Oxymatrine attenuates TNBS-induced colinutis in rats through TLR9/Myd88/NF-κB signal pathway

Abstract

Objective: Due to its well-known anti-inflammatory property, oxymatrine (OMT) has received more attention on the aspect of treating ulcerative colitis. Although efforts have been undertaken to understand the therapeutic mechanism of OMT on ulcerative colitis (UC), the remedial principle is still ambiguous. Numerous studies have shown that TLR9/Myd88/NF-κB signal pathway played a key role in the pathogenesis of UC. Moreover, TLR9/Myd88/NF-κB signal pathway is a part of the most important pathways for regulating the immune response.Methods: We explored the influence of OMT with different dosages on UC by establishing a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model. Moreover, the participation of TLR9/Myd88/NF-κB signal pathway and whether OMT protects against UC though targeting this pathway are further studied.Results: Our data revealed that OMT could significantly relieve the symptom of TNBS-induced colitis in rats by reactivating the tight junction protein and, more important, by inhibiting the activation of TLR9/Myd88/NF-κB pathway and protein expression levels of its downstream inflammatory factors.Conclusion: OMT could relieve colitis in rat models by impacting tight junction proteins’ TLR9/Myd88/NF-κB signal pathways and activity.

Combining multi‐omics analysis to identify host‐targeted targets for the control of Brucella infection

“…MPA showed an effective inhibition of hIMPDH2 with an inhibitory concentration (IC50) value of 28.79 ± 0.68 μm. Among these compounds, oxymatrine (purity >98%, purchased from Undersun Biologics, Xi'an), one of the major alkaloid components of Sophora roots (Li et al, 2022 ), showed the strongest inhibitory effect on hIMPDH2 with an IC 50 value of 4.10 ± 0.14 μm (Figure 7E ). These data suggested that oxymatrine is a novel inhibitor of hIMPDH2.…”

Phytochemicals and Regulation of NF-kB in Inflammatory Bowel Diseases: An Overview of In Vitro and In Vivo Effects

“…Li et al [ 80 ] used oxymatrine, a quinolizidine alkaloid extracted from Sophora flavescens , to evaluate its mechanism in TNBS-induced colitis. After treatment, there was a reduction in IL-1β mRNA, TNF-α mRNA, and IL-6 mRNA, in addition to a reduction in NF-kB activation and decreases in toll-like receptor 9 (TLR9) and Myd88 expression in the TLR9/Myd88/NF-kB pathway.…”

Traditional Chinese medicine treats ulcerative colitis by regulating gut microbiota, signaling pathway and cytokine: Future novel method option for pharmacotherapy

“…OMT effectively increased muribaculaceae, bifidobacterium abundance, lachnospiraceae, and ruminococcaceae, inhibited staphylococcaceae and bacteroides growth and regulated the intestinal flora structure in DSS-induced colitis [ 97 ]. OMT can inhibit PI3K/AKT and TLR9/MyD88/NF-κB signaling pathways and down-regulate pro-inflammatory cytokines such as IFN-γ, and MCP-1 to alleviate the disorder of gut microbiota caused by the decline of intestinal immune function caused by pro-inflammatory cytokines, thus alleviating the inflammatory damage of intestinal tissues [ 98 , 99 ]. OMT can protect the colonic mucosal barrier in DSS-induced colitis, inhibit inflammatory and oxidative responses and its mechanism is related to the RhoA/ROCK signaling pathway inhibiting the differentiation of Th17 cells and promoting the differentiation of Treg cells.…”