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作 者:白美玲[1] 刘星亮[2] 焦宏[1] BAI Meiling;LIU Xingliang;JIAO Hong(Basic Medical College of Hebei North University,Hebei Zhangjiakou 075000,China;The First Affiliated College of Hebei North University,Hebei Zhangjiakou 075000,China)
机构地区:[1]河北北方学院基础医学院,河北张家口075000 [2]河北北方学院附属第一医院,河北张家口075000
出 处:《中国中医基础医学杂志》2022年第10期1673-1676,共4页JOURNAL OF BASIC CHINESE MEDICINE
基 金:河北省高等学校科学研究青年基金资助项目(QN2018031)-蛋白质硝基化在一氧化碳中毒所致迟发型脑病的机制探讨;河北北方学院2020年度校级科研项目(YB2020017)-MCT1羰基化在CO中毒引起脑白质及髓鞘损伤的作用机制。
摘 要:目的通过观察芹菜素在一氧化碳(carbon monoxide,CO)中毒后对神经元凋亡的影响,探讨其干预作用与机制。方法制作CO中毒的神经元模型,即用外源性一氧化碳释放分子2(carbon monoxide releasing molecules2,CORM-2)作用于PC12细胞,筛选出CORM-2作用的最佳时间和最佳浓度,通过流式细胞术观察对照组、CORM-2组、低浓度芹菜素干预组(5μM)和高浓度芹菜素干预组(20μM)的PC12细胞凋亡率,Western blot检测各组凋亡相关蛋白半胱氨酸蛋白酶-3(Caspase-3)、BCL2-Associated X(BCL2-Associated X,Bax)和B淋巴细胞瘤-2(B-cell lymphoma-2,Bcl-2)的表达。结果给予芹菜素干预后PC12细胞凋亡率较CORM-2组下降(P<0.05)。其中加入高、低浓度芹菜素后促凋亡蛋白Caspase-3和Bax的表达明显低于CORM-2组(P<0.05),而抑制凋亡蛋白Bcl-2的表达明显高于CORM-2组(P<0.05)。结论芹菜素可以有效缓解CO中毒导致的PC12细胞的凋亡,具体机制与凋亡蛋白相互作用有关。Objective:To explore the therapeutic effect of apigenin on carbon monoxide poisoning via investigating the effect of apigenin on neuronal apoptosis induced by carbon monoxide poisoning.Methods:A neuronal model of carbon monoxide poisoning is established by carbon monoxide releasing molecule 2(CORM-2)acted on PC12 cells.The optimal time and concentration of CORM-2 were screened out.The apoptosis rate of PC12 cells in control group,CORM-2 group,5μM apigenin treatment group and 20μM apigenin treatment group were detected by flow cytometry.Western blot was used to detect the expressions of Caspase-3,Bax and Bcl-2 in different groups.Results:Compared with CORM-2 group,the apoptosis rate of PC12 cells decrease after apigenin treatment(P<0.05).The expressions of Caspase-3 and Bax were significantly lower than those of CORM-2 group(P<0.05),while the expression of Bcl-2 was significantly higher than that of CORM-2 group(P<0.05).Conclusion:Apigenin can alleviate the apoptosis of PC12 cells induced by carbon monoxide poisoning effectively,and the mechanism is related to the interaction of apoptotic proteins.
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