BK通道对大鼠脑缺血再灌注损伤神经细胞内钙离子浓度及神经细胞凋亡的影响
发布时间：2018-07-26 18:31
【摘要】：目的:研究大鼠脑缺血再灌注损伤模型BK通道对神经元细胞内钙离子浓度([ Ca~（2+）]i)的影响和对神经细胞凋亡的作用 方法:将108只SD(Sprague Dawley)大鼠随机分为假手术组(SS组,n=36)、缺血再灌注组(IR组,n=36)、BK通道特异拮抗剂依比蝎毒素IBTX(iberiotoxin)处理组(IBTX组,n=36),采用线栓法建立大鼠大脑中动脉阻塞(Middle cerebral artery occlusion,MCAO)模型,持续缺血90min后每组再分为3个亚组,分别再灌注6h(n=12)、12h(n=12)、24h(n=12),比较各组在相同再灌注各时间点神经功能缺损评分(NDS)、脑梗死面积,激光共聚焦显微镜技术测定各组[Ca~（2+）]i浓度,免疫组化和TUNEL法分别检测测BK通道表达和神经元细胞凋亡情况。 结果: IBTX组各相应再灌注时间点神经功能缺损评分优于IR组(P0.05);脑梗死体积明显大于SS组和IR组(P0.05);IBTX组与SS组和IR组相比较,各相应时点[Ca~（2+）]i明显增加,TUNEL法细胞凋亡亦有明显升高,差异具有统计学意义(P0.05),免疫组化结果显示缺血再灌注损伤后BK通道的表达增加,但IR组和IBTX组比较无统计学意义(P0.05)。 结论:BK通道可以降低脑缺血再灌注损伤后神经细胞内[Ca~（2+）]i,减少细胞凋亡的发生。
[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.
【学位授予单位】：华中科技大学
【学位级别】：硕士
【学位授予年份】：2011
【分类号】：R363
本文编号：2146921
[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.
【学位授予单位】：华中科技大学
【学位级别】：硕士
【学位授予年份】：2011
【分类号】：R363
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相关期刊论文 前2条
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2 杨光田,陈齐国,汤彦;一氧化氮和Ca~(2+)含量对缺血再灌注大鼠脑细胞凋亡的影响[J];微循环学杂志;2005年03期
，本文编号：2146921
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