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目的 观察丁酸盐和非甾体抗炎药 (NSAIDs)对大肠腺癌细胞HT 2 9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 2 9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 0 5 ) ;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。
Objective To observe the effect of butyrate and non-steroidal anti-inflammatory drugs (NSAIDs) on colorectal adenocarcinoma cell line HT 2 9 and to explore its possible mechanism. Methods The prostaglandin (PG) E2 secreted by HT 2 9 cells was quantitatively detected by enzyme-linked immunosorbent assay (ELISA). The apoptosis rate of cells was detected by flow cytometry. The morphology of apoptotic cells was observed by electron microscopy. Results Butyrate stimulated cells to secrete a large amount of PGE2, while aspirin and NS 398 inhibited the secretion of PGE2. All the three drugs had the effect of promoting apoptosis, and their effects were concentration-dependent and time-dependent (P <0.05) ; Drug combination can enhance its role to varying degrees. Conclusions Both butyrate and two NSAIDs preparations can induce apoptosis, and the combination can further enhance the therapeutic effect by down-regulating the expression of cyclooxygenase-2.