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Non‐alcoholic fatty liver disease (NAFLD) is a major health problem. However, no effective treatments are currently available. Thus, there is a critical need to develop novel drugs that can prevent and treat NAFLD with few side effects. In this study, Tussilagone (TUS), a natural sesquiterpene isolated from Tussilago farfara L, was explored in vitro and in vivo for its potential to treat NAFLD. Our results showed that in vitro TUS reduced oleic acid palmitate acid‐induced triglyceride and cholesterol synthesis in HepG2cells, reduced intracellular lipid droplet accumulation, improved glucose metabolism disorders and increased energy metabolism and reduced oxidative stress levels. In vivo, TUS significantly reduced fat accumulation and improved liver injury in high‐fat diet (HFD)‐induced mice. TUS treatment significantly increased liver mitochondrial counts and antioxidant levels compared to the HFD group of mice. In addition, TUS was found to reduce the expression of genes involved in lipid synthesis sterol regulatory element binding protein‐1 (SREBP1), fatty acid synthase (FASN), and stearoy‐CoA desaturase 1 (SCD1) in vitro and in vivo. Our results suggest that TUS may be helpful in the treatment of NAFLD, suggesting that TUS is a promising compound for the treatment of NAFLD. Our findings provided novel insights into the application of TUS in regulating lipid metabolism. [ABSTRACT FROM AUTHOR]

Acute pancreatitis (AP) is a clinical emergency characterized by elevated levels of inflammation and oxidative stress, urging the need for the development of new and more efficacious treatments. Tussilagone (TSL), a compound from Tussilago farfara flower buds, is known to exhibit diverse properties, including anti-inflammatory activity, but its precise role in AP remains unclear. In this study, we investigated TSL’s impact on the progression of AP. To establish AP animal models, mice were intraperitoneally administered hyranolin. Our findings demonstrate that TSL effectively suppresses the progression of AP in these mice and decreases inflammation in their pancreatic tissues, as evidenced by reduced secretion of inflammatory cytokines such as interleukin (IL)- 1β, Tumor necrosis factor (TNF)-α and IL-6 (p < 0.05). Notably, TSL also mitigates neutrophil infiltration into the pancreatic tissues of AP-afflicted mice and alleviates oxidative stress in AP mice, as confirmed by the measurements of Superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), and myeloperoxidase (MPO) (p < 0.05). Remarkably, TSL exerts its inhibitory effects on inflammation and oxidative stress by blocking the nuclear factor (NF)-κB pathway and activating the NF-E2-related factor 2 (Nrf2) pathway. In conclusion, TSL can mitigate inflammation and oxidative stress, offering potential as a promising therapeutic agent for AP. [ABSTRACT FROM AUTHOR]