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Background: Studies have indicated that X-linked microRNAs (miRNAs) play a role in the pathogenesis of rheumatoid arthritis (RA) and its gender-specific differences. However, research on specific miRNAs remains limited. This study aims to investigate the possible role of X-linked miR-542-5p in RA pathogenesis and gender differences., Methods: We investigated the impact of miR-542-5p on RA pathogenesis and gender differences by manipulating its expression in various rat models., Results: Our findings revealed a significant overexpression of miR-542-5p in RA patients compared with healthy individuals, with a notable gender difference among RA patients. In vivo experiments confirmed that upregulation of miR-542-5p could accelerate RA pathogenesis. Further analysis showed that the onset of adjuvant-induced arthritis (AIA) in rats exhibited significant gender differences, with more severe clinical phenotypes found in female rats. This may be attributed to their stronger immune responses and elevated levels of miR-542-5p. Subsequent in vitro and in vivo experiments demonstrated that miR-542-5p contributes to the regulation of gender differences in RA pathogenesis by promoting the differentiation of Th17 cells., Conclusions: This study offers new insights into the sex-specific nature of RA, suggesting X-linked miR-542-5p as a potential target for both diagnostic and therapeutic purposes. These findings lay the groundwork for the development of gender-specific therapeutic strategies for RA and underscore the importance of gender consideration in RA research., Competing Interests: Declarations. Ethics approval and consent to participate: All subjects were provided written informed consent was signed by all legal guardians prior to inclusion. The study was approved by the Ethics Committee of the Macau Medical Science & Technology Research Association (Approval No.2021OCT01). All animal experimental were approved by the Municipal Affairs Bureau(Approval No. AL008/DICV/DIS/2022), Macau, Special Administrative Region of China. Consent for publication: Consent for publication was signed by all legal guardians prior to inclusion. Competing interests: The authors declare no competing interests., (© 2025. The Author(s).)

Background: Neonatal hypoxic-ischemic brain damage, characterized by tissue loss and neurologic dysfunction, is a leading cause of mortality and a devastating disease of the central nervous system. We have previously shown that vitexin has been attributed various medicinal properties and has been demonstrated to have neuroprotective roles in neonatal brain injury models. In the present study, we continued to reinforce and validate the basic understanding of vitexin (45 mg/kg) as a potential treatment for epilepsy and explored its possible underlying mechanisms., Methods: P7 Sprague-Dawley (SD) rats that underwent right common carotid artery ligation and rat brain microvascular endothelial cells (RBMECs) were used for the assessment of Na + -K + -Cl - co-transporter1 (NKCC1) expression, BBB permeability, cytokine expression, and neutrophil infiltration by western blot, q-PCR, flow cytometry (FCM), and immunofluorescence respectively. Furthermore, brain electrical activity in freely moving rats was recorded by electroencephalography (EEG)., Results: Our data showed that NKCC1 expression was attenuated in vitexin-treated rats compared to the expression in the HI group in vivo. Oxygen glucose deprivation/reoxygenation (OGD) was performed on RBMECs to explore the role of NKCC1 and F-actin in cytoskeleton formation with confocal microscopy, N-(ethoxycarbonylmethyl)-6-methoxyquinolinium bromide, and FCM. Concomitantly, treatment with vitexin effectively alleviated OGD-induced NKCC1 expression, which downregulated F-actin expression in RBMECs. In addition, vitexin significantly ameliorated BBB leakage and rescued the expression of tight junction-related protein ZO-1. Furthermore, inflammatory cytokine and neutrophil infiltration were concurrently and progressively downregulated with decreasing BBB permeability in rats. Vitexin also significantly suppressed brain electrical activity in neonatal rats., Conclusions: Taken together, these results confirmed that vitexin effectively alleviates epilepsy susceptibility through inhibition of inflammation along with improved BBB integrity. Our study provides a strong rationale for the further development of vitexin as a promising therapeutic candidate treatment for epilepsy in the immature brain.