4.7 Article

Salvianolic acid B ameliorates non-alcoholic fatty liver disease by inhibiting hepatic lipid accumulation and NLRP3 inflammasome in ob/ob mice

期刊

INTERNATIONAL IMMUNOPHARMACOLOGY
卷 111, 期 -, 页码 -

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ELSEVIER
DOI: 10.1016/j.intimp.2022.109099

关键词

NAFLD; SalB; Lipid metabolism; NLRP3 inflammasome

资金

  1. Administration of Traditional Chinese Medicine of Guangdong Province [20211179]
  2. 2020 Guangdong Provincial Science and Technology Innovation Strategy Special Fund (Guangdong-Hong Kong-Macau Joint Lab) [2020B1212030006]

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In this study, the protective effects of Salvianolic acid B (SalB) on non-alcoholic fatty liver disease (NAFLD) were investigated. The results showed that SalB significantly reduced body and liver weights, improved plasma markers of liver damage, and reduced hepatic lipid accumulation in a mouse model of NAFLD. SalB also inhibited inflammation and the activation of NLRP3 inflammasome. These findings suggest that SalB has potential as a hepatoprotective agent against NAFLD.
Non-alcoholic fatty liver disease (NAFLD) has high occurrence in the global world, which poses serious threats to human health. Salvianolic acid B (SalB), an extract of the root of Salvia miltiorrhiza, has the protective effect on metabolic homeostasis. However, the mechanism is still unknown. In this study, we used ob/ob mice, a model of NAFLD, to explore the hepatoprotective effects of SalB. The results showed that SalB significantly reduced the body weights and liver weights, and ameliorated plasma alanine aminotransferase (ALT), aspartate amino-transferase (AST), triglyceride (TG), hepatic free fatty acid (FFA), total cholesterol (TC) levels, and hepatic TG and TC levels in ob/ob mice. SalB reduced the number of lipid droplets and inhibited hepatic lipogenesis by regulating peroxisome proliferator-activated receptor gamma (PPAR gamma), fatty acid synthase (FASN), stearoyl-Co A desaturase 1 (SCD1), and cluster of differentiation 36 (CD36). Compared to ob/ob mice, the lower expressions of the pro-inflammatory cytokines, such as interleukin-18 (IL-18), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and F4/80, were observed after SalB treatment. Importantly, SalB treatment inhibited the activation of NLRP3 inflammasome and reduced the severity of liver inflammation. Our findings suggested that SalB improved NAFLD pathology in ob/ob mice by reducing hepatic lipid accumulation and NLRP3 inflammasome activation, which might be the potential hepatoprotective mechanism of SalB.

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