摘要
目的 研究褪黑素对糖尿病大鼠肾脏氧化应激反应和肾功能的影响。方法 链脲佐菌素诱导的糖尿病大鼠给予褪黑素治疗 8周后 ,检测褪黑素对糖尿病大鼠血及肾脏氧自由基代谢状态和肾功能的影响。结果 与正常对照组大鼠比较 ,糖尿病大鼠肾皮质丙二醛 (MDA)含量明显增加 ,而肾组织内在抗氧化酶包括超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH Px)活性显著降低 ,同时伴尿蛋白排泄量升高 ,肾重 /体重比值降低。褪黑素治疗可明显增加糖尿病大鼠肾脏SOD和GSH Px活性、降低肾皮质MDA含量 ,并使尿蛋白排泄量减少、肾重 /体重比值降低。结论 褪黑素能有效抑制糖尿病大鼠肾脏氧化应激反应 ,改善肾功能。
Objective To in ve stigate the effects of melatonin on oxidative stress and renal function in kidne ys of diabetic rats. Methods Diabetic model of rats was induced by streptozocin. Male diabetic SD rats were assigned to 3 group s: (1) Untreated (DMC); (2) DM+Mel 1, melatonin 0.2 mg·kg -1 ·d -1 b y gavage, and (3) DM+Mel 2, melatonin 5 mg·kg -1 ·d -1 by gavage, se ven rats were in each group. Seven normal rats were assigned to normal control ( NC) group. Eight weeks later, systemic and renal intrinsic anti-oxidant enzyme activities, lipid peroxide levels and urinary protein excretion, creatinine clea rance rate and kidney weight were evaluated. Results Glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities were lower and lipid peroxide levels were higher in renal cortex of diabetic ra ts than those in NC group. SOD and GSH-Px activities in renal cortex increased and plasma triglycerides level and urinary protein excretion decreased in DM+Mel 1 group. DM+Mel 2 group showed changes similar to DM+Mel 1 group. These dose s also reduced lipid peroxide levels in renal cortex and kidney weight/body weig ht ratio of diabetic rats. Moreover, larger dose melatonin reversed the lowered SODactivitiesine rythrocytesand the raised lipid peroxide levels in plasma of dia betic rats. Conclusion Melatonin may inhibit oxi dative stress in kidneys and improve renal function in diabetic rats. Overproduc tion of reactive oxygen free radicals and insufficieny in intrinsic anti-oxidan t enzymes may contribute to the development of diabetic nephropathy.
出处
《中华内分泌代谢杂志》
CAS
CSCD
北大核心
2003年第1期60-62,共3页
Chinese Journal of Endocrinology and Metabolism
关键词
抑制作用
实验性糖尿病
肾
褪黑激素
氧化性应激
Diabetes mellitus, experimental
Kidney
Melatonin
Oxidative stress (Chin J Endocrinol Metab, 2003,19:60-62)
