Abstract
Nonalcoholic fatty liver disease (NAFLD) is characterized by lipotoxicity and ectopic lipid deposition within hepatocytes. Sulforaphane (SFA), an active compound used for inhibiting tumors, was found to have the potency to improve lipid metabolism. However, its molecular mechanisms on ameliorating NAFLD are still incompletely understood. This research evaluated if SFA could inhibit hepatic steatosis and apoptosis. The effects of SFA on cell viability, lipid accumulation, triglyceride (TG) contents, apoptosis, ceramide contents, and reactive oxygen species (ROS) levels were analyzed in palmitic acid (PA)-treated HepG2 cells and high-fat diet (HFD)-fed mice. The related molecular mechanisms were further explored in hepatocytes. The results showed SFA alleviated lipid accumulation and regulated AMPK/SREBP1c/FAS signaling pathway in PA-stressed HepG2 cells. In addition, SFA alleviated PA-mediated apoptosis, downregulated the expressions of cleaved caspase 3, as well as reduced ceramide contents and ROS levels. Moreover, SFA treatment reduced HFD-induced body weight gain, alleviated insulin resistance, decreased serum TG, total cholesterol (TC), and alanine aminotransferase (ALT) levels, and prevented lipid deposition and apoptosis in the liver. This study showed SFA suppressed lipid deposition and apoptosis both in vitro and in vivo, indicating that SFA may be a potential candidate for preventing and treating NAFLD.
Highlights
Nonalcoholic fatty liver disease (NAFLD) is characterized by the excessive lipid deposition in hepatic cells and describes a spectrum of complicated pathological processes, such as nonalcoholic simple fatty liver, nonalcoholic steatohepatitis, liver fibrosis, and even predisposes one to liver-related complications, such as cirrhosis and hepatocellular carcinoma [1]
BCA protein concentration determination kit, total cholesterol (TC) assay kit, triglycerides (TG) assay kit, aspartate aminotransferase (AST) assay kit, and alanine aminotransferase (ALT) assay kit were from Nanjing Jiancheng Bioengineering Institute, China
These results suggested that SFA alleviated palmitic acid (PA)-mediated cytotoxicity in HepG2 cells, and we chose 5 and 10 μM of SFA in the following experiments
Summary
Nonalcoholic fatty liver disease (NAFLD) is characterized by the excessive lipid deposition in hepatic cells (more than 5% fat contents in the liver) and describes a spectrum of complicated pathological processes, such as nonalcoholic simple fatty liver, nonalcoholic steatohepatitis, liver fibrosis, and even predisposes one to liver-related complications, such as cirrhosis and hepatocellular carcinoma [1]. NAFLD is the most frequent cause of liver diseases around the world, with an increasing population from 17% to 46% in Western countries [2,3]. The incidence of NAFLD is rapidly increasing due to its strong association with obesity, dyslipidemia, insulin resistance, type 2 diabetes mellitus, as well as cardiovascular disease [4]. The “second hit” is caused by oxidative stress and inflammation, resulting in further damage and apoptosis in the liver [6]. Many clinical and animal research studies have shown the pivotal roles of lipid deposition and apoptosis in the progression of NAFLD [7,8]. The discovery of functional foods or food-derived active ingredients with the least side effects could offer an effective strategy to ameliorate and treat NAFLD [11]
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