AIM:The protective effects of sodium butyrate and NSAIDs(especially the highly selective COX-2 inhibitors)haveattracted considerable interest recently.In this study,primary adenoma cells and HT-29 were used to investigatewhether the above drugs would be effective for reducingproliferation and inducing apoptosis.Additionally,it wasinvestigated whether NSAIDs would strengthen the effectsof sodium butyrate and its possible mechanisms.METHODS:In vitro primary cell culture of colorectaladenomas and HT-29 were used for this investigation.PGE_2isolated from HT-29 cell culture supematants was investigatedby ELISA.MTT was employed to detect the anti-proliferativeeffects on both adenoma and HT-29 culture cells.FCMwas used for apoptosis rate and cell cycle analysis.Themorphology of apoptotic cells was investigated by meansof electromicroscopy.RESULTS:Sodium butyrate could stimulate the secretionof PGE_2,while NSAIDs inhibited it to below 30 pg/10~6 cells.Both butyrate and NSAIDs could inhibit cell proliferationand induce apoptosis.The effects were time-and dose-dependent(P<0.05).Aspirin and NS-398 could enhancethe effects of sodium butyrate.The effects were strongerwhile sodium butyrate was used in combination with NS-398than it was used in combination with Aspirin.CONCLUSION:Butyrate and NSAIDs could inhibit cellproliferation and induce apoptosis respectively.NSAIDscould enhance the effects of sodium butyrate by down-regulating COX-2 expression.Selective COX-2 inhibitor isbetter than traditional NSAIDs. AIM: The protective effects of sodium butyrate and NSAIDs (particularly the highly selective COX-2 inhibitors) have attracted may interest recently. In this study, primary adenoma cells and HT-29 were used to investigate whether the above drugs would be effective for reducing proliferation and inducing apoptosis.Additionally, it wasinvestigated whether NSAIDs would strengthen the effectsof sodium butyrate and its possible mechanisms. METHODS: In vitro primary cell culture of colorectaladenomas and HT-29 were used for this investigation. PGE_2isolated from HT-29 cell culture supematants was investigatedby ELISA. MTT was employed to detect the anti-proliferative effects on both adenoma and HT-29 culture cells. FCM was used for apoptosis rate and cell cycle analysis. Themorphology of apoptotic cells was investigated by means of electromicroscopy .RESULTS: Sodium butyrate could stimulate the secretionof PGE_2, while NSAIDs inhibited it to 30 pg / 10 ~ 6 cells.Both butyrate and NSAIDs could inhibit cel l proliferation and induce apoptosis. These effects were time-and dose-dependent (P <0.05) .Aspirin and NS-398 could enhance the effects of sodium butyrate.The effects were stronger then sodium butyrate was used in combination with NS-398 than it was used in combination with Aspirin.CONCLUSION: Butyrate and NSAIDs could inhibit cellproliferation and induce apoptosis respectively. NSAIDscould enhance the effects of sodium butyrate by down-regulating COX-2 expression. Selective COX-2 inhibitor isbetter than traditional NSAIDs.