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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。
The Wistar male rats were restrained and challenged with intraperitoneal injection of 6% alloxan (100 mg / kg) for 24 h and the blood glucose level was 7.3 ± 0.2 mol / L, while the rats without stress treatment had a blood glucose level of 9 .9 ± 0.6mmol / L. The blood glucose level of neither alloxan nor alloxan was 7.0 ± 0.6mmol / L, indicating that restraint stress has the effect against alloxan-induced diabetes. The rats were injected intraperitoneally with the same dose of alloxan after restraint stress-induced inhibition of rat abdominal lymph node extraction. The results showed that the blood glucose of rats injected with lymph node extract was 7.3 ± 0.6mmol / L, while that of rats injected with alloxan alone was 9.8 ± 0.8mmol / L (P <0.05) These results suggested that the binding stress may antagonize the alloxan-induced diabetes by inhibition of stress-induced inhibitors.