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首页> 外文期刊>International Journal of zoological research >Repossession of Brain Complications in a Streptozotocin Induced Diabetic Rat by Exogenous Melatonin Administration
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Repossession of Brain Complications in a Streptozotocin Induced Diabetic Rat by Exogenous Melatonin Administration

机译:通过外源性褪黑激素给药恢复链脲佐菌素诱导的糖尿病大鼠脑并发症

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Background and Objective: Diabetes is one of the foremost culprit responsible in degrading the health of a person in this stressful life. The present study focused on protective effect of melatonin (MEL) on brain of streptozotocin (STZ) induced diabetic rat. Materials and Methods: Thirty six male rats were randomly divided into six groups, each group contain six rats, Control, STZ induced, STZ+Mel, Mel, STZ+GB (Glibenclamide) and GB. Streptozotocin was injected for six days continuously thereafter blood glucose level were censored after 72 h. The animals showing blood glucose level above 250 mg dL–1 were considered as diabetic and were administered with exogenous Mel for 4 weeks. Animals were euthanized after 4 weeks. Brain of all respective groups were dissected, weighed and fixed in Bouin’s fixative for histological studies as well as processed for the assessment of biochemical variables viz lipid peroxidation (LPO), antioxidative defense system; reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) activity and total protein quantification. Data were analyzed by students t-test followed by one-way ANOVA to compare between different experimental groups. Results: Streptozotocin (STZ)-induced diabetic rats exhibited significant increase in rate of LPO (p<0.001) but a significant decrease in organ weight, GSH, SOD, CAT and total protein content (p<0.05, 0.01 and 0.001). However, melatonin treatment restored LPO, weight of brain, total protein, catalase (CAT) SOD, GSH (p<0.05, 0.01 and 0.001). Decrement in hippocampal volume signifies the brain cell damaged might have resulted due to increased free radical load during diabetes. Further, histophotomicrographs of diabetic rats showed decrease in astrocyte number indicating compromised state of immune defense system. Melatonin administration however revived the brain architecture because of its antiapoptotic and antioxidant nature. Conclusion: Therefore, melatonin might be suggested as neuroprotective therapeutic molecule regulating morphological, anatomical and biochemical functions of brain during diabetes induced brain impairments.
机译:背景与目的:糖尿病是造成这种压力大的人的健康下降的罪魁祸首之一。本研究的重点是褪黑激素(MEL)对链脲佐菌素(STZ)诱导的糖尿病大鼠脑的保护作用。材料与方法:36只雄性大鼠随机分为6组,每组6只,对照组,STZ诱导,STZ + Mel,Mel,STZ + GB(格列本脲)和GB。连续连续六天注射链脲佐菌素,然后在72小时后检查血糖水平。血糖水平高于250 mg dL-1的动物被认为是糖尿病动物,并给予外源性梅尔4周。 4周后对动物实施安乐死。将所有组的脑解剖,称重并固定在Bouin固定剂中进行组织学研究,并进行处理以评估生化变量,即脂质过氧化(LPO),抗氧化防御系统;降低了谷胱甘肽(GSH),超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活性以及总蛋白定量。通过学生t检验和单向方差分析对数据进行分析,以比较不同实验组之间的差异。结果:链脲佐菌素(STZ)诱导的糖尿病大鼠的LPO率显着增加(p <0.001),但器官重量,GSH,SOD,CAT和总蛋白含量却显着降低(p <0.05、0.01和0.001)。然而,褪黑激素治疗可恢复LPO,脑重量,总蛋白,过氧化氢酶(CAT)SOD,谷胱甘肽(p <0.05、0.01和0.001)。海马体积的减少表明,由于糖尿病期间自由基负荷增加,可能导致脑细胞受损。此外,糖尿病大鼠的组织显微照片显示星形胶质细胞数量减少,表明免疫防御系统的状态受损。然而,褪黑激素的给药具有抗凋亡和抗氧化的特性,因此可以使大脑结构恢复活力。结论:因此,褪黑激素可能被建议作为调节糖尿病引起的脑损伤期间脑的形态,解剖和生化功能的神经保护性治疗分子。

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