摘要
目的研究藏红花素(crocin)对2型糖尿病大鼠胰腺组织并发症损伤的保护作用并初探其机制。方法120只实验用SD大鼠经过体重分层后随机分为正常组、模型对照组、藏红花素25、50、100mg/(kg·d)组和二甲双胍25mg/(kg·d)组,灌胃给药,疗程12周;采用链脲佐菌素(STZ)连续3天腹腔注射30mg/(kg·d)的方法制备实验性2型糖尿病大鼠模型。测定各组大鼠空腹血糖(FBG)、空腹胰岛素(FINS)和糖化血红蛋白(GHb),计算胰岛素抵抗指数(ISI)和敏感指数(HOMA-IR),采用HE染色对胰岛组织进行病理学检查,TUNEL法观察胰岛细胞凋亡状况,测定胰腺组织中抗氧化酶活性和丙二醛(MDA)含量。结果经藏红花素50~100mg/(kg·d)治疗12周,糖尿病大鼠FBG显著降低、FINS显著升高、GHb显著降低、ISI和HOMA-IR显著降低,差异均有统计学意义(P<0.05);胰岛组织病变明显改善,胰岛组织细胞凋亡数量明显减少,凋亡指数(apoptosisindex,AI)显著降低(P<0.01);胰腺组织抗氧化酶[超氧化物歧化酶(SOD)、过氧化氢酶(CAT)]活性显著升高且MDA含量显著降低(P<0.05)。结论藏红花素对2型糖尿病大鼠胰腺组织损伤具有一定的保护作用,其机制可能与抑制氧化应激损伤有关。
Objective To investigate the protective effects of crocin on pancreatic tissue injury in type 2 diabetic rats and its mechanism.Methods Totally 120 SD rats were randomized according to body weight divided into normal control group,model group,crocin [25,50,100mg/(kg·d)] groups and metformin hydrochloride 25mg/(kg·d) group.The drugs were given by gastric administration for 12 weeks.The diabetic rat models were made by intraperitoneal injecting STZ [30mg/(kg·d)] for 3days continuously.The general condition of the rats in every group were observed.The FBG,FINS,GHb were detected.The ISI and HOMA-IR were calculated.HE staining was used for pathological examination of islet tissues and TUNEL was used to observe the apoptosis of islet cells.The antioxidant enzyme activity and malondialdehyde (MDA) content in pancreatic tissues were detected.Results After treatment with crocin 50~100mg/(kg·d) for 12 weeks,the FBG decreased significantly,FINS increased significantly,GHb decreased significantly,ISI and HOMA-IR significantly decreased.All of the differences above were statistically significant ( P <0.05).The islet tissue lesions significantly improved,islet cell apoptosis was significantly reduced,apoptotic index was significantly reduced ( P <0.01).The antioxidant enzymes (SOD,CAT) activity increased significantly and MDA content decreased significantly in pancreatic tissue ( P <0.05).Conclusion Crocin has a protective effect on diabetic pancreatic tissue injury,and its mechanism may be related to the inhibition of oxidative stress injury.
作者
王立哲
王振贤
马晓伟
Wang Lizhe;Wang Zhenxian;Ma Xiaowei(Department of Rehabilitation Medicine,First Department of Endocrinology,First Department of Neurology,Handan Central Hospital,Hebei 056001,China)
出处
《医学研究杂志》
2019年第5期102-106,共5页
Journal of Medical Research
基金
河北省邯郸市科学技术研究与发展计划项目(1623208059ZC)