Abstract
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.
Highlights
Diabetes has the distinguished manifestation of high blood glucose level, or the so-called hyperglycemia
We found that high glucose treatment induced hypertrophy in H9C2 cells
Results showed that berberine didn’t have significant effect on H9C2 cell viability unless the concentration is higher than 400 nM (Supplementary Figure S1B); this showed that berberine is safe under 400 nM
Summary
Diabetes has the distinguished manifestation of high blood glucose level, or the so-called hyperglycemia. It is reported wildly that mitochondria are under ceaseless fission and fusion whole through the cell life and its morphology can somehow reflect mitochondrial function (Chan, 2012). Dynamic-related protein 1 (Drp1) is the key motor protein that governs mitochondrial fission (Otera et al, 2013) Unlike those mitochondrial fusion proteins, Drp is mainly located at cytoplasm, and it needs several mitochondrial adaptors like mitochondrial fission factor (MFF) to be recruited to mitochondria (Zheng et al, 2018). What’s more, several articles have reported that hyperglycemia may induce myocardium hypertrophy via interfering mitochondrial normal function (Adeghate and Singh, 2014; Mali et al, 2016; Li et al, 2017). The present study investigated the protective effect and the underlying mechanism of berberine on high glucose-induced H9C2 cell line
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