Department of Pharmacology, Medical Research and Clinical Studies Institute, National Research Centre (ID: 60014618), Cairo, Egypt.
Department of Pathology, Medical Research and Clinical Studies Institute, National Research Centre (ID: 60014618), Cairo, Egypt.
Drug Chem Toxicol. 2023 Nov;46(6):1193-1202. doi: 10.1080/01480545.2022.2141773. Epub 2022 Nov 2.
Antibiotic use, especially fluoroquinolones, has been linked to extensive renal and hepatic injury thus inflicts a considerable health problem. Fifty rats were allocated into five groups ( = 10). Group 1 represented the normal-control group. Group 2 received moxifloxacin only (MOX; 8 mg/kg/day, i.p.) for seven days and represented the MOX-control group. Groups 3, 4, and 5 received MOX for seven days accompanied by royal jelly (RJ; 100 mg/kg/day, p.o.), (ECH; 40 mg/kg/day, p.o.), and a combination of both at the aforementioned doses respectively for 30 days. All groups were investigated for renal and hepatic function tests. Renal tissue content of kidney injury molecule-1 (KIM-1) along with renal and hepatic tissue contents of reduced glutathione (GSH) and malondialdehyde (MDA) were assessed for all groups. Histopathological examination was performed followed by immunohistochemical staining for caspase-3 in renal and hepatic tissues. MOX administration resulted in significant renal and hepatic damage. RJ and ECH significantly improved the serum parameters of renal and hepatic functions along with increasing GSH and decreasing MDA in renal and hepatic tissues. Renal contents of KIM-1 were also reduced. Moreover, RJ, ECH, and their combination amended MOX-induced histopathological changes and significantly reduced caspase-3 immunohistochemical staining in both renal and hepatic tissues. The current study is the first to elucidate the effect of RJ, ECH, and their combination against MOX-induced renal and hepatic injury in rats. The study suggests that these protective effects are mainly via the reduction of oxidative stress induced by MOX administration.
抗生素的使用，尤其是氟喹诺酮类药物，与广泛的肾和肝损伤有关，从而造成相当大的健康问题。将 50 只大鼠分配到 5 组（每组 10 只）。第 1 组为正常对照组。第 2 组仅给予莫西沙星（MOX；8mg/kg/天，腹腔注射）7 天，代表 MOX 对照组。第 3、4 和 5 组分别给予莫西沙星 7 天，同时给予蜂王浆（RJ；100mg/kg/天，口服）、（ECH；40mg/kg/天，口服）和两者的组合，剂量分别为上述剂量 30 天。所有组均进行肾功能和肝功能检查。评估各组肾损伤分子-1（KIM-1）的肾组织含量以及肾和肝组织的还原型谷胱甘肽（GSH）和丙二醛（MDA）含量。进行组织病理学检查，随后进行肾和肝组织中 caspase-3 的免疫组织化学染色。MOX 给药导致明显的肾和肝损伤。RJ 和 ECH 显著改善了血清肾功能和肝功能参数，同时增加了肾和肝组织中的 GSH，减少了 MDA。肾组织中的 KIM-1 含量也降低。此外，RJ、ECH 及其组合纠正了 MOX 诱导的肾和肝组织的组织病理学变化，并显著减少了肾和肝组织中 caspase-3 的免疫组织化学染色。本研究首次阐明了 RJ、ECH 及其组合对大鼠 MOX 诱导的肾和肝损伤的作用。研究表明，这些保护作用主要是通过减少 MOX 给药引起的氧化应激。
