摘要
目的观察桑叶总黄酮对2型糖尿病大鼠胰岛β细胞氧化损伤的影响及作用机制。方法给大鼠腹腔注射30 mg·kg-1链脲佐菌素,建立2型糖尿病动物模型。造模后随机分成模型组,桑叶总黄酮低、中、高剂量组(50,100,150 mg·kg-1)和罗格列酮组(1.8 mg·kg-1),另取正常大鼠作为对照组,每组均为10只。灌胃给药,每日1次,连续5周后测定大鼠血清空腹血糖(FBG)、空腹胰岛素(FINS)水平和胰腺组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)含量。免疫组化法检测Bcl-2、Bax蛋白的表达,末端脱氧核糖核酸缺口标记法(TUNEL)加免疫组化法测定胰岛β细胞凋亡率。结果桑叶总黄酮能显著降低胰腺组织MDA水平,提高SOD和GSH-Px水平(P<0.05或P<0.01),显著上调抗凋亡基因Bcl-2表达,下调促凋亡基因Bax表达(P<0.05或P<0.01),使胰岛细胞凋亡率显著降低(P<0.05或P<0.01),并能显著降低FBG水平,升高FINS含量(P<0.05或P<0.01),其中以150 mg·kg-1桑叶总黄酮最为明显。结论桑叶总黄酮对2型糖尿病大鼠具有较好的抗氧化作用,可以缓解胰岛β细胞凋亡的发生。
Objective To investigate the effect and mechanism of total flavonoid (MFTF) from mulberry leaves on β- cells oxidative injury in type-2 diabetic (T2DM) rats. Methods Diabetes was induced by a intraperitoneal injection of streptozotocin (30 mg · kg-1 body weight). Animals were randomly divided into five groups: the model, MFTF (50,100, 150 mg · kg-1 ) and rosiglitazone ( 1.8 mg ·kg-1 ) groups, with other 10 normal rats as a control group. Fasting blood glucose (FBG), insulin ( FINS ) level in serum, malondialadehyde ( MDA ) content, the activity of superoxide dismutase ( SOD ) and glutathione peroxidase (GSH-Px) in the rats pancreatic tissue were measured after being orally treated once daily for five consecutive weeks. Bel-2 and Bax expression in islet tissues were detected by using immunohistochemistry and the rate of pancreatic islet β cell apoptosis was tested by both TUNEL and immunohistochemistry. Results MFTF significantly decreased the level of MDA and FBG (P〈0.05) ,increased the activity of SOD, GSH-Px and FINS content in pancreatic tissue (P〈0.05 or P〈0. 01 ),markedly up-regulated the expression of Bcl-2 and down-regulated Bax(P〈0. 05 or P〈0. 01 )at the dose of 150 mg · kg-1. Conclusion MFTF shows strong anti-oxidation and alleviates B cell apoptosis in T2DM rats.
出处
《医药导报》
CAS
北大核心
2013年第6期701-704,共4页
Herald of Medicine
基金
河南漯河医学高等专科学校科研基金项目(2010-S04)
关键词
桑叶总黄酮
糖尿病
2型
胰岛Β细胞
氧化损伤
细胞凋亡
Mori folium total flavonoid
Diabetic mellitus, type-2
Pancreatic islet β cell
Oxidative injury
Apoptosis