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新型吡唑基吡啶衍生物治疗实验性结肠炎的治疗潜力。

Therapeutic potential of a novel pyrazolyl-pyridine derivative in the treatment of experimental colitis.

机构信息

Department of Clinical Pharmacy & Pharmacy Practice, Faculty of Pharmaceutical Sciences, The Hashemite University, Zarqa, Jordan.

Department of Biology & Biotechnology, Faculty of Science, The Hashemite University, Zarqa, Jordan.

出版信息

Future Med Chem. 2024;16(19):1971-1982. doi: 10.1080/17568919.2024.2385298. Epub 2024 Aug 19.

DOI:10.1080/17568919.2024.2385298
PMID:39157857
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11485772/
Abstract

Investigating a novel compound, DMPNP, for treating colitis in mice, a key issue in inflammatory bowel diseases (IBD). Mice with induced colitis received DMPNP (50, 100, 150 mg/kg) or sulfasalazine (SUL), evaluated via tissue assessment, Disease Activity Index (DAI), myeloperoxidase (MPO), nitric oxide (NO) levels and cytokine analysis. DMPNP significantly reduced colitis symptoms, inflammation and oxidative stress at higher doses, with marked improvements in DAI, MPO, NO and cytokines, comparable to SUL results. DMPNP shows potent anti-inflammatory and immunomodulatory properties, indicating potential as an IBD therapeutic. Further clinical trials are suggested to validate these outcomes.

摘要

研究一种新型化合物 DMPNP 治疗小鼠结肠炎的效果,结肠炎是炎症性肠病(IBD)的一个关键问题。诱导结肠炎的小鼠接受 DMPNP(50、100、150mg/kg)或柳氮磺胺吡啶(SUL)治疗,通过组织评估、疾病活动指数(DAI)、髓过氧化物酶(MPO)、一氧化氮(NO)水平和细胞因子分析进行评估。DMPNP 在较高剂量下显著减轻了结肠炎症状、炎症和氧化应激,DAI、MPO、NO 和细胞因子显著改善,与 SUL 结果相当。DMPNP 具有强大的抗炎和免疫调节特性,表明其有作为 IBD 治疗药物的潜力。建议进行进一步的临床试验来验证这些结果。

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本文引用的文献

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Nilotinib exhibits less toxicity than imatinib and influences the immune state by modulating iNOS, p-p38 and p-JNK in LPS/IFN gamma-activated macrophages.尼洛替尼的毒性小于伊马替尼,并且通过调节 LPS/IFNγ 激活的巨噬细胞中的 iNOS、p-p38 和 p-JNK 来影响免疫状态。
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Anti-inflammatory activity of peiminine in acetic acid-induced ulcerative colitis model.
佩米诺因在乙酸诱导的溃疡性结肠炎模型中的抗炎活性。
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Genistein and/or sulfasalazine ameliorate acetic acid-induced ulcerative colitis in rats via modulating INF-γ/JAK1/STAT1/IRF-1, TLR-4/NF-κB/IL-6, and JAK2/STAT3/COX-2 crosstalk.金雀异黄素和/或柳氮磺胺吡啶通过调节 INF-γ/JAK1/STAT1/IRF-1、TLR-4/NF-κB/IL-6 和 JAK2/STAT3/COX-2 串扰改善乙酸诱导的大鼠溃疡性结肠炎。
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