ArticleTheScientificWorldJournal2014
Amelioration of severe TNBS induced colitis by novel AP-1 and NF- κ B inhibitors in rats.
Article in TheScientificWorldJournal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Macrophages: emerging targets for ulcerative colitis.Frontiers in immunology · 2025Review
- Detection of the Content of Two Coumarins, IM and ISOIM, and Their Mechanism of Action on Colitis Rats in Angelica albicans.Computational and mathematical methods in medicine · 2022Article
- Review
- Sodium selenite ameliorates dextran sulfate sodium-induced chronic colitis in mice by decreasing Th1, Th17, and γδT and increasing CD4(+)CD25(+) regulatory T-cell responses.World journal of gastroenterology · 2017Article
- Abnormal differentiation of stem cells into enteroendocrine cells in rats with DSS-induced colitis.Molecular medicine reports · 2017Article
- Changes in enteroendocrine and immune cells following colitis induction by TNBS in rats.Molecular medicine reports · 2016Article
- Effects of AP‑1 and NF‑κB inhibitors on colonic endocrine cells in rats with TNBS‑induced colitis.Molecular medicine reports · 2016Article
- Anti-inflammatory effects of novel AP-1 and NF-κB inhibitors in dextran-sulfate-sodium-induced colitis in rats.International journal of molecular medicine · 2016Article
- Treatment with novel AP-1 and NF-κB inhibitors restores the colonic endocrine cells to normal levels in rats with DSS-induced colitis.International journal of molecular medicine · 2016Article
- Resolution of Inflammation: What Controls Its Onset?Frontiers in immunology · 2016Review
- Switching off key signaling survival molecules to switch on the resolution of inflammation.Mediators of inflammation · 2014Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AP-1 and NF-κ B inhibitors, namely, DTCM-G and DHMEQ, were investigated in male Wistar rats with severe colitis, induced by TNBS. The animals were randomized into 3 groups. The control group received 0.5 mL of 0.5% of the vehicle i.p., the DTCM-G group received 22.5 mg/kg body weight DTCM-G in 0.5% i.p., and the DHMEQ group received 15 mg/kg body weight DHMEQ i.p., all twice daily for 5 days. The body weight losses and mortality rates were significantly higher in the control group than those in DTCM-G-treated and DHMEQ-treated groups. The endoscopic inflammation scores in the control, DTCM-G-treated, and DHMEQ-treated groups were 6.3 ± 0.7, 1.0 ± 0.3, and 0.7 ± 0.3, respectively (P = 0.004 and 0.02, resp.). The inflammation scores as assessed by the macroscopic appearance were 4.3 ± 0.8, 0.7 ± 0.3, and 1.2 ± 0.4 in the control, DTCM-G-treated, and DHMEQ-treated groups, respectively (P = 0.01 and 0.009, resp.). The histopathological inflammation scores were 6.4 ± 0.7, 2.0 ± 1.0, and 2.2 ± 0.6 in the control, DTCM-G-treated, and DHMEQ-treated groups, respectively (P = 0.03 and 0.01, resp.). It was concluded that DTCM-G and DHMEQ exhibit strong anti-inflammatory and anticancer activities with no apparent toxicity, which make them excellent drug candidates for clinical use in inflammatory bowel diseases.
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Registered trials
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