本文選題：腦缺血再灌注　切入點(diǎn)：防己黃芪湯　出處：《中國(guó)實(shí)驗(yàn)方劑學(xué)雜志》2015年12期 　論文類型：期刊論文

【摘要】：目的:研究防己黃芪湯(FJHQT)對(duì)大鼠局灶性腦缺血再灌注(I/R)損傷的保護(hù)作用,為其臨床防治腦缺血提供實(shí)驗(yàn)依據(jù)。方法:采用線栓法制備腦缺血再灌注損傷大鼠模型1 d后。將神經(jīng)行為評(píng)分合格的大鼠隨機(jī)分為FJHQT高、低劑量組、模型組、假手術(shù)組和陽(yáng)性對(duì)照尼莫地平組。連續(xù)口服給予FJHQT(按生藥量計(jì),1,2 g·kg-1)或尼莫地平(2 mg·kg-1)7 d后,觀察腦組織的梗死面積,測(cè)定腦組織Na+-K+-三磷酸腺苷(Na+-K+-ATP),還原型谷胱甘肽(GSH),過(guò)氧化氫酶(CAT)活性及炎癥因子白介素-6(IL-6),白介素-1β(IL-1β),腫瘤壞死因子α(TNF-α)水平。采用原位末端標(biāo)記(TUNEL)法測(cè)定腦組織中細(xì)胞凋亡,并采用免疫組化和蛋白免疫印跡法(Western blot)分析測(cè)定半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)蛋白表達(dá)。結(jié)果:與正常組比較,模型組大鼠缺血腦組織中Na+-K+-ATP,GSH,CAT活性顯著降低(P0.01),IL-6,IL-1β和TNF-α水平顯著提升(P0.01),凋亡程度及Caspase-3蛋白表達(dá)顯著提升(P0.01)。與模型組相比,FJHQT各劑量組均能提高缺血腦組織中Na+-K+-ATP,GSH,CAT活性;降低炎癥因子IL-6和TNF-α含量(P0.05,P0.01);減輕細(xì)胞凋亡程度并降低Caspase-3蛋白表達(dá)(P0.05,P0.01)。結(jié)論:FJHQT能明顯減輕缺血腦組織腦梗死面積,減少細(xì)胞凋亡、氧化損傷、炎癥反應(yīng)。
[Abstract]:Objective: to study the protective effect of Fangji Huangqi decoction (FJHQT) on focal cerebral ischemia-reperfusion injury in rats. Methods: after 1 day of cerebral ischemia reperfusion injury, the rats with good neurological behavior were randomly divided into FJHQT high dose group, low dose group and model group. The infarct size of brain tissue was observed after continuous oral administration of FJHQT (2g 路kg-1) or nimodipine (2mg 路kg-1)7 d) in sham operation group and Nimodipine group. The activity of Na K ATPase, reduced glutathione glutathione (GSH), catalase (CAT) and the levels of inflammatory cytokines IL 6, IL 6, IL 1 尾 1 尾, TNF- 偽) in brain tissue were determined by in situ end labeling Tunel (Tunel) method, and the expression of TNF- 偽 in brain tissue was determined by in situ terminal end labeling (Tunel) method, and the levels of interleukin 6 (IL 6), interleukin 1 尾 (IL 1 尾), and tumor necrosis factor 偽 (TNF- 偽) were measured by in situ end labeling (Tunel). The expression of cysteine aspartate protease 3 (caspase-3) was determined by immunohistochemistry and Western blotting. In the model group, the activity of Na -K ATPase GSH cat in ischemic brain tissue decreased significantly, the levels of IL-6 IL-1 尾 and TNF- 偽 increased significantly, and the degree of apoptosis and the expression of Caspase-3 protein increased significantly. Compared with the model group, the activity of Na K ATPase GSH cat in ischemic brain tissue was increased in each dose of FJHQT group. To reduce the content of IL-6 and TNF- 偽 and to reduce the degree of apoptosis and the expression of Caspase-3 protein. Conclusion: FJHQT can significantly reduce the area of cerebral infarction, apoptosis, oxidative injury and inflammatory reaction in ischemic brain tissue.
【作者單位】： 江西省醫(yī)藥學(xué)校;
【分類號(hào)】：R285.5;R-332

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相關(guān)期刊論文 前9條

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本文編號(hào)：1641992