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胡颓子薁磺酸钠通过 NF-κB 通路增强沙门氏菌诱导的小鼠肠道屏障并减轻炎症反应。

Sodium houttuyfonate enhances the intestinal barrier and attenuates inflammation induced by Salmonella typhimurium through the NF-κB pathway in mice.

机构信息

Institute of Animal Nutrition, Northeast Agricultural University, Harbin 150030, PR China.

Institute of Animal Nutrition, Northeast Agricultural University, Harbin 150030, PR China.

出版信息

Int Immunopharmacol. 2020 Dec;89(Pt A):107058. doi: 10.1016/j.intimp.2020.107058. Epub 2020 Oct 9.

Abstract

Salmonella typhimurium (ST), as an aggressive bacterium, mainly causes intestinal inflammation and diarrhea. Sodium houttuyfonate (SH) is a derivative of houttuynin in the active oil of Houttuynia cordata, which is stable in nature and has anti-inflammatory activity. In this study, we used BALB/c mice infected with ST as experimental subjects and aimed to study the regulatory effect of SH on the intestinal tract and to explain its anti-inflammatory mechanism. Compared with the ST group, SH treatment improved the morphology of jejunum mucosa and alleviated the pathological damage to colon tissue. In addition, SH protected the intestinal barrier by regulating the localization and distribution of tight junction proteins. Meanwhile, SH significantly decreased the production of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and inflammation-related enzymes (iNOS, COX-2). Moreover, further western blot results suggested that SH inhibited the expression of p-IκBα and p-p65 in intestinal tissues. These results demonstrated that SH maintained the intestinal barrier and attenuated the production of intestinal proinflammatory cytokines by regulating the NF-κB signaling pathway, thereby providing protection for the intestine.

摘要

鼠伤寒沙门氏菌(Salmonella typhimurium,ST)作为一种侵袭性细菌,主要引起肠道炎症和腹泻。虎杖苷(Sodium houttuyfonate,SH)是虎杖活性油中虎杖素的衍生物,性质稳定,具有抗炎活性。本研究以感染 ST 的 BALB/c 小鼠为实验对象,旨在研究 SH 对肠道的调节作用,并阐明其抗炎机制。与 ST 组相比,SH 处理改善了空肠黏膜的形态,减轻了结肠组织的病理损伤。此外,SH 通过调节紧密连接蛋白的定位和分布来保护肠道屏障。同时,SH 显著降低了促炎细胞因子(TNF-α、IL-1β、IL-6)和炎症相关酶(iNOS、COX-2)的产生。此外,进一步的 Western blot 结果表明,SH 抑制了肠道组织中 p-IκBα 和 p-p65 的表达。这些结果表明,SH 通过调节 NF-κB 信号通路维持肠道屏障并减弱肠道促炎细胞因子的产生,从而为肠道提供保护。

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