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作 者:窦姗姗 高丽颖 林馨怡 孟尧 董康 程葆华 DOU Shanshan;GAO Liying;LIN Xinyi;MENG Yao;DONG Kang;CHENG Baohua(College of Basic Medicine,Jining Medical University,Jining 272067,China)
出 处:《济宁医学院学报》2022年第4期234-238,共5页Journal of Jining Medical University
基 金:济宁医学院教师扶持基金(JYFC2018KJ003);大学生创新训练项目(CX2019205)。
摘 要:目的探讨apelin-36对鱼藤酮诱导的SH-SY5Y细胞凋亡及线粒体功能的影响。方法培养SH-SY5Y细胞,随机分为对照组、apelin-36组、鱼藤酮组和apelin-36+鱼藤酮组。通过鱼藤酮处理SH-SY5Y细胞建立帕金森病(Parkinson's disease,PD)体外模型,在给予apelin-36预处理后,通过CCK-8观察细胞活力,Hoechst 33342检测细胞凋亡,Western blotting检测Bax、bcl-2、α-synuclein的表达,试剂盒检测线粒体复合物I(complex I)的表达和ADP/ATP的比值来观察线粒体功能。结果与对照组相比,鱼藤酮组细胞活力下降,细胞凋亡增加,α-synuclein的表达增加,bcl-2/Bax比值下降,complex I表达降低,ADP/ATP比率升高(均P<0.05);而给予apelin-36预处理后,与鱼藤酮组相比,apelin-36+鱼藤酮组细胞活力上升,细胞凋亡降低,α-synuclein的表达减少,bcl-2/Bax比值增高,complex I表达升高,ADP/ATP比率降低(均P<0.05)。结论Apelin-36对鱼藤酮引起的SH-SY5Y细胞凋亡具有抑制作用,可减轻鱼藤酮所致的SH-SY5Y细胞线粒体功能紊乱,起到神经保护作用。Objective To investigate the effects of apelin-36 on rotenone-induced apoptosis and mitochondrial dysfunction of SH-SY5Y cells.Methods SH-SY5Y cells were cultured and randomly divided into control group,apelin-36 group,rotenone group and apelin-36+rotenone group.The vitro model of Parkinson's disease(PD)was established by treating SH-SY5Y cells with rotenone.After apelin-36 pretreatment,the cell viability was measured by CCK-8 assay.The apoptosis was measured by Hoechst 33342 staining.The expression of Bax,bcl-2 andα-synuclein was measured by western blotting.Mitochondrial function was detected by complex I and ADP/ATP ratio.Results Compared with the control group,the cell viability was decreased and apoptosis was increased in rotenone group.Andα-synuclein expression was increased significantly in SH-SY5Y cells with rotenone treatment.Bcl-2/Bax ratio was decreased due to rotenone exposure.Complex I expression was decreased and ADP/ATP ratio was increased after rotenone treatment in SH-SY5Y cells.However,apelin-36 pretreatment significantly inhibited rotenone neurotoxicity including increasing cell viability and decreasing apoptosis of SH-SY5Y cells.Compared with rotenone group,α-synuclein expression was decreased and bcl-2/Bax ratio was increased significantly.And complex I expression was increased and ADP/ATP ratio was decreased significantly due to apelin-36 prereatment.Conclusion Apelin-36 inhibited rotenone-induced the apoptosis of SH-SY5Y cells and alleviated rotenone-induced mitochondrial dysfunction,which played a neuroprotective role against rotenone neurotoxicity.
关 键 词:Apelin-36 鱼藤酮 帕金森病 线粒体损伤 凋亡
分 类 号:R742.5[医药卫生—神经病学与精神病学]
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