瑞替加濱對缺血性腦卒中模型大鼠星形膠質(zhì)細胞及Caspase-3的表達影響
發(fā)布時間：2018-07-25 08:54
【摘要】：目的通過Longa5方法比較神經(jīng)功能缺損評分,TTC染色法測量腦梗死體積變化,應(yīng)用免疫組化檢測星形膠質(zhì)纖維酸性蛋白(GFAP)陽性表達細胞(即星形膠質(zhì)細胞)數(shù)和細胞凋亡蛋白酶-3(Caspase-3)陽性表達細胞數(shù)。探討瑞替加濱對腦梗死大鼠GFAP、Caspase-3表達水平的影響,進而探討瑞替加濱(Retigabine RTG)對缺血性腦卒中模型大鼠的保護作用及機制。方法選取SD大鼠75只,隨機分為假手術(shù)組(15只,Sham組),模型組(15只,MCAO組),干預(yù)組(45只,RTG組)。干預(yù)組按照梗死再灌注后給藥時間的不同又分為RTG 0h組;RTG 1h組;RTG 3h組,各組15只。通過大鼠尾靜脈給藥。給藥劑量:RTG(10mg/kg)。假手術(shù)組和模型組不做任何處理,僅給予等量生理鹽水。制備經(jīng)典的大腦中動脈缺血再灌注模型大鼠,Longa5方法比較神經(jīng)功能缺損評分,應(yīng)用經(jīng)典的TTC染色法測量腦梗死體積的變化;免疫組化法觀察腦缺血后再灌注三組大鼠腦組織皮層GFAP、Caspase-3表達變化,顯微鏡下計數(shù)陽性細胞數(shù)。應(yīng)用SPSS17.0統(tǒng)計軟件進行統(tǒng)計學(xué)分析,結(jié)果用均數(shù)±標(biāo)準(zhǔn)(`X±s)表示,多組間比較采用單因素方差分析,兩兩比較采用LSD法或SNK法。P0.05認(rèn)為差異有統(tǒng)計學(xué)意義。結(jié)果1神經(jīng)功能缺損評分:假手術(shù)組未出現(xiàn)神經(jīng)功能缺損癥狀,模型組組均表現(xiàn)出一定程度的神經(jīng)功能缺損癥狀,表現(xiàn)為:或身體蜷縮,或身體平衡能力差,向左側(cè)旋轉(zhuǎn)及傾倒,或不能行走等。與模型組相比,RTG干預(yù)組神經(jīng)功能缺損癥狀評分明顯降低(P0.05),表現(xiàn)為單一的神經(jīng)功能缺損癥狀,或者合并兩種神經(jīng)功能缺損癥狀,但RTG不同作用時間各亞組間差異無統(tǒng)計學(xué)意義。2 TTC染色:TTC圖像顯示:假手術(shù)組未見缺血梗死灶;模型組腦組織可見不同程度的梗死灶。RTG 0h、1 h、3 h干預(yù)組梗死灶較模型組明顯降低(P0.05),但RTG不同作用時間各亞組間差異無統(tǒng)計學(xué)意義。3免疫組化:免疫組化檢測假手術(shù)組可見少量GFAP及細胞凋亡Caspase-3陽性細胞的表達;干預(yù)組的GFAP、細胞凋亡Caspase-3表達均較模型組明顯減少(P0.05),但干預(yù)組不同作用時間各亞組間差異無統(tǒng)計學(xué)意義。結(jié)論1瑞替加濱能明顯降低腦梗死大鼠神經(jīng)功能學(xué)評分,減少腦梗死體積。2瑞替加濱減少大鼠腦梗死中GFAP、細胞凋亡Caspase-3的表達,對大鼠缺血性腦卒中具有保護作用,其作用機制可能是瑞替加濱能夠在細胞去極化時持續(xù)使大量鉀離子外流抑制神經(jīng)元的興奮性,使神經(jīng)細胞的興奮性明顯降低,減少谷氨酸的釋放,從而進一步減輕腦梗死周圍區(qū)的炎癥反應(yīng),也抑制神經(jīng)元的細胞凋亡,但時間依賴性有待研究。
[Abstract]:Objective to compare the changes of cerebral infarction volume by Longa5. The number of (GFAP) positive cells (astrocytes) and the number of apoptotic protease-3 (Caspase-3) positive cells were detected by immunohistochemistry. Objective: to investigate the effect of retegabine on the expression of Caspase-3 in cerebral infarction rats, and to explore the protective effect and mechanism of retegabine (Retigabine RTG) on ischemic stroke rats. Methods Seventy-five SD rats were randomly divided into sham-operated group (15 rats), model group (15 rats) and intervention group (45 rats). According to the time of administration after reperfusion, the intervention group was divided into RTG 0 h group and 1 h group with 15 rats in each group. The drug was administered through the tail vein of rats. Give the potion a dose of: RTG (10mg/kg). Sham operation group and model group did not do any treatment, only the same amount of physiological saline. A classical middle cerebral artery ischemia-reperfusion model was established to compare the neurological deficit scores in rats. The changes of cerebral infarct volume were measured by classical TTC staining. Immunohistochemical method was used to observe the changes of Caspase-3 expression in cerebral cortex of rats after cerebral ischemia and reperfusion, and the number of positive cells was counted under microscope. SPSS17.0 statistical software was used to carry out statistical analysis. The results were expressed as mean 鹵standard (`X 鹵s). The results showed that the differences were statistically significant by using LSD method or SNK method. Results 1 the neurological deficit score: there was no neurological deficit in the sham-operation group, and the model group showed some neurological deficit symptoms, such as body curling up or poor body balance. Rotate and fall to the left, or be unable to walk, etc. Compared with the model group, the score of neurological deficit symptoms in RTG intervention group was significantly lower (P0.05), showing a single neurological deficit symptom, or combined with two neurological deficit symptoms. However, there was no significant difference among subgroups of RTG at different time of action. 2. 2 TTC staining showed that there was no ischemic infarct in sham-operation group. The infarct focus of the model group was significantly lower than that of the model group (P0.05), but there was no significant difference between the subgroups of RTG at different time of action. Immunohistochemistry was used to detect sham-operation. A small amount of GFAP and apoptotic Caspase-3 positive cells were found in group A; The expression of GFAPand apoptotic Caspase-3 in intervention group was significantly lower than that in model group (P0.05), but there was no significant difference among subgroups of intervention group at different time of action. Conclusion (1) Retigabine can significantly decrease the neurological function score, reduce the volume of cerebral infarction, reduce the expression of GFAPand apoptosis Caspase-3 in cerebral infarction rats, and have protective effect on ischemic stroke in rats. The mechanism may be that retigabine can continuously inhibit the excitability of neurons and decrease the release of glutamate by retigabine, which can inhibit the excitability of neurons and inhibit the neuronal excitability by a large amount of potassium ion efflux during the depolarization of the cells. Therefore, the inflammatory reaction around cerebral infarction was further alleviated and the apoptosis of neurons was inhibited, but the time dependence needed to be studied.
