Changchun University of Chinese Medicine

The pathogenesis of autoimmune thyroiditis (AIT) is intricately linked to immune dysregulation, endocrine imbalance, and gut microbiota dysbiosis. The immune system drives autoimmune attacks against thyroid tissue through Th1/Th2 cell imbalance, Treg dysfunction, and excessive release of proinflammatory cytokines. Thyroid hormone regulation primarily occurs via the hypothalamic-pituitary-thyroid (HPT) axis. Elevated levels of TPOAb and TgAb in AIT patients can lead to hypothyroidism by affecting the HPT feedback loop. Thyroid hormone regulation of immune cell metabolism and differentiation, in turn, affects immune homeostasis, forming a bidirectional regulatory network. Recent studies further reveal that the gut microbiota influences systemic immune tolerance by regulating intestinal barrier integrity and metabolites (e.g. short-chain fatty acids and secondary bile acids). Abnormal abundance of specific genera (e.g. Bacteroides and Prevotella) can promote the production of thyroid autoantibodies (TPOAb/TgAb), and increased intestinal permeability caused by microbiota dysbiosis may facilitate cross-reactivity between microbial antigens and thyroid antigens. Furthermore, the gut microbiota indirectly regulates thyroid function through the HPT axis. This review aims to summarize the current knowledge regarding the specific molecular mechanisms of gut microbiota-immune-endocrine interactions in AIT, offer important references for researching the treatment directions of AIT.

Myricetin, a naturally occurring flavonoid abundant in fruits, vegetables, and medicinal plants, is widely recognized for its strong antioxidant, anti-inflammatory, and anti-cancer activities. However, its regulatory effect on cellular signaling pathways activated by Vibrio (V.) vulnificus cytotoxins has not been fully elucidated. In this study, we investigated the cellular mechanism by which myricetin modulates cytotoxic autophagy induced by the V. vulnificus elastase VvpE in human gastrointestinal epithelial HT-29 cells. Treatment with recombinant VvpE (rVvpE) significantly induced autophagy-dependent cell death in HT-29 cells. Notably, myricetin treatment attenuated this effect by suppressing intracellular reactive oxygen species (ROS) accumulation. The reduction of ROS by myricetin inhibited the subsequent activation of c-Src and protein kinase C (PKC), thereby blocking p38 MAPK phosphorylation in rVvpE-exposed cells. Moreover, myricetin abrogated the activation of nuclear factor-kappa B (NF-κB), leading to downregulation of LC3-II and cleaved caspase-3 expression-key markers of autophagic and apoptotic cell death. Collectively, these findings highlight myricetin as a promising antibiotic-free therapeutic candidate capable of modulating host cellular responses to V. vulnificus infection by targeting the ROS-c-Src-PKC-MAPK-NF-κB signaling axis.

To conduct an overview of existing systematic reviews and meta-analyses on magnesium sulfate for acute asthma in children and adults, and to develop evidence-based, age-specific nursing interventions.

We searched PubMed, Embase, Cochrane Library, Web of Science, CNKI, VIP, WANFANG, and CBM from inception to August 10, 2025, for systematic reviews and meta-analyses on magnesium sulfate for acute asthma in children and adults. Primary study overlap was assessed using citation matrices and the corrected covered area. Quality was evaluated with ROBIS, AMSTAR-2, PRISMA 2020, and GRADE tools. Primary outcomes were then analyzed quantitatively and qualitatively to interpret the evidence.

Eighteen systematic reviews/meta-analyses were included. Primary study overlap was mild (corrected covered area = 5.090%). ROBIS indicated low risk of bias for all studies. AMSTAR-2 ratings: 4 high, 1 moderate, 12 low, 1 critically low. PRISMA 2020 scores (22-41) corresponded to 5 high, 12 moderate, and 1 low reporting quality. GRADE outcomes were high (n = 4), moderate (n = 31), low (n = 30), or extremely low (n = 27) quality.

Magnesium sulfate demonstrates a clearer benefit in children, reducing hospitalizations and improving physiological outcomes. In adults, it primarily lowers hospitalization risk without consistently improving lung function. Safety appears acceptable in both groups.

For pediatric acute asthma, magnesium sulfate may be used as second- or third-line adjunctive therapy. For critically ill adults, it should be an individualized option, not routine. Guidelines and nursing protocols should incorporate these age-stratified recommendations.