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机构地区:[1]浙江省人民医院肾内科,浙江杭州310014 [2]温州医学院附属第一医院肾内科,浙江温州325000
出 处:《中华中医药学刊》2012年第3期628-630,共3页Chinese Archives of Traditional Chinese Medicine
基 金:温州市科技局资助项目(Y2006A002)
摘 要:目的:研究分泌性磷脂酶A2(secretory phospholipase A2,sPLA2)激活剂氯化钙能否减轻马兜铃酸(aristolochic acid AA)对人肾小管细胞(human kidney cell HKC)的损伤。方法:以体外培养的HKC为研究对象,观察CaCl2对AA肾毒性的影响。检测指标包括MTT490nm处OD值和流式细胞议测定的细胞周期。实验分为正常对照组、单用AA组和合用AA和CaCl2组,结果:(1)AA表现出剂量相关和时间相关的肾毒性。40mg/L AA组细胞490nm处OD值明显下降,联用600μmol/L CaCl2,490nm处OD值有所上升(0.631±0.123 vs 0.492±0.076,P<0.05)。(2)AA可将HKC阻滞在S期和G2/M期。联用600μmol/L CaCl2,促进S期细胞进入G2/M期,逆转S期阻滞。结论:CaCl2可在一定程度上减轻马兜铃酸肾毒性,逆转细胞的增殖受抑状况。Objective: To investigate if CaCl2 can relieve the nephrotoxicity of aristolochic acid (AA) on human kidney ceils (I-IKC) in vitro. Methods:HKC was cultured with aristolochic acid or combined with CaCl2. Cell viability was evaluated by the MTT cell proliferation assay. Flow cytometry tested the change of cell cycle. Results : ( 1 ) The OD value in d90nm of 40mg L-1 AA group is decreased, as compared with the normal group, which can be inhibited slightly by 600μmol · L^-1 CaCl2. (2) HKC could be blocked in S phase and G2/M phase in a dose - and time - dependent manner. To some extent, the following could reverse it: cells of S phase can go into G2/M phase when 600μmol/L CaCl2is present (P 〈 O. 05) . Conclusion : In a way, CaC12 can relieve inhibition of growth induced by AA.
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