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We previously reported that diallyl trisulfide (DATS), the primary organosulfur compound in garlic, reduced fibrosis and attenuated oxidative stress in rat fibrotic liver. The present study was aimed at elucidating the underlying mechanisms. The primary rat hepatic stellate cells (HSCs) were cultured and stimulated with hydrogen peroxide (H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>) for inducing HSC activation under oxidative stress. We examined the effects of DATS on the profibrogenic properties and oxidative stress in H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>\u2010treated HSCs. The results showed that DATS suppressed and reduced fibrotic marker expression in HSCs. DATS arrested cell cycle at G2\/M checkpoint associated with downregulating cyclin B1 and cyclin\u2010dependent kinase 1, induced caspase\u2010dependent apoptosis, and reduced migration in HSCs. Moreover, intracellular levels of reactive oxygen species and lipid peroxide were decreased by DATS, but intracellular levels of glutathione were increased in HSCs. Furthermore, DATS significantly elevated hydrogen sulfide (H<jats:sub>2<\/jats:sub>S) levels within HSCs, but iodoacetamide (IAM) reduced H<jats:sub>2<\/jats:sub>S levels and significantly abrogated DATS production of H<jats:sub>2<\/jats:sub>S within HSCs. IAM also abolished all the inhibitory effects of DATS on the profibrogenic properties and oxidative stress in HSCs. Altogether, we demonstrated an H<jats:sub>2<\/jats:sub>S\u2010associated mechanism underlying DATS inhibition of profibrogenic properties and alleviation of oxidative stress in HSCs. Modulation of H<jats:sub>2<\/jats:sub>S production may represent a therapeutic remedy for liver fibrosis.<\/jats:p>","DOI":"10.1155\/2017\/1406726","type":"journal-article","created":{"date-parts":[[2017,2,20]],"date-time":"2017-02-20T21:00:46Z","timestamp":1487624446000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":37,"title":["Diallyl Trisulfide Suppresses Oxidative Stress\u2010Induced Activation of Hepatic Stellate Cells through Production of Hydrogen 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