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Abstract : Sepsis-induced renal impairment, which is carried on by polymicrobial sepsis, is one of the greatest clinical problems in medical practice. Even though numerous treatment approaches have been applied in such clinical challenges, a new efficient therapeutic approach is still required. celastrol is a substance derived from the medicinal plant Tripterygium wilfordii. Celastrol's impact on acute kidney damage (AKI) is not yet known. To ascertain how well celastrol works to reduce oxidative stress and inflammation during sepsis & examine its impact on TLR - 4/NF- kB signaling. Cecal ligation and puncture, CLP), Celastrol (2 mg/kg/1 hour intraperitoneally before CLP. After 24 hrs. we sacrificed the animals and blood was aspirated from each mouse’s heart. Kidney tissue was homogenated and then used in the ELISA procedure to identify markers (TNF-α, IL-6, IL-10, MIF, TNFα, F2- isoprostane, Caspase- 3, Bcl- 2, and TLR- 4) [1]. Pro-inflammatory cytokines [interleukin-6 (IL-6)], macrophage migration factor, and tumor necrosis factor (TNF)] are released in response to pathogen infection. Anti-inflammatory cytokine (IL-10) levels, oxidative stress marker (F2-isoprostane), pro-apoptotic factor (caspase-3), anti-apoptotic factor (Bcl-2) levels, and toll-like receptor- 4 levels all raised in sepsis patients. By inhibiting TLR-4/NF-kB downstream signal transduction pathways, celastrol was found to reduce kidney damage in male mice during CLP-induced polymicrobial sepsis.

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