Buddleoside alleviates nonalcoholic steatohepatitis by targeting the AMPK-TFEB signaling pathway.

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Tác giả: Meng Chen, Xiliang Du, Zhiyuan Fang, Wenwen Gao, Lin Lei, Xinwei Li, Guowen Liu, Yuxiang Song

Ngôn ngữ: eng

Ký hiệu phân loại: 809.008 History and description with respect to kinds of persons

Thông tin xuất bản: United States : Autophagy , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 717051

Nonalcoholic steatohepatitis (NASH) is a combination of hepatic steatosis, inflammation, and fibrosis, and it often follows simple hepatic steatosis in nonalcoholic fatty liver disease (NAFLD). However, no pharmacological treatment is currently available for NASH. Given the important role of TFEB (transcription factor EB) in regulating the macroautophagy/autophagy-lysosomal pathway, TFEB is potentially a novel therapeutic target for treatment of NASH, which function can be regulated by AMP-activated protein kinase (AMPK) and MTOR (mechanistic target of rapamycin kinase) complex 1 (MTORC1). Buddleoside (Bud), a natural flavonoid compound, has recently emerged as a promising drug candidate for liver diseases. Here, we shown that Bud treatment alleviated hepatic steatosis, insulin resistance, inflammation, and fibrosis in mice fed a high-fat and high-cholesterol (HFHC) diet. Notably, Bud activated AMPK, inhibited MTORC1, and enhanced TFEB transcriptional activity as well as autophagic flux
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