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本工作用四氧嘧啶(皮下注射)造成大鼠实验性糖尿病模型。若预先由腹腔注射剂量为10μg/kg 的前列腺素E_2(PGE_2),则可使大鼠的糖尿病发病率由75％下降到12.5％;在注射四氧嘧啶72h后,血浆葡萄糖浓度的平均值由498.0±86.6mg％下降到141.9±30.5mg％。PGE_2的这种对四氧嘧啶的细胞毒性作用的缓解具有一定的剂量依从关系。通过口服葡萄糖耐量试验观察到,经过PGE_2处理的糖尿病鼠,在注射四氧嘧啶后120h,其胰岛素分泌的功能,较未处理的糖尿病鼠得到明显恢复。组织学切片也显示,胰岛β细胞内胰岛素分泌颗粒含量在PGE_2处理组较单独四氧嘧啶处理组明显增多。因此,从机能和形态学观察结果均表明,预防性注射PGE_2能减轻四氧嘧啶对胰岛β细胞造成的急性损伤,提示PGE_2对胰岛β细胞似具有细胞保护作用。
This work with alloxan (subcutaneous injection) rat experimental diabetic model. The pretreatment of intraperitoneal injection of prostaglandin E 2 (PGE 2) at a dose of 10 μg / kg decreased the incidence of diabetes in rats from 75% to 12.5%. After 72 hours of injection of alloxan, the mean plasma glucose concentration decreased from 498.0 ± 86.6 mg% to 141.9 ± 30.5 mg%. This PGE 2 has a dose-dependent dependence on the cytotoxic effects of alloxan. Oral glucose tolerance test showed that the function of insulin secretion of PGE 2 -treated diabetic mice 120 h after alloxan injection was significantly recovered compared with untreated diabetic mice. Histological sections also showed that the content of insulin secreted granules in pancreatic β-cells was significantly increased in PGE 2 -treated group compared with that in alloxan-treated group. Therefore, from the functional and morphological observations showed that prophylactic injection of PGE 2 can reduce alloxan induced pancreatic β-cell acute injury, suggesting that PGE 2 has a cytoprotective effect on pancreatic β cells.