机构地区:[1]安徽省第二人民医院神经内科,安徽合肥230041
出 处:《安徽医药》2021年第9期1727-1731,I0002,共6页Anhui Medical and Pharmaceutical Journal
摘 要:目的研究山茱萸环烯醚萜苷(CIG)对急性脑梗死小鼠的神经保护作用,并探讨其可能机制。方法将18只ICR小鼠采用随机数字表法分为对照组、模型组、实验组,每组6只。参考大脑中动脉栓塞法对小鼠进行造模,实验组小鼠腹腔注射150 mg/kgCIG,连续给药7 d,对比三组小鼠的神经损伤评分,并观察小鼠的脑梗死体积,使用TUNEL检测测定小鼠神经元的凋亡率,使用实时荧光定量PCR和蛋白质印迹法检测脑组织中磷酸化胞外信号调节激酶1/2(p-ERK1/2)蛋白、胞外信号调节激酶1/2(ERK1/2)、B细胞淋巴瘤-2(Bcl-2)、Bcl-2相关X(Bax)蛋白及mRNA的表达情况。结果与对照组相比,模型组小鼠神经功能缺损评分、脑梗死体积、神经元凋亡率、BaxmRNA及其蛋白和p-ERK1/2蛋白表达升高,Bcl-2 mRNA及其蛋白表达降低(P<0.05),其中神经元凋亡率(79.678±7.203)%、BaxmRNA(3.84±0.29)及其蛋白表达(1.01±0.07)、p-ERK1/2蛋白表达(0.90±0.08)高于对照组的(1.983±1.071)%、(1.04±0.09)、(0.21±0.07)、(0.41±0.08),Bcl-2 mRNA(1.00±0.07)及其蛋白表达(0.50±0.07)低于对照组的(3.86±0.32)、(1.29±0.08)。与模型组相比,实验组小鼠神经功能缺损评分、脑梗死体积、神经元凋亡率、BaxmRNA及其蛋白降低,Bcl-2 mRNA及其蛋白表达和p-ERK1/2蛋白表达升高(P<0.05),其中神经元凋亡率(49.171±10.914)%、BaxmRNA(2.04±0.23)及其蛋白表达(0.51±0.08)低于模型组,Bcl-2 mRNA(2.58±0.24)及其蛋白表达(0.93±0.34)、p-ERK1/2蛋白表达(1.52±0.09)高于模型组。结论CIG可能是通过ERK信号通路发挥对急性脑梗死小鼠的神经保护作用。Objective To study the neuroprotective effect of cornel iridoid glycoside(CIG)on acute cerebral infarction in mice and explore its possible mechanism.Methods Eighteen ICR mice were divided into control group,model group and experiment group by random number table method,with 6 mice in each group.Experimental models were established according to the middle cerebral artery embolization method,mice in the experimental group were intraperitoneally injected with 150 mg/kg CIG for 7 days.The neurological injury scores of three groups of mice were compared and the cerebral infarction volume of mice was observed.Apoptotic rate of mice neurons was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling(TUNEL).The expression of phosphorylation extracellular regulated protein 1/2(p-ERK1/2)protein,ERK1/2,B cell lymphoma/leukemia-2(Bcl-2),Bcl-2 associated X protein(Bax)protein and mRNA in brain tissue were detected by quantitative Real-time PCR and Western blotting.Results Compared with the control group,the neurological deficit score,cerebral infarction volume,neuronal apoptosis rate,Bax mRNA and protein and p-ERK1/2 protein expression in the model group were increased,while Bcl-2 mRNA and protein expression were decreased(P<0.05).The neuronal apoptosis rate(79.678±7.203)%,Bax mRNA(3.84±0.29)and protein expression(1.01±0.07),p-ERK1/2 protein(0.90±0.08)were higher than those of the control group(1.983±1.071)%,(1.04±0.09),(0.21±0.07),(0.41±0.08),and the expression of Bcl-2 mRNA(1.00±0.07)and protein(0.50±0.07)were lower than that of the control group(3.86±0.32),(1.29±0.08).Compared with the model group,the neurological deficit score,cerebral infarction volume,neuronal apoptosis rate,Bax mRNA and protein in the experimental group were decreased,while Bcl-2 mRNA and protein expression,p-ERK1/2 protein expression were increased(P<0.05).The neuronal apoptosis rate(49.171±10.914)%,Bax mRNA(2.04±0.23)and protein expression(0.51±0.08)were lower than those of the model group,and the expression
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