{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T15:26:53Z","timestamp":1783524413874,"version":"3.55.0"},"reference-count":41,"publisher":"Canadian Science Publishing","issue":"10","license":[{"start":{"date-parts":[[2023,10,1]],"date-time":"2023-10-01T00:00:00Z","timestamp":1696118400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":["cdnsciencepub.com"],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[2023,10,1]]},"abstract":"<jats:p> Liver fibrosis is a typical pathological state\/stage involved in most chronic liver diseases and its persistence results in cirrhosis. Inflammasomes are cytoplasmic sensors that induce inflammation in response to stress. Glibenclamide (GLB) is an USFDA-approved drug for type 2 diabetes and is reported to possess anti-inflammatory activity by inhibiting inflammatory cytokines. Dimethyl fumarate (DMF) is an USFDA-approved drug for multiple sclerosis and has been reported to activate the Nrf2\/ARE pathway to maintain the cellular antioxidant balance. A total of 36 rats were randomized into six groups ( n\u00a0=\u00a06 each). The rats were injected with thioacetamide (TAA) 200\u00a0mg\/kg, intraperitoneally every third day for eight consecutive weeks to induce liver fibrosis and oral treatment of GLB 0.5\u00a0mg\/kg\/day and DMF 25\u00a0mg\/kg\/day, and their combinations were provided for the last four consecutive weeks. Treatment with GLB, DMF, and GLB+DMF significantly protected against TAA-mediated oxidative stress and inflammatory conditions by improving hepatic function test, triglycerides, hydroxyproline, and histopathological alterations, by inhibiting the NLRP3 inflammasome signaling and fibrogenic markers, and by activating Nrf2\/ARE pathway in Wistar rats. The present results suggest that simultaneous Nrf2\/ARE activation and NLRP3 inflammasome inhibition could significantly contribute to developing a novel therapy for patients with liver fibrosis. <\/jats:p>","DOI":"10.1139\/cjpp-2023-0018","type":"journal-article","created":{"date-parts":[[2023,9,4]],"date-time":"2023-09-04T11:01:07Z","timestamp":1693825267000},"page":"509-520","update-policy":"https:\/\/doi.org\/10.1139\/csp-crossmark-policy","source":"Crossref","is-referenced-by-count":5,"title":["Simultaneous intervention against oxidative stress and inflammation by targeting Nrf2\/ARE and NLRP3 inflammasome pathway mitigates thioacetamide-induced liver fibrosis in rat"],"prefix":"10.1139","volume":"101","author":[{"given":"Durgesh Kumar","family":"Dwivedi","sequence":"first","affiliation":[{"name":"National Institute of Pharmaceutical Education and Research","place":["S.A.S. 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