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作 者:张美齐[1] 翟昌林[1] 涂建锋[1] 杨向红[1]
出 处:《中华急诊医学杂志》2012年第6期626-630,共5页Chinese Journal of Emergency Medicine
摘 要:目的探讨丹参酮ⅡA(tanshinone,TSN)对大鼠脑缺血·再灌注损伤的保护作用及对高迁移率族蛋白1(highmobilitygroupbox1,HMGB1)表达的影响。方法雄性sD大鼠32只随机(随机数字法)分为4组(n=8),分别为假手术组(Sham组)、缺血一再灌注组(I/R组)、丹参酮ⅡA低剂量组(TaLD组)与丹参酮ⅡA高剂量组(TaHD组)。采用右侧大脑中动脉栓塞(MCA0)法建立大鼠脑缺血一再灌注损伤模型。Trc染色法检测大鼠脑梗死体积,Tunnel法检测大脑皮质区细胞凋亡并计算凋亡指数,免疫印迹法检测大脑HMGBl的表达,ELISA法检测大鼠血清HMGBl水平,并测定大脑皮质钙调蛋白(calmodulin,CaM)活性及丙二醛(malondiadehyde,MDA)含量的变化。结果与Sham组比较,I/R组、TaLD组与TaHD组大鼠脑梗死体积增大,凋亡细胞增多,CaM活性显著增强,MDA含量升高,脑组织及血清HMGBI水平明显升高(P〈0.01)。与I/R组比较,TaLD、TaHD组脑梗死体积缩小、凋亡细胞减少,CaM活性显著减弱,MDA含量降低,脑组织及血清HMGB1水平明显降低(P〈0.01),且TaLD组与TaHD组之间上述各指标值差异具有统计学意义(P〈0.01)。结论丹参酮ⅡA能够减轻大鼠脑缺血-再灌注损伤,其机制可能与减轻脑缺血.再灌注阶段HMGBl介导的晚期炎症反应有关。Objective To investigate the influence of Tanshinone H A on the expression of HMGB1 in rats with cerebral ischemia-reperfusion (I/R) injury and its neural function protection. Methods The 32 male SD rats were randomly (random number) divided into 4 groups (8 rats per group) : Sham group, I/ R group, group with low dose of Tanshinone Ⅱ A ( TaLD group) and group with high dose of Tanshinone Ⅱ A (TaHD group). The cerebral I/R models were established by the method of right middle cerebral artery occlusion (MCAO). Cerebral infarct volume was detected by Trc staining. Apoptotic cell and apoptotic index were calculated by Tunnel assay. The HMGB1 levels in brain and serum was detected by Western blot and ELISA. Calmedulin (CaM) activity and malondialdehyde (malondiadehyde, MDA) content in the brain were also detected. Results Compared with the Sham group, the volume of cerebral infarction, the number of apoptotie cells, CaM activity, MDA content, HMGB1 levels in the brain tissue and serum in group I/R, TaLD group and TaHD group increased significantly (P 〈 0.01 ) . Compared with the group I/ R, the volume of cerebral infarction, the number of apoptotic cells, CaM activity, MDA content and the HMGB1 levels in brain tissue and serum in TaLD groupand TaHDgroup decreased significantly (P 〈 0. 01 ). The difference of the above index between TaLD groupand TaHDgroup was significant ( P 〈 0. 01 ). Conclusions Tan Ⅱ A could reduce the cerebral ischemic reperfusion injury in rats which was likely related with decreasing the inflammatory response in the late stage via HMGB1.
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