ArticleWorld journal of gastroenterology2004
Targeting cyclooxygenase-2 with sodium butyrate and NSAIDs on colorectal adenoma/carcinoma cells.
Article in World journal of gastroenterology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- The impact of gut microbial short-chain fatty acids on colorectal cancer development and prevention.Gut microbes · 2025Review
- The Risk of Colorectal Polyps after Weight Loss Therapy Versus Obesity: A Propensity-Matched Nationwide Cohort Study.Cancers · 2023Article
- Butyrate suppresses mRNA increase of osteopontin and cyclooxygenase-2 in human colon tumor tissue.Carcinogenesis · 2011Article
- The effects of short-chain fatty acids on colon epithelial proliferation and survival depend on the cellular phenotype.Journal of cancer research and clinical oncology · 2006Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimThe protective effects of sodium butyrate and NSAIDs (especially the highly selective COX-2 inhibitors) have attracted considerable 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 was investigated whether NSAIDs would strengthen the effects of sodium butyrate and its possible mechanisms.
methodsIn vitro primary cell culture of colorectal adenomas and HT-29 were used for this investigation. PGE2 isolated from HT-29 cell culture supernatants was investigated by 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. The morphology of apoptotic cells was investigated by means of electromicroscopy.
resultsSodium butyrate could stimulate the secretion of PGE2, while NSAIDs inhibited it to below 30 pg/10(6) cells. Both butyrate and NSAIDs could inhibit cell proliferation and induce apoptosis. The effects were time- and dose-dependent (P<0.05). Aspirin and NS-398 could enhance the effects of sodium butyrate. The effects were stronger while sodium butyrate was used in combination with NS-398 than it was used in combination with aspirin.
conclusionButyrate and NSAIDs could inhibit cell proliferation and induce apoptosis respectively. NSAIDs could enhance the effects of sodium butyrate by down-regulating COX-2 expression. Selective COX-2 inhibitor is better than traditional NSAIDs.
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