SACM - Egypt
Permanent URI for this collectionhttps://drepo.sdl.edu.sa/handle/20.500.14154/9653
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Item Restricted Effect of some drugs on Concanavain A- inducedliver injury(Saudi Digital Library, 2025) Alenezi, FAHAD O; Nader, Manar Ahmed; Elkashef, Dalia Hassan; Abdelmageed, Marwa ElsayedLiver injury is a persistent inflammatory liver condition wherein the immune system erroneously targets liver cells, resulting in continuous inflammation and hepatic damage. The precise etiology remains ambiguous; however, it is thought to stem from genetic susceptibility that undermine immunological tolerance. In our study we found that the intraperitoneal administration of Dapan noticeably ameliorated Con A-induced hepatic enzyme impairment and histopathological disruption. Moreover, Dapan-treated mice had significantly lower MDA hepatic content and elevated GSH, SOD, and TAC levels than non-treated mice in a dose-dependent manner. The Dapansutril-treated groups showed significantly lower levels of the inflammatory mediators, NLRP3, TNF-α, IL-6, and IL-1β, in addition to the immunomodulators CD8, CD4, INF-γ, and NFκB, and inhibition of JNK and p38 MAPK levels compared to the Con A-treated group. Pretreatment with canagliflozin significantly alleviated the hepatic enzymes elevation and histopathological changes produced by Con A. CANA pretreatment also reduced liver injury produced by Con A administration via inhibition of CD4+, CD8+, IFN-γ, C-JNK, p38 MAPK and NF-κB-p65 production. Additionally, canagliflozin pretreatment significantly ameliorated antioxidant system depletion as it significantly elevated hepatic Nrf2, HO-1, SOD, GPX4 and GSH, and lowered iNOS, MDA) and 4HNe. Furthermore, pretreatment with CANA significantly inhibited hepatocytes apoptosis. Secukinumab significantly ameliorated Con A-induced biochemical and histopathological impairment. Secu significantly reduced hepatic MDA content and decreased SOD, GSH and TAC depleting effect of Con A, along with inhibition of autophagy as evidenced by reduced beclin1 expression and LC3 level. Moreover, there was a dramatic inhibition of the inflammatory, apoptotic and autophagic pathways; IL-6 and MAPK/JNK in a dose-dependent manner.24 0
