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Introduction: In the highly competitive field of sports, impulsive behavior by athletes not only threatens personal and team harmony but also poses significant risks to their careers and public image. Despite these behaviors often becoming the focus of public attention, their underlying causes and prevention strategies remain relatively unknown. This study delves deep into the impact of mindfulness on athletes' impulsive behavior, revealing the mediating roles of self-reflection and coping effectiveness. Methods: Using a combination of snowball and convenience sampling, a sample of 403 athletes from high-level sports teams in the Central China region participated in a questionnaire survey. The data were analyzed using Amos v.23 software. Results: The findings indicate a positive correlation between mindfulness and coping effectiveness (standardized coefficient = 0.336, p < 0.001), as well as between self-reflection and coping effectiveness (standardized coefficient = 0.406, p < 0.001). There is a negative correlation between coping effectiveness and impulsive behavior (standardized coefficient = -0.476, p < 0.001). The positive impact of mindfulness on impulsive behavior (standardized coefficient = -0.371, p < 0.01) is mediated by self-reflection and coping effectiveness. The explanatory power of this study is R2 = 0.35. Discussion: Mindfulness reduces impulsive behavior by enhancing self-reflection capabilities and improving coping effectiveness. Based on these substantive research results, to mitigate impulsive behavior in athletes, it is recommended that the National Sports Administration and coaches actively implement mindfulness training. Additionally, targeted psychological intervention strategies should be developed to enhance athletes' mental health levels and optimize their sports performance.
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BACKGROUND: Osteoarthritis (OA) is a common degenerative disease of synovial joints caused by inflammation. Acteoside (ACT), a major component and lipase inhibitor from the Chinese tea Ligustrum purpurascens kudingcha, has been reported to regulate the inflammation and immune response. The study aims to investigate the effects of ACT on inflammatory responses and joint protection in OA rats. METHODS: Cell proliferation was examined by MTT and colony formation assay. Apoptosis was analyzed using flow cytometry with Annexin V/PI staining. ELISA was employed to examine the concentration of inflammatory cytokines. OA rat model was established by surgery stimulation. RESULTS: ACT treatment significantly inhibited the upregulation of inflammatory cytokines induced by IL-1ß in primary chondrocytes, including IL-6, IL-12, TNF-α and IFN-γ. ACT stimulation also enhanced the cell proliferation, while inhibited cell apoptosis in IL-1ß-treated chondrocytes. Consistently, ACT treatment led to downregulation of cleaved-caspase-3 and apoptosis regulator Bax, and upregulation of Bcl-2. Furthermore, ACT treatment inhibited IL-1ß-induced activation of JAK/STAT pathway. The results were confirmed in surgery-induced OA rat model. Moreover, ACT treatment significantly inhibited synovial inflammation and articular chondrocyte apoptosis in OA rats. CONCLUSION: Our findings indicate that ACT has the potential therapeutic effect on OA through inhibiting the inflammatory responses via inactivating JAK/STAT signaling pathway.