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丁酸盐与非甾体抗炎药对大肠腺癌细胞HT-29的作用
引用本文:Zhang Z,Ouyang Q,Gan H. 丁酸盐与非甾体抗炎药对大肠腺癌细胞HT-29的作用[J]. 中华内科杂志, 2002, 41(3): 153-155
作者姓名:Zhang Z  Ouyang Q  Gan H
作者单位:华西医科大学附属第一医院消化内科,成都,610041
基金项目:四川省科技项目基金资助 (2 0 0 0 174)
摘    要:目的 观察丁酸盐和非甾体抗炎药(NSAIDs)对大肠腺癌细胞HT-29的作用,并探讨其可能的作用机制。方法 用酶联免疫法定量检测HT-29细胞所分泌的前列腺素(PG)E2;流式细胞仪检测细胞的凋亡率;电镜观察凋亡细胞的形态学。结果 丁酸盐可刺激细胞分泌大量的PGE2,阿司匹林和NS-398则抑制PGE2的分泌,3种药物均具有促进细胞凋亡的作用,且其作用呈浓度和时间依赖性(P<0.05);药物联用可使其作用不同程度地增强。结论 单用丁酸盐和2种NSAIDs制剂均有促凋亡作用,联用可通过下调环氧化酶-2的表达进一步增强疗效。

关 键 词:化学预防 非甾类消炎药 脱噬作用 丁酸盐 大肠腺癌 HT-29 癌细胞
修稿时间:2001-07-23

The effects of butyrates and non-steroidal anti-inflammatory agents on HT-29 colonic carcinoma cells
Zhang Zhihong,Ouyang Qin,Gan Huatian. The effects of butyrates and non-steroidal anti-inflammatory agents on HT-29 colonic carcinoma cells[J]. Chinese journal of internal medicine, 2002, 41(3): 153-155
Authors:Zhang Zhihong  Ouyang Qin  Gan Huatian
Affiliation:Department of Gastroenterology, The First Affiliated Hospital, Western China University of Medical Sciences, Chengdu 610041, China.
Abstract:Objective Adenocarcinoma cells HT 29 were used to investigate whether butyrates and non steroidal anti inflammatory agents (NSAIDs, aspirin and NS 398)would be effective adjuvants for inducing apoptosis and to probe its possible mechanisms. Methods Prostaglandin E 2(PGE 2) isolated from HT 29 cell culture supernants was investigated with ELISA. Flow cytometry was used for estimating apoptosis. The morphology of apoptotic cells was investigated by means of electron microscopy. Results Butyrates could stimulate the secretion of PGE 2. In contrast, NSAIDs inhibited it to a level below 30 ng/L. Both butyrates and NSAIDs could induce apoptosis. The effects showed the obvious tendency of time and concentration dependency ( P <0.05). Combination with two drugs could enhance the above effects. Conclusions Butyrates and NSAIDs could induce apoptosis individually. Combination with the two drugs could enhance the above effects by down regulating cyclooxygenase 2 expression.
Keywords:Chemoprevention  Anti inflammatory agents   non steroidal  Apoptosis  
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