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Baicalin and its nanoliposomes ameliorates nonalcoholic fatty liver disease via suppression of TLR4 signaling cascade in mice

非酒精性脂肪肝 黄芩苷 TLR4型 化学 肝细胞 纤维化 内分泌学 内科学 炎症 药理学 脂肪肝 生物化学 信号转导 医学 体外 高效液相色谱法 疾病 色谱法
作者
Jin Liu,Yinglin Yuan,Xia Gong,Liangke Zhang,Qin Zhou,Shengwang Wu,Xue Zhang,Jun Hu,Ge Kuang,Xinru Yin,Jingyuan Wan,Yonghua Yuan
出处
期刊:International Immunopharmacology [Elsevier]
卷期号:80: 106208-106208 被引量:46
标识
DOI:10.1016/j.intimp.2020.106208
摘要

As a natural flavonoid compound, baicalin(BA)has been reported to exhibit hepatoprotective and anti-inflammatory properties. However, the characteristic of poor solubility and low bioavailability greatly limits its application. In addition, the effects and underlying mechanisms of BA in nonalcoholic fatty liver disease (NAFLD) remain elusive. In this study, Methionine and choline deficient diet (MCD)-induced NAFLD mice were treated with baicalin or baicalin-loaded nanoliposomes (BA-NL), then hepatic histopathological changes, biochemical parameters and inflammatory molecules were observed. We found that mice in MCD group showed significant increases in plasma transaminase, hepatocyte apoptosis, hepatic lipid accumulation, liver fibrosis, and infiltration of neutrophils and macrophages compared with control group, however, BA and BA-NL markedly attenuated MCD-induced the above changes. Besides, further analysis indicated that BA and BA-NL also inhibited the up-regulation of toll-like receptor 4 (TLR4) signal and the production of inflammatory mediators in MCD mice. Importantly, BA-NL was found to be more effective than baicalin on MCD-induced NAFLD in mice. These data suggested that BA and its nanoliposomes BA-NL could effectively protect mice against MCD-induced NAFLD, which might be mediated through inhibiting TLR4 signaling cascade.
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