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作 者:唐志刚[1] 薛华[2] 乔进[2] 顾锦华[2] 徐济良[2]
机构地区:[1]南通大学附属医院药剂科 [2]南通大学医学院药理学教研室,江苏南通226001
出 处:《苏州大学学报(医学版)》2010年第5期922-925,935,F0003,共6页Suzhou University Journal of Medical Science
基 金:科技部十一五国家科技支撑计划子课题(2006DAI06A20-02)
摘 要:目的观察灵芝多糖对2型糖尿病大鼠胰岛损伤的保护作用。方法建立高脂饲料联合小剂量链脲佐菌素所诱发的2型糖尿病大鼠模型,应用灵芝多糖灌胃治疗10周后,检测大鼠空腹血糖和胰腺中NO、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)的活性以及丙二醛(MDA)的含量。通过胰腺HE染色和胰岛素免疫组化分析胰岛的病理变化。结果灵芝多糖能降低糖尿病大鼠的空腹血糖,提高胰岛素敏感性,提高血清和胰腺中GSH-Px、SOD和CAT的活性,显著降低NO和MDA含量(均P<0.05或0.01);HE染色等形态学检测显示能减轻大鼠胰岛萎缩,增加胰岛B细胞的数目。结论灵芝多糖能减轻2型糖尿病大鼠的胰岛损伤,可能是通过减轻氧化应激水平发挥保护作用的。Objective To investigate the protective effects of ganoderma lucidum polysaccharides ( GLPs) on pancreatic islet in T2DM rats. Method SD rats were fed high-fat diet for 4 weeks and then were injected STZ ( 30 mg/kg) to induce the type 2 diabetes mellitus( T2DM) . Once the T2DM model were set successfully,rats were divided into six groups randomly: the normal group ( NG) ,diabetes mellitus group ( DMG) ,GPLs low dosage group ( GLPs-LG) ,GPLs middle dosage group ( GLPs-MG) ,GLPs high dosage group ( GLPs-HG) and the berberine group ( BerG) . They received GLPs with different dosages ( 200,400,or 800 mg/kg) and berberine ( 30 mg/kg) continually for 10 weeks. At 10th weekend, the following indexes of rats in each group were measured respectively: blood glucose,insulin sensivity index( ISI) ,the contents of NO、SOD、MDA、GSH-Px、CAT in pancreas tissue. At the same time pathological change of pancreas was evaluated by hematoxylin/eosin staining and immunohistochemistry of insulin. Result As compared with the diabetic model,the decrease of blood glucose with GLPs treatment for 10 weeks were observed. There was also notably increased antioxidant enzyme activity such as superoxide dismutase( SOD) ,catalase( CAT) as well as decreased MDA content in the pancreatic homogenate. Under light microscope,GLPs-HG treated T2DM showed significantly ameliorated pathological changes,increased islet area and enhanced insulin staining intensity in islets. Conclusion GLPs has protective effect on the STZ-induced islet injury in T2DM rats through increasing antioxidant enzyme activity and reducing oxidative stress.
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