【摘要】：目的:研究大鼠腦缺血再灌注損傷模型BK通道對(duì)神經(jīng)元細(xì)胞內(nèi)鈣離子濃度([ Ca~（2+）]i)的影響和對(duì)神經(jīng)細(xì)胞凋亡的作用 方法:將108只SD(Sprague Dawley)大鼠隨機(jī)分為假手術(shù)組(SS組,n=36)、缺血再灌注組(IR組,n=36)、BK通道特異拮抗劑依比蝎毒素IBTX(iberiotoxin)處理組(IBTX組,n=36),采用線栓法建立大鼠大腦中動(dòng)脈阻塞(Middle cerebral artery occlusion,MCAO)模型,持續(xù)缺血90min后每組再分為3個(gè)亞組,分別再灌注6h(n=12)、12h(n=12)、24h(n=12),比較各組在相同再灌注各時(shí)間點(diǎn)神經(jīng)功能缺損評(píng)分(NDS)、腦梗死面積,激光共聚焦顯微鏡技術(shù)測(cè)定各組[Ca~（2+）]i濃度,免疫組化和TUNEL法分別檢測(cè)測(cè)BK通道表達(dá)和神經(jīng)元細(xì)胞凋亡情況。 結(jié)果: IBTX組各相應(yīng)再灌注時(shí)間點(diǎn)神經(jīng)功能缺損評(píng)分優(yōu)于IR組(P0.05);腦梗死體積明顯大于SS組和IR組(P0.05);IBTX組與SS組和IR組相比較,各相應(yīng)時(shí)點(diǎn)[Ca~（2+）]i明顯增加,TUNEL法細(xì)胞凋亡亦有明顯升高,差異具有統(tǒng)計(jì)學(xué)意義(P0.05),免疫組化結(jié)果顯示缺血再灌注損傷后BK通道的表達(dá)增加,但I(xiàn)R組和IBTX組比較無(wú)統(tǒng)計(jì)學(xué)意義(P0.05)。 結(jié)論:BK通道可以降低腦缺血再灌注損傷后神經(jīng)細(xì)胞內(nèi)[Ca~（2+）]i,減少細(xì)胞凋亡的發(fā)生。
[Abstract]:Objective: to study the effect of BK channel on intracellular calcium concentration ([Ca ~ (2)] I) and apoptosis of neurons in rats with cerebral ischemia-reperfusion injury. Methods: 108 SD (Sprague Dawley) rats were randomly divided into prosthetic hands. The operation group (SS group), the ischemia reperfusion group (IR group) and the control group (IBTX group) treated with IBTX (iberiotoxin), a BK channel specific antagonist, were used to establish the (Middle cerebral artery occlusion model of middle cerebral artery occlusion in rats. Each group was subdivided into 3 subgroups after continuous ischemia 90min. The cerebral infarction area of (NDS), was compared at the same time points after reperfusion for 6 h (nh 12) and 12 h (nna 12). The concentration of [Ca ~ (2)] I in each group was measured by confocal laser microscopy. The expression of BK channel and apoptosis of neurons were detected by immunohistochemistry and TUNEL method respectively. Results: the neurological deficit score at different reperfusion time points in IBTX group was better than that in IR group (P0.05), and the volume of cerebral infarction in IBTX group was significantly larger than that in SS group and IR group (P0.05). The difference was statistically significant (P0.05), the immunohistochemical results showed that the expression of BK channels increased after ischemia-reperfusion injury, but there was no significant difference between IR group and IBTX group (P0.05). Conclusion [Ca ~ (2)] I in neurons after cerebral ischemia-reperfusion injury can be reduced by WBK channel, and apoptosis can be reduced.
【學(xué)位授予單位】：華中科技大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2011
【分類(lèi)號(hào)】：R363

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本文編號(hào)：2146921