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

• Published in: International immunopharmacology Vol. 89; no. Pt A; p. 107058
• Main Authors: Zhang, Lei, Lv, Hao, Li, Ying, Dong, Na, Bi, Chongpeng, Shan, Anshan, Wu, Zhihan, Shi, Baoming
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.12.2020; Elsevier BV
• Subjects: Anti-inflammatory agents; Colon; Cyclooxygenase-2; Cytokines; Diarrhea; IL-1β; Inflammation; Interleukin 6; Intestinal barrier; Intestine; Jejunum; Localization; Morphology; Mucosa; NF-κB protein; Nitric-oxide synthase; Salmonella; Salmonella typhimurium; Signal transduction; Sodium; Sodium houttuyfonate; Tumor necrosis factor-α; Intestinal barrier; Inflammation; Sodium houttuyfonate; Salmonella typhimurium
• ISSN: 1567-5769; 1878-1705; 1878-1705
• DOI: 10.1016/j.intimp.2020.107058

Sodium houttuyfonate enhances the intestinal tight junction barrier and ameliorates inflammation in Salmonella typhimurium-induced diarrhea in mice via the NF-κB pathway. [Display omitted] •SH alleviates intestinal inflammation by inhibiting the NF-κB pathway.•SH reduces intestinal damage and enhances intestinal barrier function.•SH can prevent intestinal inflammation caused by bacterial infections. 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.