期刊
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
卷 233, 期 -, 页码 -出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2022.113327
关键词
Verbascoside; Sepsis-induced cardiomyopathy; Mitochondrial biogenesis
资金
- National Natural Science Foundation of China [81470273]
- Clinical Medicine Science and Technology Spe-cial Project of Jiangsu Province [BL2014083]
- Six talent peak project of Jiangsu Province [2012-WS-114]
- Science and Technology Plan Project of Nanjing [201803064]
This study demonstrates that verbascoside can exert cardioprotective effects in septic heart injury by inhibiting oxidative stress, inflammation, and apoptosis, as well as promoting mitochondrial biogenesis.
Background: Verbascoside (VB), as an active component of multiple medicinal plants, has been proved to exert anti-oxidative, anti-aging and neuroprotective effects. This study was designed to investigate whether VB could play a cardioprotective role in septic heart injury.Methods: Mice were injected with lipopolysaccharide (LPS; 10 mg/kg) to induce sepsis. The treatment group received an intraperitoneally injection of VB (20 mg/kg) before LPS challenge. Transthoracic echocardiography, ELISA, immunofluorescence, and qPCR were performed to assess the effect of VB on heart function, oxidative stress, inflammation and apoptosis. Transmission electronic microscopy and immunoblotting were used to evaluate the mitochondrial morphology and biogenesis of the septic heart. In vitro experiments were also performed to repeat above-mentioned assays.Results: Compared with LPS group, the VB treatment group showed improved cardiac function in sepsis. VB alleviated oxidative stress and inflammatory cell infiltration, as well as cardiomyocyte apoptosis. Specifically, VB could restore sepsis-induced mitochondrial alterations via regulating mitochondrial biogenesis. These results were also confirmed in in vitro experiments. Conclusion: Verbascoside could protected from sepsis-induced cardiomyopathy by inhibiting oxidative stress, inflammation, and apoptosis, as well as promoting mitochondrial biogenesis.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据