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This mechanism involves: Sequestration of monomeric actin (G-actin) to prevent premature polymerization Promotion of actin polymerization into functional microfilaments (F-actin) when needed Enhanced cellular migration through cytoskeletal reorganization Facilitation of cell shape changes necessary for wound healing Research indicates TB-500 may work with the Arp2/3 protein complex to orchestrate actin polymerization, though this mechanism requires further clarification[4]

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Higher relative abundance of proinflammatory bacteria like Eggerthella, Atopobium was found to be increased, and decreased relative abundance of Faecalibacterium in the subjects with MDD (Knudsen et al., 2021)