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S-allyl-l-cysteine Attenuates Bleomycin-Induced Pulmonary Fibrosis and Inflammation via AKT/NF-κB Signaling Pathway in Mice

S-allyl-l-cysteine Attenuates Bleomycin-Induced Pulmonary Fibrosis and Inflammation via AKT/NF-κB Signaling Pathway in Mice

Yunjuan Nie, Kaikai Yu, Boyu Li, Yudong Hu, Hui Zhang, Ruiting Xin, Yue Xiong, Peng Zhao, Gaoshang Chai

J Pharmacol Sci. 2019 Apr;139(4):377-384.

PMID: 30928090

Abstract:

Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease characterized by inflammation, multifocal fibrotic lesions and excessive collagen deposition with limited therapies. As a major bioactive compound in garlic, S-allyl-l-cysteine (SAC) is a neuroprotective drug candidate to prevent cognitive decline, however, its anti-pulmonary fibrotic activity remains unknown. Here, we investigated whether SAC could attenuate bleomycin (BLM)-induced pulmonary fibrosis and inflammation in mice. Our results showed that SAC dose-dependently reduced the infiltration of inflammatory cells, pulmonary lesions and collagen deposition in BLM treated mice with downregulated mRNA expression levels of fibrotic genes including alpha smooth muscle actin (α-SMA), fibronectin, collagen I and collagen III as well as the protein level of α-SMA. In addition, SAC could also reduce the mRNA expression of inflammatory mediators such as TNF-α and iNOS. Furthermore, higher phosphorylation of AKT and NF-κB p65 in IPF patient samples and murine samples was verified by immunohistochemistry while SAC could decrease the phosphorylation level of AKT and NF-κB p65 in mice stimulated with BLM. These findings, for the first time, indicate that SAC might mediate AKT/NF-κB signaling pathway to inhibit BLM-induced pulmonary fibrosis and support the potential role of SAC as an anti-pulmonary fibrosis agent.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP21593771	S-Allyl-L-cysteine		21593-77-1	Price

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