本文關(guān)鍵詞：電針水溝穴對腦缺血再灌注大鼠神經(jīng)細胞自噬的影響　出處：《第二軍醫(yī)大學》2016年碩士論文　論文類型：學位論文

  更多相關(guān)文章： 電針 水溝穴 腦缺血再灌注 自噬 LC3B p62 Bcl-2

【摘要】：目的:探討電針水溝穴對MCAO/R大鼠神經(jīng)細胞自噬的影響及其可能的作用機制。方法:本實驗參照Longa法并改良制備大鼠大腦中動脈缺血再灌注(MCAO/R)模型,大鼠腦缺血2h后再灌注24h和72h。將雄性SD大鼠隨機分為假手術(shù)組、模型組和治療組,每組按時相分為24h和72h 2個亞組。運用Bederson評分法對各組大鼠進行神經(jīng)功能評分。于再灌注后24h和72h 2個時間點取材,TTC染色法觀察并計算各組大鼠腦梗死體積比;光鏡觀察各組大鼠神經(jīng)細胞形態(tài)結(jié)構(gòu);透射電鏡觀察神經(jīng)細胞自噬體情況;western blot法檢測各組大鼠自噬相關(guān)蛋白LC3B、p62的表達;免疫組化法檢測Bcl-2陽性細胞的表達并計算Bcl-2陽性細胞率。結(jié)果:1.與同時相假手術(shù)組比較,模型24h組和模型72h組Bederson評分升高(p0.01),腦梗死體積比上升(p0.05),神經(jīng)細胞病理損害加重。治療24h組和治療72h組較同時相模型組Bederson評分降低(p0.05),梗死體積比減小(p0.05),神經(jīng)細胞損傷減輕。2.模型24h組透射電鏡下觀察到神經(jīng)細胞自噬體數(shù)量較多;與模型24h組比較,治療24h組神經(jīng)細胞自噬體數(shù)量減少。模型72h組和治療72h組未觀察到自噬體。3.模型24h組和模型72h組LC3B-II/LC3B-I的比值較假手術(shù)24h組升高(p0.01)。治療24h組和治療72h組LC3B-II/LC3B-I的比值與同時相模型組比較無統(tǒng)計學差異(p0.05)。4.模型24h組p62表達較假手術(shù)24h組降低(p0.05);模型72h組p62表達與假手術(shù)24h組比較無統(tǒng)計學差異(p0.05)。治療24h組p62表達較模型24h組升高(p0.05);治療72h組p62表達與模型72h組比較無統(tǒng)計學差異(p0.05)。5.與假手術(shù)24h組比較,模型24h組和模型72h組Bcl-2陽性細胞表達率升高,差異有統(tǒng)計學意義(p0.01);治療24h組Bcl-2陽性細胞表達率較模型24h組升高(p0.01),治療72h組Bcl-2陽性細胞表達率與模型72h組比較無統(tǒng)計學差異(p0.05)。結(jié)論:1.電針水溝穴縮小腦缺血再灌注損傷大鼠腦梗死體積,促進腦缺血再灌注損傷大鼠神經(jīng)功能恢復,對腦缺血再灌注損傷大鼠起到腦保護作用。2.電針水溝穴下調(diào)神經(jīng)細胞自噬水平可能是其對腦缺血再灌注損傷大鼠發(fā)揮腦保護作用的機制之一。3.電針水溝穴減輕腦缺血再灌注損傷大鼠神經(jīng)細胞自噬可能與其上調(diào)p62、Bcl-2表達水平有關(guān)。
[Abstract]:Objective: to investigate the effect of electroacupuncture at Shuigou point on neuronal autophagy in MCAO/R rats and its possible mechanism. MCAO / R) model. Male Sprague-Dawley rats were randomly divided into sham-operation group, model group and treatment group. Each group was divided into 2 subgroups at 24 h and 72 h. The neurological function of rats in each group was evaluated by Bederson scoring method. The samples were collected at 24 and 72 hours after reperfusion. The volume ratio of cerebral infarction was observed and calculated by TTC staining. The morphologic structure of nerve cells in each group was observed by light microscope. The neuronal autophagy was observed by transmission electron microscope. The expression of autophagy associated protein LC3BP62 was detected by western blot. Immunohistochemical method was used to detect the expression of Bcl-2 positive cells and calculate the rate of Bcl-2 positive cells. The Bederson scores of 24 h model group and 72 h model group were increased (p0.01), and the cerebral infarction volume ratio was increased (p0.05). Compared with the model group, the Bederson score and the infarct volume ratio of the 24 h and 72 h groups were lower than those of the model group (P 0.05 and P 0.05 respectively). The number of neuronal autophagy was observed under transmission electron microscope in the model group. The results were compared with the model group for 24 hours. The number of neuronal autophagy decreased in 24 h treatment group. No autophagy was observed in model group and 72 h group. The ratio of LC3B-II/LC3B-I in model group 24 h and model group 72 h was not observed. The value was higher than that in the 24 h sham operation group (. The ratio of LC3B-II/LC3B-I in 24 h group and 72 h group was not significantly different from that in the simultaneous model group (p 0.05). The expression of p62 in the 24 h model group was lower than that in the sham operation 24 h group. There was no significant difference in the expression of p62 between the model group and the sham operation group (24 h), but the expression of p62 in the 24 h treatment group was higher than that in the 24 h model group. There was no significant difference in p62 expression between the 72 h treatment group and the model 72 h group, and there was no significant difference between the treatment group and the sham operation 24 h group. The expression rate of Bcl-2 positive cells in 24 h model group and 72 h model group was higher than that in model 24 h group and 72 h group, the difference was statistically significant (P 0.01). The expression rate of Bcl-2 positive cells in the treatment group was higher than that in the model group (P 0.01). There was no significant difference in the expression rate of Bcl-2 positive cells between the 72 h group and the model group (P 0.05). Conclusion: electroacupuncture at Shuigou point can reduce the volume of cerebral infarction in rats with cerebral ischemia-reperfusion injury. To promote the recovery of nerve function in rats with cerebral ischemia-reperfusion injury. Electroacupuncture at Shuigou point down-regulating the level of neuronal autophagy may be one of the mechanisms of its protective effect on cerebral ischemia-reperfusion injury in rats. The effect of Acupoint on neuronal autophagy in rats with cerebral ischemia-reperfusion injury may be related to its up-regulation of p62. The expression level of Bcl-2 is related.
【學位授予單位】：第二軍醫(yī)大學
【學位級別】：碩士
【學位授予年份】：2016
【分類號】：R245.97

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