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Therapeutic Effects and Mechanisms of Sodium New Houttuyfonate in a Murine Model of Intra-AbdominalInfection.

Source: PubMed, NCBI / U.S. National Library of Medicine

International journal of molecular sciencesPeng Xiaoyu, Xie Yuxin, Wang Rong, et al.Published 7/20/2026Last synced 7/29/2026Status: syncedPMID: 42511779DOI: 10.3390/ijms27146437

Excessive use of immunosuppressive agents compromises host immune defenses and broad-spectrum antimicrobial drugs disrupts the normal microbiota, thereby promoting the overgrowth and dissemination of. As an opportunistic pathogen that commonly resides in the intestinal microbiota,can subsequently translocate across the intestinal barrier and cause intra-abdominal infections. To investigate this process, a murine model of peritonealinfection was established, in which sodium new houttuyfonate was administered for therapeutic evaluation. The therapeutic potential of sodium new houttuyfonate against abdominalinfection was evaluated through assessment of immune cell composition, peritoneal macrophage polarization, tissue fungal burden, and histopathological features. The molecular mechanisms of sodium new houttuyfonate therapy were also investigated with cellular experiments, including colony counting, real-time quantitative PCR, Western blotting, and the detection of reactive oxygen species (ROS) in RAW264.7 macrophages. Our results revealed that sodium new houttuyfonate exerts a dual anti-infective effect through its fungicidal activity and via the immunomodulation of immunoinflammatory states. Sodium new houttuyfonate also stimulates cytokine production (e.g., IL-1β, IL-6, IL-10, TNF-α, and MCP-1) via the TLR2/p38/NF-κB pathway and promotes the release of ROS and nitric oxide. Overall, these findings highlight the potential of exogenous sodium new houttuyfonat

Abstract

Excessive use of immunosuppressive agents compromises host immune defenses and broad-spectrum antimicrobial drugs disrupts the normal microbiota, thereby promoting the overgrowth and dissemination of. As an opportunistic pathogen that commonly resides in the intestinal microbiota,can subsequently translocate across the intestinal barrier and cause intra-abdominal infections. To investigate this process, a murine model of peritonealinfection was established, in which sodium new houttuyfonate was administered for therapeutic evaluation. The therapeutic potential of sodium new houttuyfonate against abdominalinfection was evaluated through assessment of immune cell composition, peritoneal macrophage polarization, tissue fungal burden, and histopathological features. The molecular mechanisms of sodium new houttuyfonate therapy were also investigated with cellular experiments, including colony counting, real-time quantitative PCR, Western blotting, and the detection of reactive oxygen species (ROS) in RAW264.7 macrophages. Our results revealed that sodium new houttuyfonate exerts a dual anti-infective effect through its fungicidal activity and via the immunomodulation of immunoinflammatory states. Sodium new houttuyfonate also stimulates cytokine production (e.g., IL-1β, IL-6, IL-10, TNF-α, and MCP-1) via the TLR2/p38/NF-κB pathway and promotes the release of ROS and nitric oxide. Overall, these findings highlight the potential of exogenous sodium new houttuyfonate as a therapeutic option for abdominalinfection.

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