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目的:研究决明子提取物Cassia obtusifolia extract(COE)对链脲佐菌素(STZ)诱发糖尿病小鼠晶状体氧化应激状态的改善作用。方法:雄性昆明种小鼠尾静脉注射STZ 130 mg·kg-1造成糖尿病模型后,分成STZ模型组、二甲双胍组(300mg·kg-1,ig)、决明子提取物低、中、高给药组(50,150,450 mg·kg-1,ig),每组10只,每天ig 1次,连续给药10 d后。检测小鼠血糖浓度和晶状体氧化应激状态相关指标抗氧化能力指数(ORAC)、丙二醛(MDA)、一氧化氮(NO)、谷胱甘肽(GSH)、超氧化物歧化酶(T-SOD)和谷胱甘肽过氧化物酶(GSH-Px)的改善作用。结果:小鼠尾静脉注射STZ 7 d后,诱发小鼠血糖值明显增高(P<0.01),同时造成晶状体的氧化损伤。同时与模型组相比,决明子提取物没有显示有效的降血糖作用,但决明子给药均能显著降低小鼠晶状体的氧化应激产物NO和MDA含量(P<0.01),同时提高晶状体的抗氧化能力指数ORAC和GSH水平(P<0.01),并提高小鼠晶状体组织内抗氧化的自由基清除系统相关酶(T-SOD和GSH-Px)的活性(P<0.01)。结论:决明子提取物可以改善STZ诱导糖尿病小鼠晶状体内的过氧化状态,其作用机制可能通过清除自由基和抑制脂质过氧化过程实现的。
Objective: To study the effect of extract Cassia obtusifolia extract (COE) on the oxidative stress in mice with streptozotocin (STZ) -induced diabetic mice. Methods: The STZ model group, metformin group (300mg · kg-1, ig) and the Cassia seed extract low, middle and high dosage group were given into the caudal vein of male Kunming mice after injection of STZ 130 mg · kg- (50,150,450 mg · kg-1, ig), 10 rats in each group, once a day for 10 days. The levels of blood glucose and the indicators of oxidative stress in the lens were measured for the antioxidant index (ORAC), malondialdehyde (MDA), nitric oxide (NO), glutathione (GSH), superoxide dismutase -SOD) and glutathione peroxidase (GSH-Px). Results: After injection of STZ for 7 days in tail vein of mice, the blood glucose level of mice induced by STZ was significantly increased (P <0.01) and oxidative damage of lens was induced. Compared with the model group, Cassia seed extract did not show effective hypoglycemic effect, but Cassia seed administration could significantly reduce the content of NO and MDA in the lens of mice (P <0.01), and at the same time improve the antioxidation of the lens (P <0.01), and increased the activity of antioxidant free radical scavenging enzymes (T-SOD and GSH-Px) in the lens epithelial cells of mice. CONCLUSION: Cassia seed extract can improve peroxisome state in STZ-induced diabetic mice. Its mechanism may be through the elimination of free radicals and inhibition of lipid peroxidation.