血红素加氧酶/一氧化碳系统在百令胶囊水提物对抗STZ损伤大鼠胰岛细胞的作用

Role of HO/CO in STZ Induced Pancreatic Islet Cell Damage and the Effect of Water Extract of Corbrins Capsule

目的观察百令胶囊(Corbrin Capsule,CC)水提物对胰岛细胞的保护作用及其机制与血红素加氧酶/一氧化碳系统的关系。方法Wistar大鼠腹腔注射链脲佐菌素(Streptozotocin,STZ)建立Ⅰ型糖尿病模型,腹腔注射CC水提物和(或)HO的特异抑制剂锌原卟啉(Zinc protoporphrin IX,ZnPP),分糖尿病组(DM)、正常对照组(NC)、CC水提物组、CC水提物组+ZnPP,28 d后检测血糖,血清胰岛素分泌量、CO含量、HO-1活性。离体培养乳鼠的胰岛细胞,检测STZ、CC以及ZnPP作用后细胞活性、细胞培养上清液中胰岛素的基础、高糖刺激分泌量,细胞HO-1以及CO的变化,同时设立正常对照组。结果经CC水提物作用后,STZ糖尿病大鼠血清中血糖降低,胰岛素增加,CO、HO-1水平升高(P<0.01)。ZnPP作用后血清HO-1水平降低,CO含量减少。STZ与胰岛细胞孵育20 h后与ZnPP加入CC组,均表现出细胞活性降低,基础和高糖刺激胰岛素分泌减少;细胞HO-1活性降低,CO生成减少(P<0.01)。与CC共同孵育细胞活性显著升高,胰岛素基础和高糖分泌量增多,HO-1活性水平和CO生成量显著提高(P<0.01)。结论通过实验证实CC水提物对STZ损伤的胰岛细胞有保护作用,机制与增加HO-1活性,CO生成增多有关。

Objective To observe the proteetive effect of water extract of Corbrins Capsule（ CC ） on pancreatic islet cell injury induced by streptozocin（STZ） mechanisms. Methods The pancreases of the rats were removed to collect islet cells. The cells were incubated with STZ with/or CC or ZnPP. Cell activity , insulin secretion , HO - 1 activity , CO content were detected. Type 1 diabetic rats model was induced by injection of the STZ, and water extract of CC and/or ZnPP were given by injection for twenty eight days. Blood glucose level was measured by glucometer. HO - 1 activity , CO content were detected. Results Water extract of CC obviously improved the islet cell activity damaged by STZ, and the amount of basic insulin secretion and stimulated by high glucose were improved（ P 〈 0.05 ）. The eontent of CO and activity of Coo synthase in supernatant were obviously increased in the STZ damaged group and in the serum of diabetic rats, and there were significant differences between the CC groups and STZ damaged groups . Activities of HO - 1 and CO were decreased in STZ damaged group and diabetie rats as compared to normal control group, and the water extract of CC could signifieantly elevated the abrivities of hot aual Co as compared to STZ damaged group and diabetic rats. Conclusion Water extract of CC plays a protective role in the pancreatic islet cell damage induced by STZ, and the protective mechanism may be correlated with elevation of HO - 1 - 1 activity and generation of CO.