黄芪甲苷对慢性萎缩性胃炎大鼠的影响

被引:49
作者
李祎群 [1 ,2 ]
谢建群 [3 ]
龚雨萍 [1 ]
孙玉娇 [2 ]
机构
[1] 上海中医药大学龙华医院脾胃病科
[2] 上海交通大学医学院附属仁济医院中医科
[3] 上海中医药大学龙华医院脾胃病研究所
关键词
胃炎; 萎缩; 黄芪甲苷; 一氧化氮; 诱导型一氧化氮合成酶; 超氧化物歧化酶; 大鼠;
D O I
暂无
中图分类号
R285.5 [中药实验药理];
学科分类号
100806 [中药药理学];
摘要
目的探讨黄芪甲苷(astragalosideⅣ,ASⅣ)对慢性萎缩性胃炎(chronic atrophic gastritis,CAG)大鼠的作用及机制。方法将32只SD大鼠采用随机数字表法分为空白对照组、CAG模型组、ASⅣ低剂量组和ASⅣ高剂量组,每组8只。空白对照组按照常规进行喂养,CAG模型组给予蒸馏水2 mL/d灌胃,ASⅣ低剂量组给予ASⅣ10 mg/kg灌胃,ASⅣ高剂量组给予ASⅣ40 mg/kg灌胃,观察各组大鼠的生长情况,并于21周后采用脊椎脱臼法处死大鼠。观察胃黏膜病理情况并对炎症和萎缩评分,测试血清一氧化氮(nitric oxide,NO),诱导型一氧化氮合成酶(induced nitric oxide synthase,iNOS),总一氧化氮合成酶(total nitric oxide synthase,TNOS),超氧化物歧化酶(super oxide dismutase,SOD)抑制率和SOD活力。结果病理显示CAG模型组造模成功,ASⅣ组炎性反应及萎缩程度较模型组轻,其中高剂量组更明显。ASⅣ治疗组体质量高于较模型组,且差异有统计学意义(P<0.05)。ASⅣ高剂量可以降低CAG大鼠血清升高的NO、iNOS、TNOS。ASⅣ高剂量可以升高CAG大鼠血清降低的SOD活力及SOD抑制率。而ASⅣ低剂量组仅在iNOS中表现出显著性差异。结论 ASⅣ干预可以改善CAG模型SD大鼠的胃黏膜病理病变,其作用机制可能是其抑制CAG大鼠血清NO和iNOS,增加SOD活力,从而促进机体清除氧自由基,减轻或阻断组织的脂质过氧化反应,保护胃黏膜。
引用
收藏
页码:601 / 606
页数:6
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