In this study, we found Sal B significantly inhibited lipid accumulation in hepatocytes should be a possible explanation for its benefit on improving metabolic syndrome. Excessive LDs accumulation in hepatocytes can result in lipotoxicity, patients with hepatic lipid accumulation are at risk of serious complications, including progression to NAFLD, steatohepatitis, type 2 diabetes, fibrosis, cirrhosis, liver failure and hepatocellular carcinoma, currently, the only effective treatment option for NAFLD is weight loss, there are no pharmaceutical treatments approved. [21–23] our finding provided its clinical value of Sal B by decreasing lipid drop accumulation of hepatocytes.
Autophagy is beneficial to the metabolism and decomposition of nutrients, therefore it is very important for the regulation of nutrients metabolism and the maintenance of intracellular balance. Study reported an important role of autophagy involved in regulating lipid metabolism. The impairment of autophagy caused accumulation of lipid in cells leads to obesity, dyslipidemia and fatty liver disease. 
LDs undergoes degradation partly through autophagy lysosomal pathway. Lipid accumulation could stimulate autophagy. The endoplasmic reticulum forms the early autophagic structure, encapsulates the newly formed lipid droplets and transports them to lysosomes.  Our result indicated an increasing autophagy by upregulation of LC3B and Beclin1expression whereas a decreasing P62 expression in hepatocytes, which suggested the increasing autophagy stimulated by Sal B might be related to improvement of hepatic lipid drop accumulation.
We also found inhibition of autophagy by 3-MA induced intracellular lipid droplet accumulation and increased TG level in hepatocytes. Meanwhile, Sal B reduced LD accumulation and TG level in hepatocytes was abrogated by 3-MA. Although Sal B has been reported a variety of beneficial metabolic effects including ameliorated the histopathological alterations of pancreas, increased muscle glycogen content, increased p-AMPK protein expression in skeletal muscle and liver; increased protein expressions of PPARαand p-ACC in liver. [17, 18] Our study showed that Sal B reduced intracellular accumulation of LDs and TG level whereas stimulated autophagosome formation by increasing expression of autophagosome formation marker LC3 II and decreasing autophagy substrates marker p62 expression in hepatocytes. Meanwhile, Beclin-1, another aytophagy biomarker which mainly activated autophagy by formation of class III PI3-kinase complex to stimulate ATG proteins, was found significantly higher expression in Sal B treated hepatocytes. It suggested Sal B activated autophagy and stimulated autophagosome formation. Previous studies reported pharmaceutical inhibition of autophagy significantly increased LD accumulation in hepatocytes.  We also found inhibition of autophagy by 3-MA induced intracellular lipid droplet accumulation and increased TG level in hepatocytes. Meanwhile, Sal B reduced LD accumulation and TG level in hepatocytes was abrogated by 3-MA, which indicated Sal B inhibited hepatic lipid accumulation through stimulation of autophagy.
In conclusion, our study exhibited another function of Sal B on decreasing lipid drop accumulation in hepatocyte, and provided a possible mechanism of Sal B regulating hepatic lipid metabolism through activation of autophagy, that may contribute to its benefit on liver disease related to hepatic lipid accumulation.