摘要
目的探讨人参皂苷Rb1是否可以增加脑缺血再灌注损伤小鼠脑梗死半暗带区LncRNA Malat1的表达。方法将30只C57/B6小鼠按随机数字表法分成假手术组、模型+生理盐水对照组、模型+人参皂Rb1组,每组10只。采用大脑中动脉闭塞(MCAO)法建立小鼠脑缺血再灌注损伤模型。人参皂苷Rb1组和模型组大鼠在制模后即刻分别腹腔注射人参皂苷Rb1(40 mg/kg)和等量生理盐水。再灌注损伤后24 h观察各组小鼠的神经行为学评分、脑梗死体积、Bcl-2蛋白表达量和LncRNA Malat1含量。结果与假手术组相比,模型组小鼠神经行为学评分和脑梗死体积明显增加(P<0.05),Bcl-2蛋白表达量和LncRNA Malat1表达水平明显增加(P<0.05);与模型组相比,人参皂苷Rb1组小鼠神经行为学评分和脑梗死体积明显减少(P<0.05),Bcl-2蛋白表达量和LncRNA Malat1表达水平进一步增加(P<0.05)。结论人参皂苷Rb1可以改善MCAO小鼠的神经行为学评分、减小脑梗死体积和增加Bcl-2蛋白表达量。人参皂苷Rb1具有脑保护作用,其可能的机制与增加小鼠脑梗死半暗带区LncRNA Malat1的表达有关。
Objective To investigate whether ginsenoside Rb1 can increase the expression of LncRNA Malat1 in the penumbra of cerebral infarction in mice with cerebral ischemia-reperfusion injury.Methods Thirty C57/B6 mice were divided into sham operation group,model+normal saline control group,model+ginsenoside Rb1 group according to random number table method,with 10 mice in each group.The cerebral ischemia-reperfusion injury model in mice was established by using middle cerebral artery occlusion(MCAO)method.Rats in the ginsenoside Rb1 group and model group were injected intraperitoneally with ginsenoside Rb1(40 mg/kg)and the same amount of normal saline immediately after modeling.The neuroethology score,cerebral infarction volume,Bcl-2 protein expression and LncRNA Malat1 content of mice in each group were observed 24 hours after reperfusion injury.Results Compared with those of the sham operation group,the neurobehavior score and cerebral infarction volume of the model group were significantly increased(P<0.05),the expression levels of Bcl-2 protein and LncRNA Malat1 were significantly increased(P<0.05).Compared with those of the model group,the neurobehavioral score and cerebral infarction volume of the ginsenoside Rb1 group were significantly reduced(P<0.05),and the expression levels of Bcl-2 protein and LncRNA Malat1 were further increased(P<0.05).Conclusion Ginsenoside Rb1 can improve the neuroethology,reduce the volume of cerebral infarction and increase the expression of Bcl-2 protein in MCAO mice.Ginsenoside Rb1 has a protective effect,and its possible mechanism is related to the increased expression of LncRNA Malat1 in the penumbra of cerebral infarction in mice.
作者
王雷雷
戴勤学
WANG Leilei;DAI Qinxue(The First Affiliated Hospital of Wenzhou Medical University,Wenzhou325800,China)
出处
《中国现代医生》
2020年第23期41-44,49,F0003,共6页
China Modern Doctor
基金
国家自然科学基金青年基金项目(81704180)。