摘要
为探讨马兜铃酸 (AA)对体外培养的肾小管上皮细胞释放内皮素 (ET)、血管紧张素(Ang II)的影响 ,以及甘草酸的干预作用 ,以不同浓度AA作为刺激物 ,观察AA对体外培养的肾小管上皮细胞系 (LLC PK1)分泌和释放Ang II、ET的影响 ;另各培养体系中分别加入AA (4 0 μg/ml)和不同浓度甘草酸 ,观察甘草酸对AA作用下LLC PK1释放AngII、ET的干预作用。各组培养 2 4h后 ,提取培养上清 ,用放射免疫法测定ET、Ang II的浓度。结果显示 :①AA(4 0、80、16 0 μg/ml)可明显刺激细胞释放ET、Ang II(P <0 0 1)。②甘草酸在 5 0 μg/ml、10 0 μg/ml、2 0 0 μg/ml浓度时可使AA刺激细胞分泌和释放ET、Ang II水平下降 (P <0 0 5或P <0 0 1)。提示 :AA可刺激肾小管上皮细胞分泌和释放ET、Ang II ,此作用可能与AA的细胞毒性损害有关 ;甘草酸可使AA刺激细胞分泌和释放ET、Ang II水平下降 ;甘草酸的保护作用可能与抑制AA作用下细胞分泌和释放ET、Ang II有关。
To investigate the aristolochic acid (AA) affecting the renal tubular epithelial cells (LLC-PK1) releasing endothelin and angiotensin-Ⅱ, and the effects of Glycyrrhizic acid (GA) on ET and Ang-Ⅱ, LLC-PK1 cells were cultured in different concentrations of AA and GA. The concentrations of ET and Ang-Ⅱ were determined by radiation immunity. Results: AA of the concentrations of 40, 80 and 160μg/ml could stimulate cells to release ET and Ang-Ⅱ, as compared to AA group, P<0.01; in the concentration of GA of 50μg/ml, 100μg/m and 200μg/m, the release of ET and Ang-Ⅱ declined, P<0.01-0.05. Conclusions: AA can stimulate LLC-PK1 to release ET and Ang-Ⅱ, while GA can reduce the excretion and release of ET and Ang-Ⅱ, indicating that the protective effects of GA from renal tubular epithelial cells injury may word by inhibiting the excretion and release of ET and Ang-Ⅱ.
出处
《上海中医药杂志》
北大核心
2004年第9期47-49,共3页
Shanghai Journal of Traditional Chinese Medicine
基金
上海市自然科学基金项目 (0 3ZR14 0 31)
关键词
马兜铃酸
肾小管上皮细胞
内皮素
血管紧张素
甘草酸
Aristolochic acid (AA)
renal tubular epithelial cell
ET
Ang-Ⅱ
Glycyrrhizic acid