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机构地区:[1]三峡大学医学院药理教研室,湖北省443002 [2]三峡大学医学院生物技术研究中心,湖北省443002
出 处:《江苏医药》2012年第5期506-508,共3页Jiangsu Medical Journal
基 金:湖北省教育厅自然科学研究计划中青年项目(Q20101206);宜昌市科学技术与开发项目(A01301-02)
摘 要:目的探讨丹参酮Ⅱ-A对局灶性脑缺血大鼠脑组织环氧化酶2(COX-2)及其下游产物含量的影响。方法 46只SD大鼠随机分为假手术(S)组(n=10)、缺血模型(I)组(n=11)和丹参酮Ⅱ-A低(T1)(n=12,丹参酮Ⅱ-A腹腔预注射1周,每日2mg/kg)、高(T2)(n=13,丹参酮Ⅱ-A腹腔预注射1周,每日4mg/kg)剂量预防组。采用持续性大脑中动脉线栓法制作局灶性脑缺血模型。持续栓塞3h后进行神经行为学评分,6h后断头取脑,干湿重法求出脑组织含水量,ELISA法测定脑组织中COX-2、6-酮前列腺素F1α(6-keto-PGF1α)、血栓素B2(TXB2)含量。结果与I组相比,T1、T2组神经功能损伤改善,脑组织含水量减少,COX-2、6-keto-PGF1α和TXB2的产生呈剂量依赖性的降低(P<0.01)。结论抑制COX-2及其下游产物TXA2、前列环素(PGI2)可能是丹参酮Ⅱ-A保护局灶性脑缺血大鼠神经功能的作用机制之一。Objective To investigate the effect of tanshinoneⅡ-A on the contents of cyclooxygenase 2(COX-2),prostacyclin(PGI2) and thromboxane A2(TXA2) in rats with focal cerebral ischemia in vivo.Methods Forty-six SD rats were divided into four groups of S(10 rats,sham operation),I(11 rats,ischemic model),T1(12 rats,pretreated by intraperitoneal injection of tanshinoneⅡ-A 2 mg·kg-1·d-1 for 7 days) and T2(13 rats,pretreated by intraperitoneal injection of tanshinoneⅡ-A 4 mg·kg-1·d-1 for 7 days).Focal cerebral ischemia model was established by permanent middle cerebral artery occlusion(pMCAO).Neurology deficit score was evaluated at 3 h after pMCAO.All animals were sacrificed for measuring water content of brain tissue by the wet and dry weight method and detecting the contents of COX-2,6-keto-PGF1αand TXB2 in the hippocampus by ELISA at 6 h after pMCAO.Results Compared with group I,neurological deficit score was improved,water content of brain tissue was reduced and COX-2,6-keto-PGF1α and TXB2 were decreased in a dose-dependent manner in groups of T1 and T2(P0.01).Conclusion The neuroprotective effect of tanshinoneⅡ-A on focal cerebral ischemia rats is partly due to its inhibition of the contents of COX-2,PGI2 and TXA2.
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