虫草菌丝药物血清对白细胞介素-1β损伤胰岛细胞的保护作用的实验研究

Protective Effect of Medicated Sera of Cordyceps sinensis(cs) on Islet Cell Damage Induced by Interleukin-1β

目的通过白细胞介素1β(Interleukin-1β,IL-1β)损伤离体胰岛细胞,研究虫草菌丝(Cordyceps sinensis,CS)含药血清对胰岛细胞的保护作用以及其机制与抗氧化酶和一氧化氮(Nitric oxide,NO)的关系。方法离体培养乳鼠胰岛细胞,用IL-1β损伤胰岛细胞,与不同浓度CS含药血清共同孵育,应用MTT法检测细胞活性,放免法检测基础和高糖胰岛素分泌量,比色法检测细胞培养上清液中一氧化氮(NO)的含量,诱生型一氧化氮合酶(Nitric oxide synthase,iNOS)、超氧化物歧化酶(superoxide dismutase,SOD)和谷胱甘肽过氧化物酶(glutathione perioxidase,GSH-Px)的活性。结果CS含药血清显著提高IL-1β损伤的胰岛细胞活性,并且胰岛细胞基础和高糖刺激胰岛素分泌量明显提高。IL-1β作用后细胞培养上清液中NOS活性升高,NO含量增加,而SOD,GSH-Px的活性水平降低,经与不同浓度CS含药血清共同孵育后,细胞培养上清液中NO含量减少、iNOS活性降低,SOD,GSH-Px的水平明显升高,呈剂量依赖性,具有统计学意义(P<0.05,P<0.01)。结论CS含药血清对IL-1β损伤的胰岛细胞分泌功能和细胞活性有保护作用,其机制与降低iNOS的活性,从而减少NO生成以及提高SOD,GSH-PX的活性水平有关。

Objective To investigate the effects and mechanism of medicated sera of cs on the islet cell damage induced by IL - 1β. Methods The pancreases of the rats were removed to collect islet cells , and then the cells were divided into normal control group, IL - 1β damadaged group, IL -1β ＋ medicated sera of cs groups. The cellular activity was detected with methyl - thiazol - tetrazolium（MTT） assay, basic amount of insulin secretion and stimulated by high glucose was detected by radioimmunoassay,the content of nitric oxide and activities of nitric oxide synthase superoxide dismutase and glutathione perioxidase were determued according to the kit direction. Results Medicated sera of cs obviously improved the islet cellular activity damaged by IL - 1β, and basic amount of insulin secretion and stimulated by high glucose were improved（ P 〈 0.01 ）. content of nitric oxide and activity of nitric oxide synthase in the supernatant were obviously higher in IL -1β damaged group, and there were significant differences between the medicated sera of es groups and IL -1β damaged group. Compared with IL - 1β damage group, medicated sera of cs could significantly elevate the activities of superoxide dismutase and glutathione perioxidase（P 〈 0.05 ,P 〈 0.01 ）. ConcLusion - Medicated sera of cs plays a protective role in the pancreatic islets damaged by IL -1β. The protective mechanism may be correlated with the decrease of iNOS activity and the content of nitric oxide, and the increase of the activities of superoxide dismutase and glutathione perioxidase.