【學(xué)位授予單位】：華北理工大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R743.3;R-332
本文編號：2143295
[Abstract]:Objective to compare the changes of cerebral infarction volume by Longa5. The number of (GFAP) positive cells (astrocytes) and the number of apoptotic protease-3 (Caspase-3) positive cells were detected by immunohistochemistry. Objective: to investigate the effect of retegabine on the expression of Caspase-3 in cerebral infarction rats, and to explore the protective effect and mechanism of retegabine (Retigabine RTG) on ischemic stroke rats. Methods Seventy-five SD rats were randomly divided into sham-operated group (15 rats), model group (15 rats) and intervention group (45 rats). According to the time of administration after reperfusion, the intervention group was divided into RTG 0 h group and 1 h group with 15 rats in each group. The drug was administered through the tail vein of rats. Give the potion a dose of: RTG (10mg/kg). Sham operation group and model group did not do any treatment, only the same amount of physiological saline. A classical middle cerebral artery ischemia-reperfusion model was established to compare the neurological deficit scores in rats. The changes of cerebral infarct volume were measured by classical TTC staining. Immunohistochemical method was used to observe the changes of Caspase-3 expression in cerebral cortex of rats after cerebral ischemia and reperfusion, and the number of positive cells was counted under microscope. SPSS17.0 statistical software was used to carry out statistical analysis. The results were expressed as mean 鹵standard (`X 鹵s). The results showed that the differences were statistically significant by using LSD method or SNK method. Results 1 the neurological deficit score: there was no neurological deficit in the sham-operation group, and the model group showed some neurological deficit symptoms, such as body curling up or poor body balance. Rotate and fall to the left, or be unable to walk, etc. Compared with the model group, the score of neurological deficit symptoms in RTG intervention group was significantly lower (P0.05), showing a single neurological deficit symptom, or combined with two neurological deficit symptoms. However, there was no significant difference among subgroups of RTG at different time of action. 2. 2 TTC staining showed that there was no ischemic infarct in sham-operation group. The infarct focus of the model group was significantly lower than that of the model group (P0.05), but there was no significant difference between the subgroups of RTG at different time of action. Immunohistochemistry was used to detect sham-operation. A small amount of GFAP and apoptotic Caspase-3 positive cells were found in group A; The expression of GFAPand apoptotic Caspase-3 in intervention group was significantly lower than that in model group (P0.05), but there was no significant difference among subgroups of intervention group at different time of action. Conclusion (1) Retigabine can significantly decrease the neurological function score, reduce the volume of cerebral infarction, reduce the expression of GFAPand apoptosis Caspase-3 in cerebral infarction rats, and have protective effect on ischemic stroke in rats. The mechanism may be that retigabine can continuously inhibit the excitability of neurons and decrease the release of glutamate by retigabine, which can inhibit the excitability of neurons and inhibit the neuronal excitability by a large amount of potassium ion efflux during the depolarization of the cells. Therefore, the inflammatory reaction around cerebral infarction was further alleviated and the apoptosis of neurons was inhibited, but the time dependence needed to be studied.
【學(xué)位授予單位】：華北理工大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R743.3;R-332
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