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机构地区:[1]北京医科大学生理学系,北京电子部402医院内科,佳木斯医学院生理教研室
出 处:《中国神经免疫学和神经病学杂志》1996年第2期95-98,共4页Chinese Journal of Neuroimmunology and Neurology
基 金:国家自然科学基金
摘 要:将Wistar雄性大鼠束缚应激,腹腔注射6%四氧嘧啶(100mg/kg),24h后血糖值为7.3±0.2mol/L,而未做应激处理的大鼠血糖值为9.9±0.6mmol/L;既不应激也不注射四氧嘧啶动物的血糖值为7.0±0.6mmol/L,说明束缚应激具有对抗四氧嘧啶致糖尿病的作用。以束缚应激后大鼠腹腔淋巴结提取的抑制因子给大鼠静脉注射,然后再腹腔注射同样剂量的四氧嘧啶。结果显示,注射淋巴结提取物大鼠血糖值为7.3±0.6mmol/L,而单纯注射四氧嘧啶大鼠血糖值为9.8±0.8mmol/L(P<0.05),说明束缚应激对抗四氧嘧啶致糖尿病作用可能由束缚应激产生的抑制因子所致。Wistar rats were subjected to restraint stress overnight(15~18h),and then were intraperitoneally injected with 6%alloxan(100mg/kg).Blood glucose in control group(without stress)was 9.9±0.6mmol/L,however,blood glucose in experimental group was7. 3±0.2mmol/L. There is a statistically significant difference between them(P<0.01,t test).In order to study the role of the suppressive protein induced by restraint stress in the elevation of blood glucose induced by alloxan,a partially purified product of the protein derived from lymph nodes of stressed rats was intraperitoneally injected in rats.It was found that the elevation of blood glucose was suppressed. The results suggest that the suppressive protein induced by restraint stress may have an inhibitory effect on diabetes induced by alloxan.
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