Key result
Baicalin improves cardiac function and reduces diabetic myocardial hypertrophy and fibrosis in preclinical models.
Why the study?
Although baicalin had been shown to prevent cardiac injuries in other disease models, whether it protects against T2DM-associated cardiomyopathy remained unknown.
Does Baicalin improve cardiac function and reduce cardiomyocyte injury in a mouse model of diabetic cardiomyopathy?
Does Baicalin improve cardiac function and reduce cardiomyocyte injury in a mouse model of diabetic cardiomyopathy?
Baicalin protects against diabetic cardiomyopathy through Keap1/Nrf2/AMPK-mediated antioxidative and lipid-lowering effects in preclinical models.
Answers are grounded in this paper and cite their sources.
Baicalin merits dose-optimization studies in diabetic cardiomyopathy models; human efficacy and safety remain untested.
Previous studies demonstrated that Bailcalin (BAI) prevented cardiac injuries under different disease models. Whether BAI protected against type 2 diabetes mellitus- (T2DM-) associated cardiomyopathy was investigated in this study. T2DM was established by the combination of streptozotocin injection and high-fat diet in mice. BAI was administered daily for 6 months. After evaluating cardiac functions, mice hearts were removed and processed for morphological, biochemical, and molecular mechanism analyses. Neonatal rat cardiomyocytes (NRCM) were isolated and treated with high glucose and palmitate (HG/Pal) for in vitro investigation. BAI significantly ameliorated T2DM-induced cardiomyocyte hypertrophy, interstitial fibrosis, and lipid accumulation accompanied by markedly improved cardiac functions in diabetic mice. Mechanically, BAI restored decreased phosphorylation of AMPK and enhanced expression and nuclei translocation of Nrf2. In in vitro experiments, BAI also prevented NRCM from HG/Pal-induced apoptosis and oxidative stress injuries by increasing p-AMPK and Nrf2 accumulation. The means by which BAI restored p-AMPK seemed to be related to the antioxidative effects of Nrf2 after silencing AMPK or Nrf2 in NRCM. Furthermore, BAI regulated Nrf2 by inhibiting Nrf2 ubiquitination and consequent degradation mediated by Keap1. This study showed that BAI alleviated diabetes-associated cardiac dysfunction and cardiomyocyte injuries in vivo and in vitro via Keap1/Nrf2/AMPK-mediated antioxidation and lipid-lowering effects. BAI might be a potential adjuvant drug for diabetes cardiomyopathy treatment.
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Li et al. (2019) studied Diabetic cardiomyopathy (n=56). Baicalin vs. Vehicle was evaluated on Cardiac function and cardiomyocyte injuries (p=<0.05). Baicalin significantly ameliorated T2DM-induced cardiomyocyte hypertrophy, interstitial fibrosis, and lipid accumulation accompanied by markedly improved cardiac functions in diabetic mice.
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