Ligularia fischeri and its constituent 3,4-dicaffeoylquinic acid improve obesity-induced nonalcoholic fatty liver disease by regulating lipid metabolism and activating AMPK

- Ligularia fischeri suppressed lipid accumulation and activated AMPK in HepG2 cells.
- L. fischeri inhibited liver injury and steatosis in HFD-induced mice
- L. fischeri reduced oxidative stress and insulin resistance in HFD-induced mice

This study revealed the activity of a Ligularia fischeri extract (LFE) and its constituents to protect against obesity-induced NAFLD using in vitro and in vivo models. In HepG2 cells, LFE and its chemical constituent 3,4-dicaffeoylquinic acid inhibited lipid accumulation by altering lipid metabolism towards fatty acid oxidation through activation of the AMP-activated protein kinase (AMPK) pathway. In high-fat diet-induced obese C57BL/6J mice, oral administration of LFE attenuated the progression of obesity and improved signs of insulin resistance. LFE treatment attenuated development of NAFLD by decreasing fat droplet accumulation and the triacylglycerol content. In vivo activity of LFE was displayed through regulation of hepatic lipid metabolism and activation of hepatic AMPK. Furthermore, LFE was protected against NAFLD by lowering the level of lipid peroxidation through activation of the antioxidant defence system via NRF2 activation. These results indicate that LFE is a potent agent to improve NAFLD.