Amikacin (AMK) is one of the most effective aminoglycoside antibiotics. However, nephrotoxicity is a major deleterious and dose-limiting side effect associated with its clinical use especially in high dose AMK-treated patients. The present study assessed the ability of taurine (TAU) to alleviate or prevent AMK-induced nephrotoxicity if co-administrated with AMK focusing on inflammation, apoptosis, and fibrosis. Male Sprague Dawley rats were assigned to six equal groups. Group 1: rats received saline (normal control), group 2: normal rats received 50 mg kg⁻¹ TAU intraperitoneally (i.p.). Groups 3 and 4: received AMK (25 or 50 mg kg⁻¹; i.p.). Groups 5 and 6: received TAU (50 mg kg⁻¹; i.p.) concurrently with AMK (25 or 50 mg kg⁻¹; i.p.) for 3 weeks. AMK-induced nephrotoxicity is evidenced by elevated levels of serum creatinine (CRE), blood urea nitrogen (BUN), and uric acid (UA). Histopathological investigations provoked damaging changes in the renal tissues. Heat shock proteins (HSP)25 and Toll-like receptor-4 (TLR-4) elevated levels were involved in the induction of inflammatory reactions and focal fibrosis. The improved activation of TLR-4 may stimulate monocytes to upgrade Interleukin (IL)-18 production rather than IL-10. TAU proved therapeutic effectiveness against AMK-induced renal toxicity through downregulation of HSP25, TLR-4, caspase-3, and IL-18 with up-regulation of IL-10 levels.

阿米卡星 (AMK) 是最有效的氨基糖苷类抗生素之一。然而，肾毒性是与其临床应用相关的主要有害和剂量限制性副作用，尤其是在高剂量 AMK 治疗的患者中。本研究评估了牛磺酸 (TAU) 在与 AMK 共同给药时减轻或预防 AMK 引起的肾毒性的能力，重点是炎症、细胞凋亡和纤维化。雄性 Sprague Dawley 大鼠被分配到六个相等的组。第 1 组：大鼠接受盐水（正常对照），第 2 组：正常大鼠腹膜内 (ip) 接受 50 mg kg ^-1 TAU。第 3 组和第 4 组：接受 AMK（25 或 50 mg kg ^-1；ip）。第 5 组和第 6 组：同时接受 TAU（50 mg kg ^-1 ; ip）和 AMK（25 或 50 mg kg ^-1; ip) 3 周。AMK 诱导的肾毒性表现为血清肌酐 (CRE)、血尿素氮 (BUN) 和尿酸 (UA) 水平升高。组织病理学研究引起了肾组织的破坏性变化。热休克蛋白 (HSP)25 和 Toll 样受体 4 (TLR-4) 水平升高与炎症反应和局灶性纤维化的诱导有关。TLR-4 激活的改善可能会刺激单核细胞升级白细胞介素 (IL)-18 的产生，而不是 IL-10。TAU 通过下调 HSP25、TLR-4、caspase-3 和 IL-18 以及上调 IL-10 水平证明了对 AMK 诱导的肾毒性的治疗效果。