Fisetin attenuates high fat diet-triggered hepatic lipid accumulation: A mechanism involving liver inflammation overload associated TACE/TNF-α pathway
| Autor: | Huanhuan Li, Mingxing Xiong, Tingting Long, Qin Kuang, Yu-Ting Qin, Jianxia Zhan, Xu Minxuan, Tingting Tang, Ge Chenxu, Tan Jun, Xianling Dai, Yan Sun |
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| Rok vydání: | 2019 |
| Předmět: |
Liver inflammation and lipid accumulation
0301 basic medicine medicine.medical_specialty Medicine (miscellaneous) Inflammation TACE/TNF-α 03 medical and health sciences chemistry.chemical_compound 0404 agricultural biotechnology NAFLD Internal medicine Medicine TX341-641 chemistry.chemical_classification 030109 nutrition & dietetics Nutrition and Dietetics Nutrition. Foods and food supply business.industry Fatty liver Metabolic disorder NASH nutritional and metabolic diseases 04 agricultural and veterinary sciences Fisetin medicine.disease 040401 food science Endocrinology Enzyme chemistry Tumor necrosis factor alpha Steatosis medicine.symptom Metabolic syndrome business Food Science |
| Zdroj: | Journal of Functional Foods, Vol 53, Iss, Pp 7-21 (2019) |
| ISSN: | 1756-4646 |
| DOI: | 10.1016/j.jff.2018.12.007 |
| Popis: | Excess fat-rich diet ingestion predisposes the liver to non-alcoholic fatty liver disease (NAFLD), but the mechanism is complicated. Fisetin (Fn) as a natural flavonoid with many bio-activities was determined in a number of diseases models. TACE (tumor necrosis factor-α-converting enzyme)-combined tumor necrosis factor-α (TACE/TNF-α) signaling played a significant role in inflammation-associated diseases. The study aimed to explore the protective mechanisms of Fn against high fat diet (HFD)-induced nonalcoholic steatohepatitis (NASH), with particular focus on TACE/TNF-α signaling. HFD-fed C57BL/6 mice were used as the metabolic syndrome model to explore the effects of Fn on NASH and to determine whether TACE/TNF-α activation was involved in the process. Indeed, HFD increases systemic metabolic disorder, promotes circulating levels of pro-inflammatory cytokines produce, aggravates development of hepatic inflammation, resulting in inflammation overload-associated excessive activation of TACE/TNF-α, ultimately induces hepatic lipid accumulation and NASH. Fisetin protected against HFD-induced liver inflammation and lipid accumulation by decreasing metabolic disorder and inflammation overload-related TACE/TNF-α activation, inhibiting over-expression of pro-inflammatory cytokines, negatively regulating HFD-triggered abnormal lipid metabolism-related genes expression, finally restricting lipid deposition and hepatic steatosis. Fisetin suppressed HFD-induced liver inflammation and lipid accumulation by decreasing metabolic disorder and hepatic inflammation overload-related TACE/TNF-α activation. |
| Databáze: | OpenAIRE |
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