目的：探讨黄精多糖(PSP)对链脲菌素(STZ)诱导的糖尿病大鼠的降血糖作用及其可能机制。方法：采用STZ(60 mg·kg-1)腹腔注射法建立糖尿病大鼠模型。造模第30 d测定大鼠体重、进食量、进水量和尿量；末次给药24 h后，腹主动脉取血，分离血清。采用葡萄糖氧化酶法测定大鼠空腹血糖(FBG)、放射免疫方法检测血清胰岛素(INS)、化学比色法测定糖化血清蛋白(GSP)；采用胰腺组织切片HE 染色和免疫组化染色法对胰岛结构和胰岛素表达情况进行观察；原位末端标记法(TUNEL)标记STZ糖尿病大鼠胰岛凋亡细胞；采用免疫组化染色观察各组大鼠胰岛细胞caspase-3蛋白表达。结果：模型组大鼠呈现多饮多尿多食、体重下降、血糖升高和胰岛结构破坏。PSP(390，780 mg·kg-1)组大鼠的进食量、进水量和尿量指标显著低于模型组，同时FBG和GSP降低，血清INS含量上升，胰岛形态改善，INS表达增强。模型组细胞凋亡率和Caspase-3表达显著升高(P<0.01)；PSP各剂量组胰岛细胞凋亡率和Caspase-3表达显著下降。结论：PSP能够降低STZ糖尿病大鼠血糖，提高胰岛素表达，其机制可能与其抑制胰岛细胞凋亡，下调Caspase-3表达有关。
Objective: To study the effects of Polygona-polysaccharose (PSP) on blood glucose level and the mechanism of protection on diabetic rats induced by streptozotocin (STZ). Method: The animal model of diabetes was established by injecting STZ (60 mg·kg-1) into its abdominal cavity. The amount of water drinking, food intake, urinary volume and body weight were measured at the fourth week of the treatment. The blood samples were drawn to determine the indexes of blood glucose (FBG) and Glycosy lated serum protein (GSP) and blood serum insulin (INS). Pancreatic pathology was studied with morphological method and immunohistochemical method. The distribution of apoptotic cells and the expression of Caspase-3 were observed by TUNEL and immunohistochemistry. Result: The levels of FBG, GSP and the amount of water drinking, food intake, urinary volume in the PSP treated groups were obviously lower than those in the model group while INS increased. PSP decreased the rate of apoptotic cells and the level of Caspase-3. Conclusion: PSP can effectivly decrease blood glucose and increase INS. The mechanism may be related with inhibiting islet cell apoptosis and lowering Caspase-3.