地锦草对糖尿病小鼠胰岛β细胞氧化应激和凋亡的影响

Effect of Euphorbiae Humifusae Herba on Pancreatic Islet Beta Cells on Oxidative Stress and Apoptosis in Diabetic Mice

目的:研究地锦草对糖尿病小鼠胰岛β细胞氧化应激和凋亡的影响。方法:尾静脉注射四氧嘧啶溶液(80 mg·kg-1)复制糖尿病小鼠模型。将造模成功的小鼠随机分为5组:模型组,阳性对照组(盐酸二甲双胍悬浊液25 mg·kg-1·d-1),地锦草低、中、高剂量组(59,118,236 mg·kg-1·d-1),连续给药14 d后,观察其血糖、胰腺组织超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GSH-Px),丙二醛(MDA)水平的变化,采用末端脱氧核苷酸转移酶介导的d UTP缺口末端标记法(TUNEL法)检测胰岛β细胞的凋亡情况。结果:与模型组比较,地锦草各剂量组小鼠体重下降不明显(P<0.05);与给药前及模型组比较,地锦草高剂量组和二甲双胍组血糖均下降(P<0.05);与模型组比较,地锦草高剂量组和二甲双胍组胰腺组织中SOD和GSH-Px活性均升高(P<0.05),MDA的含量降低(P<0.05),胰岛β细胞凋亡指数降低(P<0.05)。结论:地锦草可明显降低糖尿病小鼠的血糖,其机制可能与增强糖尿病小鼠的抗氧化能力,减弱氧化应激对糖尿病小鼠胰岛β细胞的损伤,抑制胰岛β细胞的凋亡有关。

Objective： To observe the effects of Euphorbiae Humifusae Herba on pancreatic islet beta cells on oxidative stress and apoptosis in diabetic mice. Method： Alloxan solution （80 mg ·kg-1 ） was injected into mice＇s caudal vein to establish the model of diabetic mice. The diabetic mice were randomly divided into 5 groups： model group, positive controlled group （metformin group）, low-dose Euphorbiae Humifusae Herba group （ 59 mg ·kg - 1·d -1 ）, medium-dose Euphorbiae Humifusae Herba group （ 118 mg ·kg -1·d-1 ） and high-dose Euphorbiae Humifusae Herba group （236 mg ·kg -1·d-1）. After successive administration for 14 days, the changes of blood glucose, pancreatic superoxide dismutase （SOD）, glutathione peroxidase （GSH-Px） and malonaldehyde （MDA） were observed. TUNEL method was used to determine pancreatic islet beta cells apoptosis. Result： Compared with model group, the body weight in Euphorbiae Humifusae Herba groups was not obviously decreased （P 〈0.05）. The blood glucose in high-dose group and metformin group was lower than that of model group and before medication （P 〈 0.05 ）. Compared with model group, SOD and GSH-Px level in high-dose group and metformin group were increased （P 〈 0.05）, MDA level was decreased （P 〈 0. 05 ）, the cell apoptosis index was decreased （P 〈0. 05）. Conclusion： Euphorbiae Humifusae Herba humifusae can obviously decrease blood glucose in diabetic mice, its mechanism is probably related to increasing antioxidant capacity of diabetic mice, reducing the pancreatic islet beta cells damage caused by oxidative stress, inhibiting pancreatic islet beta cells apoptosis.