机构地区:[1]贵州医科大学附属医院,贵州贵阳550001 [2]贵州医科大学附属白云医院,贵州贵阳550001
出 处:《中国实用神经疾病杂志》2021年第11期921-927,共7页Chinese Journal of Practical Nervous Diseases
基 金:贵州省科技合作计划项目(编号:黔科合LH字[2015]7387号)。
摘 要:目的探讨不同浓度七氟醚预处理对短暂性全脑缺血(tGCI)大鼠海马组织神经细胞的影响。方法选取成年健康WKY大鼠48只,将所有WKY大鼠随机分为模型组、2%七氟醚预处理组、4%七氟醚预处理组和6%七氟醚预处理组,各组大鼠均建立tGCI大鼠模型,其中2%七氟醚预处理组、4%七氟醚预处理组和6%七氟醚预处理组分别给予浓度2%、4%和6%七氟醚处理,模型组给予等量生理盐水,HE染色观察各组海马组织,MTT比色法测定海马神经元活性,流式细胞仪检查海马神经细胞凋亡率,Westernblot检查Bax、LC3-Ⅱ蛋白、Bcl-2表达。结果模型组海马神经元结构及排列紊乱,细胞水肿,成片神经元系统核皱缩,七氟醚预处理组海马结构有所改善,其中6%七氟醚预处理组改善明显。七氟醚预处理组海马组织神经元活力OD值明显高于模型组(P<0.05),其中6%七氟醚预处理组海马神经元活力OD值为(1.55±0.26),高于2%七氟醚预处理组和4%七氟醚预处理组(P<0.05);七氟醚预处理组海马组织神经细胞凋亡率明显低于模型组(P<0.05),其中6%七氟醚预处理组海马神经细胞凋亡率为(12.24±3.11)%,低于2%七氟醚预处理组和4%七氟醚预处理组(P<0.05);七氟醚预处理组海马组织Bax蛋白相对表达量明显低于模型组(P<0.05),而Bcl-2、LC3-Ⅱ相对表达量明显高于模型组(P<0.05)。结论七氟醚预处理对tGCI大鼠模型海马组织神经细胞有保护作用,呈剂量依赖性,可能与调控Bax、LC3-Ⅱ和Bcl-2表达有关。Objective To investigate the effects of sevoflurane preconditioning on the neurons in hippocampus of transient global cerebral ischemia(tGCI)rats.Methods Forty-eight healthy adult SD rats were selected and randomly divided into model group,2% sevoflurane pretreatment group,4% sevoflurane pretreatment group and 6% sevoflurane pretreatment group,tGCI rat models were established in each group,in which 2% sevoflurane pretreatment group,4% sevoflurane pretreatment group and 6% sevoflurane pretreatment group were treated with 2%,4% and 6% sevoflurane respectively,and the model group was given the same amount of normal saline,the activity of hippocampal neurons was measured by MTT colorimetry,the apoptosis rate of hippocampal neurons was detected by flow cytometry,the expressions of Bax,LC3-Ⅱ protein and Bcl-2 were detected by Western blot.Results In the model group,the structure and arrangement of hippocampal neurons were disordered,the cells were edematous,and the nucleus of neuron system was shrunk,the hippocampal formation was improved in sevoflurane pretreatment group,6% sevoflurane pretreatment group improved significantly. The OD value of hippocampal neuron activity in sevoflurane pretreatment group was significantly higher than that in model group(P<0.05),the OD value of hippocampal neuron activity in 6% sevoflurane pretreatment group was(1.55±0.26),which was higher than that in 2% sevoflurane pretreatment group and 4% sevoflurane pretreatment group(P<0.05). The apoptosis rate of hippocampal neurons in sevoflurane pretreatment group was significantly lower than that in model group(P<0.05),the apoptosis rate of hippocampal neurons in 6% sevoflurane pretreatment group was(12.24±3.11)%,which was lower than that in 2% sevoflurane pretreatment group and 4% sevoflurane pretreatment group(P<0.05). The relative expression of Bax protein in sevoflurane pretreatment group was significantly lower than that in model group(P<0.05),while the relative expression of Bcl-2 and LC3-Ⅱwas significantly higher than that in mod
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