熊脱氧胆酸对糖尿病大鼠胰岛β细胞凋亡的保护作用
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The protective effect of ursodeoxycholic acid on pancreatic β-cell in STZ-induced diabetic rats
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    摘要:

    目的:探讨熊脱氧胆酸(UDCA)对链脲佐菌素(STZ)诱导的糖尿病(DM)大鼠胰岛β细胞抗氧化及抗凋亡的保护作用。方法:STZ 50 mg/kg一次性腹腔注射建立糖尿病大鼠模型(n = 40),并将成功制备的糖尿病大鼠(血糖持续1周≥16.7 mmol/L,n = 14)随机分为两组:DM组7只,UDCA组7 只,另外取正常对照组10只。自造模成功第10天开始UDCA组以UDCA(40 mg/kg)给大鼠灌胃30天,对照组予等量生理盐水,其间观察各组大鼠的体重、血糖,处死后留取血清和组织标本,测定血清一氧化氮(NO)、丙二醛(MDA),胰腺组织匀浆超氧化物歧化酶(SOD)及观察胰岛β细胞凋亡的形态学改变。结果:糖尿病大鼠在给予UDCA治疗后血糖浓度逐渐下降,但仍然未降到正常水平;糖尿病大鼠予UDCA治疗后减少了由STZ引起的胰岛β细胞的凋亡(P < 0.01);血清MDA、NO水平在糖尿病组大鼠显著增加,而胰腺组织匀浆SOD活性则降低;给予UDCA治疗后这些参数均有明显改善。结论:UDCA可以清除STZ 产生的NO和氧自由基,保护胰岛β细胞,使其不发生过度凋亡,从而降低血糖。[关键词] 熊脱氧胆酸; 胰腺β细胞; 细胞凋亡; 氧化应激

    Abstract:

    Objective:To clarify the protective effect of ursodeoxycholic acid(UDCA) on antioxidation and antiapoptosis of pancreatic β-cells in STZ-induced diabetic rats. Methods:Rats(n = 40) were received a single injection STZ(50 mg/kg) intraperitoneally to produce a β-cell injury model. Weight-matched normal rats(the control group,n = 10) were injected with the buffer alone. STZ-treated rats with persistent random blood glucose higher than 16.7 mmol/L for 1 week were considered as diabetic(n = 14),then were divided into the following two groups:STZ-induced diabetes group(n = 7) and UDCA-treated diabetes group(n = 7). UDCA(40 mg/kg) was administered daily by intragastric intubations during the experimental period(30 days). The control group and the STZ-induced diabetic group without UDCA treatment were given an equivalent amount of 0.9% NaCl intragastrically. During all experiments period,blood glucose and weight of all rats were assessed. Following 30-days UDCA treatment,all rats were anaesthetized and then killed to remove pancreas and collect the blood sample. The morphological changes of pancreatic β-cells apoptosis were determined by light microscope and TUNEL assay. Serum nitric oxide(NO), matondialdehyde(MDA) concentration and superoxide dismutase(SOD) level in pancreatic tissue were measured. Results:The concentration of blood glucose in diabetic rats was gradually decreased after the UDCA treatment,while still higher than the normal control group at the end of the experiment. The percentage of β-cell apoptosis of UDCA-treated group was significantly lower than that of STZ-induced diabetic group(P < 0.01). The content of serum NO and MDA was significantly elevated in STZ-induced diabetic rats with SOD decreased in pancreas,whereas these parameters became close to the normal after treated with UDCA. Conclusion:UDCA could act as an effective antioxidant agent and protect pancreatic β-cell from apoptosis in STZ-induced diabetes. It suggested that UDCA should have potential benefits in inhibiting the development of pancreas dysfunction in diabetic patients.

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朱敏,刘倩琦,郭 梅,费 莉,潘晓勤.熊脱氧胆酸对糖尿病大鼠胰岛β细胞凋亡的保护作用[J].南京医科大学学报(自然科学版),2008,28(3):286-290

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  • 收稿日期:2007-08-22
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