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J Diabetes Res：研究揭示甘氨酸保护H9C2细胞免于HG-和H/R-诱导损伤的机制

2018-06-02 MedSci MedSci原创

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糖尿病患者更容易受到心肌缺血再灌注损伤（IRI）的影响，IRI参与了PKCβ2激活和线粒体功能障碍。研究发现甘氨酸作为细胞保护剂可减轻糖尿病相关的异常并减少心肌IRI，但其基本机制仍不清楚。本研究旨在确定甘氨酸是否可以通过抑制培养的H9C2细胞中的PKCβ2激活并改善线粒体功能来减弱高葡萄糖-（HG-）和缺氧/复氧-（H/R-）诱导的损伤。 将H9C2细胞暴露于低葡萄糖（LG）或HG条件下，

糖尿病患者更容易受到心肌缺血再灌注损伤（IRI）的影响，IRI参与了PKCβ2激活和线粒体功能障碍。研究发现甘氨酸作为细胞保护剂可减轻糖尿病相关的异常并减少心肌IRI，但其基本机制仍不清楚。本研究旨在确定甘氨酸是否可以通过抑制培养的H9C2细胞中的PKCβ2激活并改善线粒体功能来减弱高葡萄糖-（HG-）和缺氧/复氧-（H/R-）诱导的损伤。

将H9C2细胞暴露于低葡萄糖（LG）或HG条件下，甘氨酸或CGP53353（PKCβ2的选择性抑制剂）处理或不处理48小时，然后缺氧4小时，然后2小时再氧合（H/R ）。使用相应的商业试剂盒检测细胞活力、乳酸脱氢酶（LDH）释放、线粒体膜电位（MMP）、超氧化物歧化酶（SOD）活性和丙二醛（MDA）浓度。 Western blot检测线粒体质量控制相关蛋白（LC-3II，Mfn-2和Cyt-C）和PKCβ2活化。

结果显示，与LG组相比，HG刺激明显降低细胞活力和SOD活性，并增加LDH释放，MDA产生和PKCβ2活化，所有这些变化都由H/R损伤进一步增加。甘氨酸或CGP53353处理显著降低了LDH释放、MDA产生、PKCβ2活化和Cyt-C表达的增加，以及诱导的细胞活力、SOD活性、MMP及Mfn-2的表达，HG和H/R刺激降低了LC-3II/LC-3I的比率。

综上所述，该研究结果表明，补充甘氨酸通过抑制PKCβ2活化并改善线粒体功能来保护H9C2细胞免于HG-和H/R-诱导的细胞损伤。

原始出处：

Zhang Y, Su W, et al., Glycine Protects H9C2 Cardiomyocytes from High Glucose- and Hypoxia/Reoxygenation-Induced Injury via Inhibiting PKCβ2 Activation and Improving Mitochondrial Quality. J Diabetes Res. 2018 Apr 4;2018:9502895. doi: 10.1155/2018/9502895. eCollection 2018.

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    2019-01-30 ms5439512287675881

    #BET#

    0

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    2018-09-11 ms9608593228839890

    #DIA#

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    2018-09-12 徐岩

    #甘氨酸#

    0

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    2019-02-04 木头人513

    #Diabetes#

    0

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    2018-06-04 ms3046638856685384

    #损伤#

    0

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    2018-06-02 131****1460

    学习了受益匪浅

    0

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    2018-06-02 清风拂面

    谢谢分享学习

    0