二氢杨梅素对小鼠局灶性脑缺血/再灌注损伤的抗凋亡作用及机制研究(1)
[摘要]目的 探討二氢杨梅素(DMY)对小鼠局灶性脑缺血再灌注(I/R)损伤的抗细胞凋亡作用和相关机制，从而研究DMY抗脑缺血损伤的保护机制。方法 将雄性昆明种小鼠随机分为假手术组、I/R模型组及DMY(500 mg/kg)组。小鼠大脑中动脉阻塞/再灌注(MCAO/R)局灶性脑I/R损伤模型利用改良线栓法来进行制备与完善。DMY组术前连续灌胃给药10 d，每天1次，并在缺血前1 h及再灌注后12 h各给药1次。缺血3 h再灌注24 h后，取脑采用原位缺口末端标记法(TUNEL)进行凋亡检测，免疫组织化学法和实时荧光定量PCR 法(RT-qPCR)分别检测凋亡相关因子Bcl-2相关X蛋白(Bax)及B细胞淋巴瘤-2蛋白(Bcl-2)蛋白及mRNA 表达。结果 与假手术组比较，在I/R模型组中，小鼠缺血脑组织中凋亡阳性细胞数量明显增高，凋亡相关因子Bcl-2蛋白及基因表达下降(P<0.01)，而Bax的蛋白及基因表达增强(均P<0.01)。与I/R模型组比较，DMY组小鼠缺血脑组织凋亡阳性细胞率显著下降，Bcl-2蛋白及基因表达增强，Bax蛋白和基因表达下降(均P<0.01)。结论 DMY可减轻小鼠局灶性脑I/R损伤所致的细胞凋亡，其抗凋亡机制可能与DMY上调Bcl-2表达、下调Bax表达有关。
[关键词]二氢杨梅素；脑缺血/再灌注损伤；大脑中动脉阻塞；细胞凋亡
[中图分类号] R332 [文献标识码] A [文章编号] 1674-4721(2018)5(b)-0004-05
Study on anti-apoptosis effect and mechanism of dihydromyrcetin on focal cerebral ischemia-reperfusion injury in mice
GAN Lu1 DENG Zhi-jing1 WANG Xian-zhe1 SHU Qi1 LIANG Cong1 GUO Zhe HE Ping
1.Pharmaceutical College of Guangxi Medical University，Nanning 530021，China；2.Department of Emergency，the Third Affiliated Hospital of Guangxi Medical University，Nanning 530031，China；3.Laboratory Animal Center，Guangxi Medical University，Nanning 530021，China
[Abstracts]Objective To study the anti-apoptosis effect of dihydromyricetin (DMY) on acute focal cerebral ischemia/reperfusion (I/R) injury in mice.Methods Male Kunming mice were randomly divided into sham group，I/R group and DMY group (500 mg/kg).Mice model of I/R injury was established by middle cerebral artery occlusion (MCAO) using modified thread method.Daily intragastric administration of DMY was carried out 10 days before the surgery，and 1 hour before ischemia and 12 hours after reperfusion.The brain tissues of the mice were harvested after ischemia for 3 hours and reperfusion for 24 hours.Myocyte apoptosis in the cerebral I/R brain was detected with in situ terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL staining) .The protein and mRNA expression of Bax and Bcl-2 were detected by immunohistochemistry assay and real-time quantitative PCR (RT-qPCR) respectively.Results Compared with sham group，apaotosis index was significantly higher，protein and mRNA expressions of Bcl-2 were lower than those of Bax were higher in I/R model group (all P<0.01).Compared with I/R model group，in DMY group，apoptosis index decreased significantly，the expressions of Bcl-2 were higher，those of Bax were lower (all P<0.01).Conclusion DMY can reduce the myocyte apoptosis induced by focal I/R injury，its anti-apoptotic mechanism might be related to regulating the expressionof Bax and Bcl-2., http://www.100md.com(甘露 邓之婧 王献哲 苏棋 梁聪 郭哲 何萍)
[关键词]二氢杨梅素；脑缺血/再灌注损伤；大脑中动脉阻塞；细胞凋亡
[中图分类号] R332 [文献标识码] A [文章编号] 1674-4721(2018)5(b)-0004-05
Study on anti-apoptosis effect and mechanism of dihydromyrcetin on focal cerebral ischemia-reperfusion injury in mice
GAN Lu1 DENG Zhi-jing1 WANG Xian-zhe1 SHU Qi1 LIANG Cong1 GUO Zhe HE Ping
1.Pharmaceutical College of Guangxi Medical University，Nanning 530021，China；2.Department of Emergency，the Third Affiliated Hospital of Guangxi Medical University，Nanning 530031，China；3.Laboratory Animal Center，Guangxi Medical University，Nanning 530021，China
[Abstracts]Objective To study the anti-apoptosis effect of dihydromyricetin (DMY) on acute focal cerebral ischemia/reperfusion (I/R) injury in mice.Methods Male Kunming mice were randomly divided into sham group，I/R group and DMY group (500 mg/kg).Mice model of I/R injury was established by middle cerebral artery occlusion (MCAO) using modified thread method.Daily intragastric administration of DMY was carried out 10 days before the surgery，and 1 hour before ischemia and 12 hours after reperfusion.The brain tissues of the mice were harvested after ischemia for 3 hours and reperfusion for 24 hours.Myocyte apoptosis in the cerebral I/R brain was detected with in situ terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL staining) .The protein and mRNA expression of Bax and Bcl-2 were detected by immunohistochemistry assay and real-time quantitative PCR (RT-qPCR) respectively.Results Compared with sham group，apaotosis index was significantly higher，protein and mRNA expressions of Bcl-2 were lower than those of Bax were higher in I/R model group (all P<0.01).Compared with I/R model group，in DMY group，apoptosis index decreased significantly，the expressions of Bcl-2 were higher，those of Bax were lower (all P<0.01).Conclusion DMY can reduce the myocyte apoptosis induced by focal I/R injury，its anti-apoptotic mechanism might be related to regulating the expressionof Bax and Bcl-2., http://www.100md.com(甘露 邓之婧 王献哲 苏棋 梁聪 郭哲 何萍)