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• W3036648443 abstract "Tec kinase is an important mediator in inflammatory immune response that enhances the activity of neutrophils and macrophages. However, information on its function in lipopolysaccharide- (LPS-) induced acute kidney injury (AKI) is limited. This study is aimed at determining whether Tec kinase was a regulator in AKI. An AKI model in mice was successfully established using intraperitoneal LPS. Results showed that the serum levels of creatinine (Cr), blood urea nitrogen (BUN), and cystatin-C (Cys-C) increased after intraperitoneal LPS injection. Renal tissue sustained significantly severe injury as measured by pathological scores. Pretreatment with LFM-A13 improved the function of the kidney in mice and decreased the renal injury score. Enzyme-linked immunosorbent assay showed that LFM-A13 significantly reduced the release of IL-1 β and TNF- α in mice exposed to LPS. LFM-A13 can evidently abrogate the expression of Tec protein, MyD88, TLR4, NF- κ B p65, and Tec’s phosphorylated protein as determined by Western blot. Immunohistochemistry analysis revealed that LFM-A13 markedly downregulated the expression of Tec kinase in renal tubular epithelial cells. In vitro, Tec kinase protein was expressed highly in NRK-52E cells after LPS exposure. Tec-siRNA also decreased IL-1 β and TNF- α production and obviously abolished phospho-p65 and phospho-I κ B α expression in NRK-52E cell stimulated by LPS; however, Tec-siRNA increased the I κ B α level. Altogether, these data suggested that Tec kinase can be a modulating protein in AKI through TLR4/NF- κ B activation." @default.
• W3036648443 created "2020-06-25" @default.
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• W3036648443 date "2020-06-20" @default.
• W3036648443 modified "2023-10-17" @default.
• W3036648443 title "Negative Regulation of Tec Kinase Alleviates LPS-Induced Acute Kidney Injury in Mice via theTLR4/NF-κB Signaling Pathway" @default.
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• W3036648443 doi "https://doi.org/10.1155/2020/3152043" @default.
• W3036648443 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7322586" @default.
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