Abstract
Objective High-fat-diet- (HFD-) induced hepatic cell apoptosis is common in mice with nonalcoholic fatty liver disease (NAFLD). We aim to investigate the effect of Ginsenoside Rb1 (GRb1) on hepatocyte apoptosis. Methods C57BL/6J mice with HFD were used to induce a liver-injured model with cell apoptosis. In addition, GRb1 was used to treat HFD-induced apoptosis in a liver with or without inhibitor of peroxisome proliferator-activated receptor γ (PPAR-γ). Results Compared with C57BL/6J mice with common chow, there are downregulated PPAR-γ but upregulated cell apoptosis in the liver of mice with HFD. Furthermore, GRb1 elevated the hepatic PPAR-γ level and suppressed hepatocytic apoptosis. However, GW9662 abolished the effects of GRb1 on apoptosis in the liver. Conclusions GRb1 alleviated HFD-induced apoptosis of hepatocytes of mice via PPAR-γ.
Highlights
With a prevalence of 25–30% in the general population [1] and 3–12% in children [2], nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases throughout the world [3]
As a ligand for Toll-like receptors (TLRs), High-mobility group box 1 protein (HMGB1) is a kind of Damage-associated molecular patterns (DAMPs) that serves to activate innate immunity [8] and trigger apoptosis
To investigate the effects of Ginsenoside Rb1 (GRb1) on obese mice with NAFLD, C57BL/6J mice were fed with HFD
Summary
With a prevalence of 25–30% in the general population [1] and 3–12% in children [2], NAFLD is one of the most common chronic liver diseases throughout the world [3]. A recent study suggested that NAFLD prevalence is increasing especially in obese children (ranging from 70 to 90%) [4]. NAFLD in obese individuals, with systemic lowgrade chronic inflammation status and IR, is a characteristic of cell apoptosis, especially in livers of patients with nonalcoholic steatohepatitis (NASH) [5]. HMGB1 is actively secreted resulting from cell death (including necrosis and severe apoptosis) [9, 10]. To exert these activities, HMGB1 must be transmitted from the nucleus to the outside of cells through the cytoplasm. Limited apoptosis is not the reason for severe inflammation, necrosis and high level of apoptosis may result in low-grade inflammation and the release of HMGB1.
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