N,N-Dimethylglycine (DMG) is a glycine derivative, and its sodium salt (DMG-Na) has been demonstrated to possess various biological activities, including immunomodulation, free radical scavenging, and antioxidation, collectively contributing to the stability of tissue and cellular functions. However, its direct effects and underlying mechanisms in wound healing remain unclear. In this study, a full-thickness excisional wound model was established on the dorsal skin of mice, and wounds were treated locally with DMG-Na. Wound healing progression was assessed by calculating wound closure rates. Histopathological analysis was conducted using hematoxylin-eosin (HE) staining, and keratinocyte proliferation, migration, and differentiation were evaluated using CCK-8 assays, scratch wound assays, and quantitative reverse transcription PCR (qRT-PCR). Inflammation-related cytokine expression in keratinocytes was analyzed via ELISA and qRT-PCR. Results revealed that DMG-Na treatment significantly accelerated wound healing in mice and improved overall wound closure quality. The wound healing rates on days 3, 6, and 9 were 49.18%, 68.87%, and 90.55%, respectively, with statistically significant differences compared to the control group (P<0.05). DMG-Na treatment downregulated the mRNA levels of keratinocyte differentiation markers while enhancing cell proliferation and migration (P<0.05). Furthermore, DMG-Na decreased the secretion of LPS-induced keratinocyte inflammatory cytokines, including IL-1β, IL-6, IL-8, TNF-α, and CXCL10 (P<0.05). These findings indicate that DMG-Na regulates inflammatory responses and promotes keratinocyte proliferation and migration, thereby facilitating the healing of skin wounds.
Osteoarthritis (OA) is a chronic degenerative disease characterized by cartilage degeneration, synovial inflammation, and abnormal bone remodeling. Emerging evidence indicates that helper T (Th) cells play a pivotal role in OA pathogenesis. In the OA joint microenvironment, a marked imbalance among Th cell subsets is observed, manifested as overactivation of Th1 and Th17 cells alongside impaired function of Th2 and regulatory T cells. This imbalance leads to elevated levels of pro-inflammatory cytokines, such as interleukin (IL)-17, interferon-gamma, and tumor necrosis factor-alpha, whereas anti-inflammatory cytokines, including IL-4 and IL-10, are relatively deficient, resulting in chondrocyte apoptosis, extracellular matrix degradation, and synovial inflammation. This article systematically summarizes the molecular mechanisms of different Th cell subsets in OA development and elucidate their synergistic interactions with macrophages, providing a theoretical basis for Th cell-targeted immunomodulatory strategies in OA therapy.
