https://www.scienceopen.com/hosted-document?doi=10.15212/AMM-2024-0074
Announcing a new publication for
Acta Materia Medica journal. Phagocytosis is a fundamental mechanism used by the body to resist pathogens and restore physiological homeostasis. Herein, to identify small molecules with anti-inflammatory properties via phagocytosis inhibition, the authors of this article constructed a library of natural products and evaluated their ability to modulate phagocytosis in RAW264.7 macrophages. Berberine (BBR) is the major constituent of traditional Chinese medicine Coptidis Rhizoma that is recorded in Chinese Pharmacopoeia with the effect of clearing heat-toxin and is used in the therapeutic management of various inflammatory diseases. BBR was found to inhibit phagocytosis and significantly alleviate inflammation via suppressing interleukin-1α (IL-1α), interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α (TNF-α), according to real-time quantitative polymerase chain reaction (RT-qPCR) analyses, and phosphorylated-p65 (p-p65), iNOS, and cyclooxygenase-2 (COX-2), according to western blot analyses. BBR inhibited the expression of F-actin, a key protein in phagosome formation. Notably, BBR exerted its phagocytosis effects through targeting phosphoinositide 3-kinase (PI3K), thereby activating the small GTPase-Cdc42 (CDC42), Wiskott-Aldrich syndrome protein (WASP), and actin-related protein 2/3 complex subunit 2 (Arp2/3). BBR attenuated LPS-mediated inflammation through promoting macrophage phagocytosis. It was determined that BBR targets the toll-like receptor 4 (TLR4)-PI3K-CDC42 pathway, thereby inhibiting the nuclear factor-kappa B (NF-κB) pathway, and consequently regulating phagocytosis and the inflammatory response. These findings suggest that BBR might serve as a candidate for the development of phagocytic inhibitors.
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Jing Chang, Chengpeng Sun and Miaomiao Wang et al. Berberine inhibits phagocytosis through the TLR4-PI3K-CDC42 pathway.
Acta Materia Medica. 2025. Vol. 4(2):280-292. DOI: 10.15212/AMM-2024-0074