The increase in infections with multidrug resistant bacteria has forced to return to the use of colistin, antibiotic with known nephrotoxicity. Mesenchymal stem cells (MSCs) are being extensively investigated for their potential in regenerative medicine. This study aimed to investigate the possible protective mechanisms of the MSCs against kidney injury induced by colistin. Forty adult female albino rats were randomly classified into 4 equal groups; the control group, the MSC-treated group (a single dose of 1 ×10⁶ /ml MSCs through the tail vein), the colistin-treated group (36 mg/kg/day colistin was given for 7 days), and the both colistin and MSC group (36 mg/kg/day colistin and 1 ×10⁶ /ml MSCs). Main outcome measures were histopathological alterations, kidney malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and immunohistological autophagy evaluation. MSC repressed the progression of colistin-induced kidney injury as evidenced by the improvement of histopathological alterations and the substantial increase MDA, and decrease SOD and CAT in serum levels. Moreover, MSC resulted in a profound reduction in oxidative stress as manifested by decreased MDA and increased SOD in serum. Notably, MSC suppressed colistin-induced autophagy; it reduced renal levels of Beclin-1, P62 and LC3A/B. Furthermore, MSC decreased renal levels of eNOS. Lastly, MSC efficiently decreased expression of the TUNEL positive cell number. MSC confers protection against colistin-induced kidney injury by alleviating oxidative stress, nitric oxide synthase besides modulating reducing autophagy and apoptosis.

多重耐药细菌感染的增加迫使人们重新使用粘菌素，这是一种已知具有肾毒性的抗生素。间充质干细胞 (MSC) 因其在再生医学中的潜力而受到广泛研究。本研究旨在探讨间充质干细胞对粘菌素诱导的肾损伤的可能保护机制。40只成年雌性白化大鼠随机分为4组；对照组、MSC治疗组（通过尾静脉单次给药1×10 ⁶ /ml MSCs）、粘菌素治疗组（36 mg/kg/天粘菌素给药7天），两者均粘菌素和 MSC 组（36 mg/kg/天粘菌素和 1 ×10 ⁶/ml 间充质干细胞）。主要结果指标是组织病理学改变、肾丙二醛 (MDA)、超氧化物歧化酶 (SOD)、过氧化氢酶 (CAT) 和免疫组织学自噬评估。MSC 抑制粘菌素诱导的肾损伤的进展，组织病理学改变的改善和 MDA 的显着增加以及血清水平中 SOD 和 CAT 的降低证明了这一点。此外，MSC 导致氧化应激显着减少，表现为血清中 MDA 减少和 SOD 增加。值得注意的是，MSC 抑制了粘菌素诱导的自噬；它降低了 Beclin-1、P62 和 LC3A/B 的肾脏水平。此外，MSC 降低了 eNOS 的肾脏水平。最后，MSC 有效地减少了 TUNEL 阳性细胞数量的表达。MSC 通过减轻氧化应激来保护粘菌素引起的肾损伤，