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摘要:

目的:观察山药对糖尿病小鼠组织丙二醛( MDA) 含量的影响。方法:采用四氧嘧啶制作糖尿病小鼠模型,并以优降糖作阳性对照,连续21 天用不同剂量山药灌胃治疗,比较各组心脏、肝脏、肾脏和胰脏过氧化脂质的终末代谢产物MDA 含量。结果:①对照组四器官MDA显著高于正常组(P< 0 .01 或P< 0 .001) ;②剂量在6 .00g/kg·d- 1 以上山药各治疗组四器官MDA显著低于对照组(P< 0 .05 或P< 0.001) ;③与优降糖组比,除肝脏MDA 较高外(P< 0.001) ,中、大剂量山药组心、胰、肾组织MDA 较低(P< 0 .05 或P< 0 .001) 。结论:山药能明显降低糖尿病小鼠组织内过氧化脂质含量,尤其对心组织作用最强,其次为胰、肾和肝组织,而优降糖对胰组织过氧化脂质无明显影响。

Abstract:

Objective To observe the effect of Dioscoren Opposita Thunb(DOT) on MDA content in tissues of alloxan induced diabetic mice.Methods The diabetic mice model was established by intra abdominal injection of alloxan.After the DOT treatment (in contrast with glibenclamide) for a period of 21 days,determine and compare the contents of malonyldiadehyde(MDA) in heart,liver,pancreas and kidney tissues of the mice of all groups.Results ①Comparing with the normal group,in diabetic control group the contents of MDA in four kinds of tissue were obviously higher(P<0.0.1 or P<0.001).②Comparing with the diabetic control group,in DOT group(dosage>6.00g/kg·d -1 ) the contents of MDA in four kinds of tissue were obviously lower(P<0.05 or P<0.01).③Comparing with glibenclamide group,in DOT group (dosage>6.00g/kg·d -1 ) the contents of MDA in heart,pancreas and kidney tissues were lower(P<0.01 or P<0.001),but in liver tissues were higher (P<0.001).Conclusion DOT is able to significantly decrease the contents of lipoperoxide in tissues of diabetic mice,and this effect is most obviously showed on heart tissue,then is on pancresa,kidney and liver tissue sequentially.The above effect of glibenclamide on pancreas tissue is not obvious.

参考文献

1  舒思洁,洪爱蓉,胡宗礼,等.山药对糖尿病小鼠血糖、血脂、肝糖元和心肌糖元含量的影响。咸宁医学院学报,1998 ;12(4) :223

2 李仪奎主编.中药药理实验方法学.上海科学技术出版社,1991 :203

3  姜兆顺.第Ⅱ型糖尿病辩证分型与血清过氧化物岐化酶、丙二醛的关系.中国中西医结合杂志,1997 ;17(10) :597

4  宋鲁成.黄连对大鼠脂质过氧化及抗氧化酶活性的影响.中国中西医结合杂志,1992 ;12(7) :421

5  苏爱锋.降糖通脉宁对糖尿病大鼠血清及组织氧自由基的影响.中国中西医结合杂志,1993 ;13(5) :291

基本信息:

DOI:10.16751/j.cnki.2095-4646.1999.03.007

中图分类号:R282.7

引用信息:

[1]舒思洁,胡宗礼,洪爱蓉,闵清,明章银.山药对糖尿病小鼠组织丙二醛含量的影响[J].咸宁医学院学报,1999(03):156-158.DOI:10.16751/j.cnki.2095-4646.1999.03.007.

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