Berberine Ameliorates High Glucose-Induced Cardiomyocyte Injury via AMPK Signaling Activation to Stimulate Mitochondrial Biogenesis and Restore Autophagic Flux.
Berberine Ameliorates High Glucose-Induced Cardiomyocyte Injury via AMPK Signaling Activation to Stimulate Mitochondrial Biogenesis and Restore Autophagic Flux.
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小檗碱通过 AMPK 信号激活刺激线粒体生物发生并恢复自噬通量，改善高糖诱导的心肌细胞损伤
DOI：
10.3389/fphar.2018.01121
复制
发表时间：
2018
影响因子：
5.6
通讯作者：
Chen J
中科院分区：
文献类型：
--
作者：
Hang W;He B;Chen J;Xia L;Wen B;Liang T;Wang X;Zhang Q;Wu Y;Chen Q;Chen J
背景：II型糖尿病（T2 D）诱导的心肌细胞肥大与线粒体功能受损密切相关。黄连素已被证明是T2 D模型中低血糖症的一种有前景的作用。高糖诱导的体外心肌细胞肥大已有报道。本研究探讨小檗碱对高糖诱导的H9 C2细胞的保护作用及其机制。方法：用高糖诱导的H9 C2细胞系模拟高糖诱导的心肌细胞肥大。采用共聚焦显微镜、免疫荧光、RT-PCR、Western blot等方法观察小檗碱对高糖诱导的H9 C2细胞的保护作用，并探讨小檗碱对高糖诱导的H9 C2细胞的保护机制。结果如下：小檗碱可显著减轻H9 C2细胞的肥大，并通过纠正线粒体动力学中融合与分裂的失衡，显著改善线粒体功能。此外，小檗碱进一步促进有丝分裂，并通过线粒体自噬清除受损的线粒体。此外，小檗碱还通过激活AMPK信号通路恢复高糖诱导的心肌细胞损伤的自噬通量。结论：黄连素通过激活AMPK信号通路促进H9 C2细胞线粒体生物合成和自噬流改善高糖诱导的心肌细胞损伤
Background: Type II diabetes (T2D)-induced cardiomyocyte hypertrophy is closely linked to the impairment of mitochondrial function. Berberine has been shown to be a promising effect for hypoglycemia in T2D models. High glucose-induced cardiomyocyte hypertrophy in vitro has been reported. The present study investigated the protective effect and the underlying mechanism of berberine on high glucose-induced H9C2 cell line. Methods: High glucose-induced H9C2 cell line was used to mimic the hyperglycemia resulting in cardiomyocyte hypertrophy. Berberine was used to rescue in this model and explore the mechanism in it. Confocal microscopy, immunofluorescence, RT-PCR, and western blot analysis were performed to evaluate the protective effects of berberine in high glucose-induced H9C2 cell line. Results: Berberine dramatically alleviated hypertrophy of H9C2 cell line and significantly ameliorated mitochondrial function by rectifying the imbalance of fusion and fission in mitochondrial dynamics. Furthermore, berberine further promoted mitogenesis and cleared the damaged mitochondria via mitophagy. In addition, berberine also restored autophagic flux in high glucose-induced cardiomyocyte injury via AMPK signaling pathway activation. Conclusion: Berberine ameliorates high glucose-induced cardiomyocyte injury via AMPK signaling pathway activation to stimulate mitochondrial biogenesis and restore autophagicflux in H9C2 cell line.
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DOI：
10.1016/j.bbamcr.2011.01.014
发表时间：
2011-07
期刊：
Biochimica et biophysica acta
影响因子：
--
作者：
Duncan JG
通讯作者：
Duncan JG
影响因子：
5.6
作者：
Li H;Xu C;Li Q;Gao X;Sugano E;Tomita H;Yang L;Shi S
通讯作者：
Shi S
影响因子：
44.1
作者：
通讯作者：
--
影响因子：
4.3
作者：
King, George L.
通讯作者：
King, George L.
小檗碱通过调节 DM 大鼠的异常炎症反应和胰岛素信号通路改善糖尿病相关的认知衰退
影响因子：
5.6
作者：
Chen Q;Mo R;Wu N;Zou X;Shi C;Gong J;Li J;Fang K;Wang D;Yang D;Wang K;Chen J
通讯作者：
Chen J