Abstract
Lentinan (LNT), a type of polysaccharide derived from Lentinus edodes, has manifested protective effects during liver injury and hepatocellular carcinoma, but little is known about its effects on nonalcoholic fatty liver disease (NAFLD). This study aimed to investigate whether LNT can affect the progression of NAFLD and the associated mechanisms. C57BL/6J mice were fed a normal chow diet or a high-fat diet (HFD) with or without LNT (6 mg/kg/d). AML12 cells were exposed to 200 μM palmitate acid (PA) with or without LNT (5 μg/mL). After 21 wk of the high-fat diet, LNT significantly decreased plasma triglyceride levels and liver lipid accumulation, reduced excessive reactive oxygen species production, and subsequently attenuated hepatic apoptosis in NAFLD mice. These effects were associated with increased PPARα levels, a decreased Bax/Bcl-2 ratio, and enhancement of the antioxidant defense system in vivo. Similar effects were also observed in cultured cells. More importantly, these protective effects of LNT on palmitate acid-treated AML12 cells were almost abolished by PPARα knockdown. In conclusion, this study demonstrates that LNT may ameliorate hepatic steatosis and decrease oxidative stress and apoptosis by activating the PPARα pathway and is a potential drug target for NAFLD.
Highlights
Nonalcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease in the world [1,2]
During Weeks 6 to 21, the HFD group exhibited rapid increases in body weight, while LNT significantly prevented the body weight gain induced by the high-fat diet (Figure 1A)
Our results suggested that LNT protected against the development and progression of NAFLD at least partially through the Peroxisome proliferator-activated receptor α (PPARα) pathway in this model
Summary
Nonalcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease in the world [1,2]. Approximately 25% of the global population is currently thought to have NAFLD [2,3]. NAFLD covers a spectrum of liver damage ranging from simple steatosis to more severe forms of liver injury, including nonalcoholic steatohepatitis (NASH), fibrosis, and hepatocellular carcinoma [4,5]. NAFLD is a strong risk factor for cardiovascular disease, atherosclerosis, Type 2 diabetes, and chronic kidney disease [3,6]. Lifestyle modifications are difficult to achieve and sustain, and approved pharmacological therapy is lacking [7,8]
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