地菍粗多糖对STZ致糖尿病小鼠血糖、血脂及抗氧化作用的影响

Effect of crude polysaccharide of Melastoma dodecandrum Lour.on blood glucose,lipid and antioxidation in STZ-induced hyperglycemic mice

目的研究地菍粗多糖对链脲佐菌素(STZ)致糖尿病小鼠血糖、血脂及抗氧化作用的影响。方法以STZ诱导小鼠糖尿病模型,将造模成功的小鼠随机分为模型组、二甲双胍组(0.6 g/kg)、地菍粗多糖低、中、高剂量组(0.25 g/kg、0.50 g/kg、1.00 g/kg),另设空白组,共6组,每组12只。治疗组分别按相应剂量每天灌胃1次,模型组、空白组给予生理盐水,给药21 d。观察小鼠空腹血糖(FPG)、总胆固醇(TG)、三酰甘油(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)含量、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、谷胱甘肽过氧化物酶(GSH-PX)活性。结果二甲双胍组及地菍多糖各剂量组体重显著高于模型组(P<0.05,P<0.01)。给药第7、14、21天,二甲双胍组及地菍多糖各剂量组FPG显著低于模型组(P<0.05,P<0.01)。与模型组比较,二甲双胍组及地菍多糖高剂量组TG、TC、LDL-C水平显著降低,HDL-C水平显著升高(P<0.05,P<0.01)。地菍多糖中剂量组TG、TC水平显著低于模型组(P<0.05,P<0.01);地菍多糖低剂量组TC水平显著低于模型组(P<0.01)。与模型组比较,二甲双胍组及地菍多糖高、中剂量组血清及肝脏MDA水平显著降低,血清及肝脏SOD、GSH-Px水平显著升高(P<0.05,P<0.01);地菍多糖低剂量组血清及肝脏MDA水平显著低于模型组(P<0.01)。结论地菍粗多糖能够降低糖尿病小鼠空腹血糖,有效调节血脂紊乱且具有抗氧化作用。

Objective To study the effect of crude polysaccharide of Melastoma dodecandrum Lour.on blood glucose,lipid and antioxidation in STZ-induced hyperglycemic mice.Methods STZ was used to induce diabetic model of mice,the mice with successful modeling were randomly divided into model group,metformin group,low,middle and high dose(0.25 g/kg,0.50 g/kg,1.00 g/kg)of crude polysaccharide of Melastoma dodecandrum Lour.group,normal group was also set,12 mice in each group.Mice in treatment group were administrated at corresponding dose by gastric perfusion once a day,normal saline to model group and normal group.Continuous administration for 21 days.The fasting blood glucose(FPG),TG,TC,LDL-C,HDL-C,SOD and GSH-Px activity and content of MDA were observed.Results Compared with model group,FPG,TG,TC,LDL-C content of the mice of the crude polysaccharide of Melastoma dodecandrum Lour.group were decrease significantly,HDL-C was increased significantly,SOD and GSH-Px vitality were increased significantly,the MDA content was decrease obviously.Conclusions Crude polysaccharide of Melastoma dodecandrum Lour.has the hypoglycemic effect,it could effectively regulate lipids disorder and has antioxidation effect in STZ-induced hyperglycemic mice.