Article Publish Status: FREE
Abstract Title:

Allyl isothiocyanate ameliorates lipid accumulation and inflammation in nonalcoholic fatty liver diseasethe Sirt1/AMPK and NF-κB signaling pathways.

Abstract Source:

World J Gastroenterol. 2019 Sep 14 ;25(34):5120-5133. PMID: 31558861

Abstract Author(s):

Chun-Xiao Li, Jian-Guo Gao, Xing-Yong Wan, Yi Chen, Cheng-Fu Xu, Ze-Min Feng, Hang Zeng, Yi-Ming Lin, Han Ma, Ping Xu, Chao-Hui Yu, You-Ming Li

Article Affiliation:

Chun-Xiao Li


BACKGROUND: Allyl isothiocyanate (AITC), a classic anti-inflammatory and antitumorigenic agent, was recently identified as a potential treatment for obesity and insulin resistance. However, little is known about its direct impact on the liver.

AIM: To investigate the effect and underlying mechanism of AITC in nonalcoholic fatty liver disease (commonly referred to as NAFLD).

METHODS: To establish a mouse and cellular model of NAFLD, C57BL/6 mice were fed a high fat diet (HFD) for 8 wk, and AML-12 cells were treated with 200μM palmitate acid for 24 h. For AITC treatment, mice were administered AITC (100 mg/kg/d) orally and AML-12 cells were treated with AITC (20 μmol/L).

RESULTS: AITC significantly ameliorated HFD-induced weight gain, hepatic lipid accumulation and inflammation. Furthermore, serum alanine aminotransferase and aspartate aminotransferase levels were markedly reduced in AITC-treated mice. Mechanistically, AITC significantly downregulated the protein levels of sterol regulatory element-binding protein 1 (SREBP1) and its lipogenesis target genes and upregulated the levels of proteins involved in fatty acidβ-oxidation, as well as the upstream mediators Sirtuin 1 (Sirt1) and AMP-activated protein kinase α (AMPKα), in the livers of HFD-fed mice. AITC also attenuated the nuclear factor kappa B (NF-κB) signaling pathway. Consistently, AITC relieved palmitate acid-induced lipid accumulation and inflammation in AML-12 cellsthrough the Sirt1/AMPK and NF-κB signaling pathways. Importantly, further studies showed that the curative effect of AITC on lipid accumulation was abolished by siRNA-mediated knockdown of either Sirt1 or AMPKα in AML-12 cells.

CONCLUSION: AITC significantly ameliorates hepatic steatosis and inflammation by activating the Sirt1/AMPK pathway and inhibiting the NF-κB pathway. Therefore, AITC is a potential therapeutic agent for NAFLD.

Study Type : Animal Study

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Sayer Ji
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