Jatrorrhizine hydrochloride attenuates hyperlipidemia in a high-fat diet-induced obesity mouse model

Yang,Weiwei; She,Liping; Yu,Kun; Yan,Shan; Zhang,Xuefeng; Tian,Xiaoyi; Ma,Shuren; Zhang,Xiwen

doi:10.3892/mmr.2016.5634

Jatrorrhizine hydrochloride attenuates hyperlipidemia in a high-fat diet-induced obesity mouse model

Authors:
- Weiwei Yang
- Liping She
- Kun Yu
- Shan Yan
- Xuefeng Zhang
- Xiaoyi Tian
- Shuren Ma
- Xiwen Zhang
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Affiliations: Department of Nephrology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu 223300, P.R. China, Department of Intensive Care Unit, Jiangsu Province Geriatric Hospital, Nanjing, Jiangsu 210000, P.R. China, Department of Cardiology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu 223300, P.R. China
Published online on: August 18, 2016 https://doi.org/10.3892/mmr.2016.5634
Pages: 3277-3284

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Abstract

Jatrorrhizine hydrochloride (JH) is an active component of the traditional Chinese herb Coptis chinensis, which has been used to prevent and treat metabolic disorders. Hyperlipidemia is one of the principal factors underlying numerous metabolic diseases, including diabetes and obesity. Therefore, the aim of the present study was to investigate the lipid lowering effects of JH treatment in vivo in an obesity mouse model. JH-treated hyperlipidemic mice exhibited a reduction in body weight, as well as improved glucose tolerance and insulin sensitivity. In addition, JH‑treated hyperlipidemic mice exhibited reduced serum triglyceride, total cholesterol and low‑density lipoprotein cholesterol levels, as well as increased high‑density lipoprotein cholesterol levels compared with untreated mice fed a high‑fat diet. Notably, JH treatment ameliorated the pathophysiological changes observed in the livers of hyperlipidemic mice. At the molecular level, JH downregulated the hepatic mRNA expression levels of SREBP‑1c and FAS, and induced PPAR‑α and CPT1A mRNA expression in hyperlipidemic mice. These findings suggest that JH ameliorates hyperlipidemia via the suppression of lipogenesis and the enhancement of lipid oxidation in the liver.

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