Zoology Department, Faculty of Science, Aswan University, Egypt.
Tissue Cell. 2013 Apr;45(2):89-94. doi: 10.1016/j.tice.2012.09.006. Epub 2012 Dec 6.
The present investigation report the effect of a bradykinin-potentiating factor (BPF) on gentamicin-induced oxidative stress in rat liver and kidney. BPF is a peptide fraction isolated from the venom of the Egyptian scorpion (Buthus occitanus) has been demonstrated to have antioxidant, free radical scavenger and anti-inflammatory effects. Thirty male Rattus norvegicus (130-150 g) were included and divided into three equal groups as follows: Group I (control), group II was (ip) injected with gentamicin alone (80 mg/kg/day) for 15 days, group III was given (ip) injection of BPF (1mg/kg/day) one hour prior to gentamicin treatment for 15 days with the same dose of gentamicin as group II. Both organs were subjected to histopathological analysis with the light microscope. The activities of alanine aminotransferase (ALT), asparate aminotransferase (AST) and alkaline phosphatase (ALP) in serum were measured as indicators of the liver function. As parameters of the kidney function, creatinine, uric acid and urea concentrations were determined. Also, malondialdehyde (MDA), reduced glutathione (GSH), super oxide dismutase (SOD) and catalase (CAT) were determined in both tissues. Gentamicin caused a significant decrease or inhibition in the activities of GSH, SOD, and CAT, with significant increase in the level of MDA, ALT, AST, ALP, as well as creatinine, uric acid and urea concentrations in versus to control groups in both liver and kidney. Co-administration of gentamicin and BPF significantly increased the activity of GSH, SOD, and CAT, with significant decrease in the level of MDA and maintained serum (ALT); (AST); (ALP), creatinine, uric acid and urea concentrations as the same level as control group. Moreover, administration of gentamicin resulted in damage to liver and kidney structures. Administration of BPF before gentamicin exposure prevented severe alterations of biochemical parameters and disruptions of liver and kidney structures. In conclusion, this study obviously demonstrated that pretreatment with BPF significantly attenuated the physiological and histopathological alterations induced by gentamicin. Also, the present study identifies new areas of research for development of better therapeutic agents for liver, kidney, and other organs dysfunctions and diseases.
本研究报告了一种缓激肽增强因子（BPF）对庆大霉素诱导的大鼠肝、肾氧化应激的影响。BPF 是从埃及蝎子（Buthus occitanus）毒液中分离得到的肽段，已被证明具有抗氧化、自由基清除和抗炎作用。
将 30 只雄性挪威大鼠（130-150g）纳入并分为三组：I 组（对照组），II 组（ip）单独注射庆大霉素（80mg/kg/天）15 天，III 组（ip）注射 BPF（1mg/kg/天）1 小时后，给予庆大霉素治疗 15 天，剂量与 II 组相同。
用光学显微镜对两种器官进行组织病理学分析。血清中天冬氨酸氨基转移酶（ALT）、丙氨酸氨基转移酶（AST）和碱性磷酸酶（ALP）的活性作为肝功能的指标。作为肾功能的参数，测定肌酐、尿酸和尿素的浓度。同时，还测定了两种组织中的丙二醛（MDA）、还原型谷胱甘肽（GSH）、超氧化物歧化酶（SOD）和过氧化氢酶（CAT）。
庆大霉素导致 GSH、SOD 和 CAT 的活性显著降低或抑制，MDA、ALT、AST、ALP 水平以及肝、肾组织中肌酐、尿酸和尿素浓度显著升高。与对照组相比，肝、肾组织中 GSH、SOD、CAT 的活性显著增加，MDA 水平显著降低，血清（ALT）；（AST）；（ALP）、肌酐、尿酸和尿素浓度与对照组相同。此外，庆大霉素给药导致肝、肾结构损伤。庆大霉素暴露前给予 BPF 可防止生化参数的严重改变和肝、肾结构的破坏。
总之，本研究明显表明，BPF 预处理可显著减轻庆大霉素引起的生理和组织病理学改变。此外，本研究为开发更好的治疗肝、肾和其他器官功能障碍和疾病的治疗药物开辟了新的研究领域。
