摘要
本实验采用四氧嘧啶损伤大鼠胰岛β细胞，复制糖尿病动物模型。若预先腹腔注射汉防己甲素（１００ｍｇ／ｋｇ）则可完全预防引发的糖尿病。预防组血糖（７．６３±０．４４ｍｍｏｌ／Ｌ）明显低于对照组（２５．４６±１．２１ｍｍｏｌ／Ｌ，Ｐ＜０．００１）；血清胰岛素水平（１１．３３±１．９７μＵ／ｍｌ）高于对照组（７．１３±０．４５μＵ／ｍｌ，Ｐ＜０．０５）；血浆胰高血糖素（６６．８５±５．０７ｐｇ／ｍｌ）明显低于对照组（９０．３５±３．１５ｐｇ／ｍｌ，Ｐ＜０．０１）．口服葡萄糖耐量实验显示预防组耐糖功能较对照组明显改善，糖耐量曲线下血糖面积预防组（２９．４５±１．６３ｍｌ·ｈ／Ｌ）低于对照组（１１３．２８±５．０２ｍｍｏｌ·ｈ／Ｌ，ｐ＜０．００１）。胰岛β细胞免疫组织化学染色结果显示，预防组胰岛β细胞数目及胰岛素分泌颗粒的含量均与正常大鼠胰岛相同，无形态学改变，而对照组胰岛内β细胞免疫反应阳性产物减少甚至消失。结果表明，汉防己甲素对四氧嘧啶引起的胰岛β细胞急性损伤有保护作用。
Tetrandrine(TET,100 mg/kg)injected intraperitoneally could prevent rats fromdiabetes induced by alloxan.After 48 h of injection of alloxan,the bital sugar of thepreventive group decreased from the control value of 25.46±1.21 mmol/L to 7.63±0.44 mmol/L(PR<0.001)while the serum insulin level increased to 11.33±1.97μU/ml and the plasma glucagon concentration to 66.85±5.07 pg/ml respectivelyfrom the control group's value of 7.13±0.45μU/ml and 90.35±8.33 pg/ml.In glucose tolerance lost,TET 100 mg/kg showed that the abnormal glucose tolerance inducedby alloxan could be improved.The blood sugar area under the glucose tolerance curveof the preventive group decreased from the control groups level of 113.28±5.02mmol·h/L to 29.45±1.63 mmol·h/L(P<0.001).Immunohistochemical observation of islet βcells confirmed that TET could markedly prevent βcells from injuries induced by alloxan and there was no obvious change in the appearance of islet βcells inthe preventive group.The above results suggested thet TET could protect pancreatic isletβ cells from injuries caused by Alloxan.
出处
《生理学报》
CAS
CSCD
北大核心
1994年第2期161-167,共7页
Acta Physiologica Sinica
