Ashafaq Mohammad, Varshney Laxmi, Khan Mohammad Haaris Ajmal, Salman Mohd, Naseem Mehar, Wajid Saima, Parvez Suhel
Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), New Delhi 110 062, India.
Department of Biotechnology, Jamia Hamdard (Hamdard University), New Delhi 110 062, India.
Biomed Res Int. 2014;2014:249031. doi: 10.1155/2014/249031. Epub 2014 Jun 19.
Oxidative stress has been implicated in pathogenesis of streptozotocin- (STZ-) induced diabetes mellitus and its complication in central nervous system (CNS). Recent studies have provided insights on antioxidants and their emergence as potential therapeutic and nutraceutical. The present study examined the hypothesis that hesperidin (HP) ameliorates oxidative stress and may be a limiting factor in the extent of CNS complication following diabetes. To test this hypothesis rats were divided into four groups: control, diabetic, diabetic-HP treated, and vehicle for HP treatment group. Diabetes mellitus was induced by a single injection of STZ (65 mg/kg body weight). Three days after STZ injection, HP was given (50 mg/kg b.wt. orally) once daily for four weeks. The results of the present investigation suggest that the significant elevated levels of oxidative stress markers were observed in STZ-treated animals, whereas significant depletion in the activity of nonenzymatic antioxidants and enzymatic antioxidants was witnessed in diabetic rat brain. Neurotoxicity biomarker activity was also altered significantly. HP treatment significantly attenuated the altered levels of oxidative stress and neurotoxicity biomarkers. Our results demonstrate that HP exhibits potent antioxidant and neuroprotective effects on the brain tissue against the diabetic oxidative damage in STZ-induced rodent model.
氧化应激与链脲佐菌素(STZ)诱导的糖尿病及其中枢神经系统(CNS)并发症的发病机制有关。最近的研究提供了关于抗氧化剂及其作为潜在治疗和营养保健品出现的见解。本研究检验了橙皮苷(HP)可改善氧化应激且可能是糖尿病后CNS并发症程度的限制因素这一假说。为验证该假说,将大鼠分为四组:对照组、糖尿病组、糖尿病-HP治疗组和HP治疗组的赋形剂组。通过单次注射STZ(65 mg/kg体重)诱导糖尿病。STZ注射后三天,每天口服给予HP(50 mg/kg体重),持续四周。本研究结果表明,在STZ处理的动物中观察到氧化应激标志物水平显著升高,而在糖尿病大鼠脑中则发现非酶抗氧化剂和酶抗氧化剂的活性显著降低。神经毒性生物标志物活性也发生了显著改变。HP治疗显著减轻了氧化应激和神经毒性生物标志物水平的改变。我们的结果表明,在STZ诱导的啮齿动物模型中,HP对脑组织表现出强大的抗氧化和神经保护作用,可抵抗糖尿病氧化损伤。