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Abstract One of the most potent aminoglycoside antibiotics is amikacin (AMK). However, nephrotoxicity is a serious and dose-limiting adverse effect associated with its therapeutic usage, particularly in patients receiving large doses of AMK. The purpose of this study was to see if taurine (TAU) might relieve or prevent AMK-induced nephrotoxicity when concurrent with AMK, with an emphasis on inflammation, apoptosis, and fibrosis. Six groups of male Sprague Dawley rats were formed. group 1: rats received saline (normal control), group 2: normal rats received 50 mg/kg TAU intraperitoneally (i.p.). Groups 3 and 4: received AMK (25 or 50 mg/kg; i.p.), respectively. Groups 5 and 6: received TAU (50 mg/kg; i.p.) concurrently with AMK (25 or 50 mg/kg; i.p.) for 3 weeks, respectively. High levels of serum creatinine (CRE), urea nitrogen (BUN) and uric acid (UA) were shown in AMK-mediated nephrotoxicity. Renal tissue damage has determined during histopathological studies. The development of inflammatory responses and localized fibrosis involves increased degree of heat shock protein (HSP) 25 and Toll-like receptors-4 (TLR-4). Improved TLR-4 enables monocytes to increase the production of interleukin (IL)-18 rather than IL-10. TAU showed therapeutic effects against AMK-caused nephrotoxicity with the downregulation of HSP25, TLR-4, caspase-3 and IL-18 with up-regulation IL-10 levels. |