河北医科大学学报
河北醫科大學學報
하북의과대학학보
JOURNAL OF HEBEI MEDICAL UNIVERSITY
2014年
8期
869-872
,共4页
温雅%祝春华%王力娜%季辉%刘莹
溫雅%祝春華%王力娜%季輝%劉瑩
온아%축춘화%왕력나%계휘%류형
脑梗死%血脑屏障%丹参酮
腦梗死%血腦屏障%丹參酮
뇌경사%혈뇌병장%단삼동
brain infarction%blood-brain barrier%tanshinone
目的:探讨丹参酮ⅡA 对大鼠脑梗死后血脑屏障的保护作用及其机制。方法线栓法建立大脑中动脉闭塞(middle cerebral artery occlusion,MCAO)大鼠模型。实验采用随机分组(n =168),分为假手术组、MCAO 组、丹参酮ⅡA 大剂量组、丹参酮ⅡA 小剂量组。丹参酮ⅡA 于术后立即腹腔注射,大鼠24h 处死。采用 Western Blot和反转录-聚合酶链反应测定 claudin-5蛋白和 IgG 变化,激光共聚焦显微镜观察双重荧光标记的 claudin-5和 IgG在脑组织的分布,并观察神经功能、脑梗死体积和脑水肿。结果与假手术组比较,MCAO 组 claudin-5表达明显减少;大剂量丹参酮ⅡA 能够显著上调 claudin-5,明显改善神经功能,减轻脑水肿,减小梗死体积,减少 IgG 渗出,保护血脑屏障。结论大剂量丹参酮ⅡA 通过上调 claudin-5表达,维持血管内皮细胞紧密连接的完整性,对血脑屏障发挥保护作用,是丹参酮ⅡA 治疗脑梗死的重要机制
目的:探討丹參酮ⅡA 對大鼠腦梗死後血腦屏障的保護作用及其機製。方法線栓法建立大腦中動脈閉塞(middle cerebral artery occlusion,MCAO)大鼠模型。實驗採用隨機分組(n =168),分為假手術組、MCAO 組、丹參酮ⅡA 大劑量組、丹參酮ⅡA 小劑量組。丹參酮ⅡA 于術後立即腹腔註射,大鼠24h 處死。採用 Western Blot和反轉錄-聚閤酶鏈反應測定 claudin-5蛋白和 IgG 變化,激光共聚焦顯微鏡觀察雙重熒光標記的 claudin-5和 IgG在腦組織的分佈,併觀察神經功能、腦梗死體積和腦水腫。結果與假手術組比較,MCAO 組 claudin-5錶達明顯減少;大劑量丹參酮ⅡA 能夠顯著上調 claudin-5,明顯改善神經功能,減輕腦水腫,減小梗死體積,減少 IgG 滲齣,保護血腦屏障。結論大劑量丹參酮ⅡA 通過上調 claudin-5錶達,維持血管內皮細胞緊密連接的完整性,對血腦屏障髮揮保護作用,是丹參酮ⅡA 治療腦梗死的重要機製
목적:탐토단삼동ⅡA 대대서뇌경사후혈뇌병장적보호작용급기궤제。방법선전법건립대뇌중동맥폐새(middle cerebral artery occlusion,MCAO)대서모형。실험채용수궤분조(n =168),분위가수술조、MCAO 조、단삼동ⅡA 대제량조、단삼동ⅡA 소제량조。단삼동ⅡA 우술후립즉복강주사,대서24h 처사。채용 Western Blot화반전록-취합매련반응측정 claudin-5단백화 IgG 변화,격광공취초현미경관찰쌍중형광표기적 claudin-5화 IgG재뇌조직적분포,병관찰신경공능、뇌경사체적화뇌수종。결과여가수술조비교,MCAO 조 claudin-5표체명현감소;대제량단삼동ⅡA 능구현저상조 claudin-5,명현개선신경공능,감경뇌수종,감소경사체적,감소 IgG 삼출,보호혈뇌병장。결론대제량단삼동ⅡA 통과상조 claudin-5표체,유지혈관내피세포긴밀련접적완정성,대혈뇌병장발휘보호작용,시단삼동ⅡA 치료뇌경사적중요궤제
Objective This study is to explore the protective role and mechanism of tanshinoneⅡA(Tan ⅡA)for the blood-brain barrier in focal cerebral ischemia of rats. Methods Male Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion(MCAO). Sprague-Dawley rats (n = 168)were randomly divided into sham-operated group,MCAO group,TanⅡA higher dose group (TanⅡA-H)and TanⅡA lower dose group(TanⅡA-L). Tan ⅡA was administered with intraperitomeal injection immediately after operation,rats were executed at 24h. Western Blot,RT-PCR and confocal microscope were used to measure claudin-5 protein and IgG expression in ischemic brain. And the neurological deficits,brain water content and infarct volume were explored. Results At 24h after focal cerebral ischemia,claudin-5 expression in MCAO group decreased. Claudin-5 in Tan Ⅱ A-H group significantly up-regulated,and also its neurologic deficit,infarct volume and brain water content were alleviated compared with MCAO group( P ﹤ 0. 05). Conclusion Tan Ⅱ A-H protected blood-brain barrier permeability by increasing claudin-5,which might be the mechanism of treating focal cerebral ischemia.