Zaki, Omnia S.Safar, Marwa M.Ain-Shoka, Afaf A.Rashed, Laila A.2019-11-272019-11-272018Cited References in Web of Science Core Collection: 560360-3997https://doi.org/10.1007/s10753-017-0659-5https://link.springer.com/article/10.1007/s10753-017-0659-5Accession Number: WOS:000419896200003Sepsis caused by lipopolysaccharide (LPS) is a life-threatening disease accompanied by multiple organ failure. This study investigated the curative effects of imatinib (IMA) against hepatic, renal, and pulmonary responses caused by a single administration of LPS (10 mg/kg, i.p.) in rats. Treatment with IMA (15 mg/kg, i.p.) 30 min after LPS antagonized the LPS-induced boost of liver enzymes (ALT, AST), kidney functions (BUN, sCr) as well as the elevated pulmonary vascular permeability and edema. IMA declined tissue contents of NF-kappa B, STAT-3, P38-MAPK, TNF-alpha, IL-1 beta, and iNOS. It also amplified the anti-inflammatory cytokine IL-10 as well as the Bcl-2/Bax ratio, a cardinal indicator of the anti-apoptotic effect. Meanwhile, the rats exhibited marked reduction of the broncho-alveolar lavage fluid (BALF) contents of TNF-alpha, IL-1 beta, IFN-gamma, and neutrophil count; however, they revealed prominent augmentation of the BALF content IL-10. In conclusion, these findings suggest that IMA is endowed with anti-inflammatory, anti-oxidant, and anti-apoptotic properties and hence may provide a novel agent for the management of sepsis.enUniversity of ACUTE LUNG INJURYMESENCHYMAL STEM-CELLSTUMOR-NECROSIS-FACTORMOLECULAR-MECHANISMSINTERFERON-GAMMAEndotoxinApoptosisTyrosine kinase inhibitorOxidative stressA Novel Role of a Chemotherapeutic Agent in a Rat Model of Endotoxemia: Modulation of the STAT-3 Signaling PathwayArticlehttps://doi.org/10.1007/s10753-017-0659-5