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本实验采用小剂量多次腹腔注射链佐霉素(Streptozotocin,STZ)选择性地破坏胰岛β细胞的方法造成高血糖的小鼠动物模型,观察α_2-肾上腺素能受体激动剂可乐宁(Clonidine)与胃肠激素生长抑素(Somatostatin,SS)在预防STZ诱导的高血糖作用中的相互关系。结果如下:(1)接受STZ处理后,小鼠在实验的第6、8、10、15天,血糖均有明显升高;(2)在每次注射STZ前注射可乐宁或SS,均可减轻STZ诱导的高血糖,(8)将可乐宁和SS合并作预防牲注射,对STZ高血糖的抑制作用大大加强,在实验的第15天,联合用药降低高血糖的作用大于两种药单独注射效果的代数和。本工作提示,某些神经因素和体液因素在预防由STZ诱导的高血糖产生中具有相互加强作用,从而为寻找减少激素用量,经济、有效的防治糖尿病方法提供了一定的线索。
In this study, a small dose of multiple intraperitoneal injections of streptozotocin (STZ) to selectively destroy pancreatic islet β cells resulted in a hyperglycemic mouse model, and an α2-adrenoceptor agonist, Clonidine, was observed. ) The interaction with gut hormone somatostatin (SS) in the prevention of STZ-induced hyperglycemia. The results were as follows: (1) After receiving STZ treatment, the mice had a significant increase in blood glucose on the 6th, 8th, 10th and 15th days of the experiment; (2) injection of clonidine or SS before each injection of STZ. Reducing STZ-induced hyperglycemia, (8) Combining clonidine and SS as a prophylactic injection, the inhibition of STZ hyperglycemia was greatly enhanced. On the fifteenth day of the experiment, the combined use of drugs reduced hyperglycemia more than the two drugs alone. Algebraic sums of injection effects. This work suggests that certain neurological factors and humoral factors have mutual reinforcing effects in preventing the production of hyperglycemia induced by STZ, thus providing certain clues for seeking to reduce the amount of hormones, and to economically and effectively prevent and treat diabetes.