing the activity of Na + -K -ATP, Ca2+ -ATP, CAT, SOD and GSH-Px in brain, inhibiting the activation of transcription factor nuclear transfer and expression of inflammatory cytokines.
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