Chinese Traditional and Herbal Drugs•2026•DOI: 10.7501/j.issn.0253-2670.2026.16.20261633
Ulcerative colitis (UC) is a chronic, non-specific inflammatory bowel disease with a continuously rising global incidence; an estimated 5 million cases were recorded worldwide in 2023, with emerging industrialized nations such as China showing the most pronounced increases. The core pathophysiological driver of UC's recurrent and refractory nature is a self-reinforcing vicious cycle between gut microbiota dysbiosis and intestinal barrier dysfunction. Reduced microbial diversity, depletion of beneficial taxa, and expansion of pathogenic bacteria disrupt short-chain fatty acid (SCFA) and tryptophan metabolism, impair the mucus layer, downregulate tight junction (TJ) proteins, and compromise immune barrier integrity, thereby exacerbating mucosal inflammation. Conventional therapies—aminosalicylates, glucocorticoids, immunosuppressants, and biologics—frequently fail to achieve durable remission and impose substantial economic burden. Traditional Chinese medicine (TCM), guided by the 'turbidity-toxin' theory, intervenes through multi-component, multi-target mechanisms: reshaping gut microbial composition, enhancing beneficial metabolite production, and upregulating TJ protein expression. This review systematically synthesizes the gut microbiota–barrier interaction in UC and the theoretical and modern biological mechanisms of TCM intervention, providing a theoretical reference for optimizing clinical strategies and highlighting the potential of TCM in UC management.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21492
BACKGROUND: Previous studies from our group have shown that triptolide exerts protective effects on nerve cells and alleviates symptoms of neurodegenerative diseases. However, whether it acts by improving mitochondrial dynamic abnormalities requires further investigation. OBJECTIVE: To explore the effect and mechanism of triptolide in regulating the mitochondrial fusion-fission balance to mitigate hydrogen peroxide (H₂O₂)-induced apoptosis in SH-SY5Y cells. METHODS: Human neuroblastoma SH-SY5Y cells were cultured and divided into three groups: control group, model group (200 μmol/L H₂O₂), and triptolide group (2.5 nmol/L triptolide + 200 μmol/L H₂O₂). After 24 hours of intervention, oxidative stress markers (superoxide dismutase activity and malondialdehyde levels), mitochondrial membrane potential, and apoptosis levels were measured. Western blot was used to detect the expression of apoptosis-related proteins, mitochondrial dynamics-related proteins, and respiratory chain-related proteins. Immunofluorescence staining was used to detect the expression of phosphorylated dynamin-related protein 1, optic atrophy protein 1, cytochrome C oxidase 1, and ATP synthase F1 subunit alpha. RESULTS AND CONCLUSION: Compared with the control group, the model group showed significantly decreased superoxide dismutase activity, mitochondrial membrane potential, anti-apoptotic protein Bcl-2, mitochondrial fusion proteins 1 and 2, optic atrophy protein 1, and oxidative phosphorylation complex proteins (NADH dehydrogenase [ubiquinone] iron-sulfur protein 8, ubiquinol-cytochrome c reductase core protein 2, cytochrome c oxidase 1, succinate dehydrogenase B, ATP synthase F1 subunit alpha) (P < 0.05). Meanwhile, malondialdehyde levels, pro-apoptotic proteins Bax and Caspase-3, mitochondrial fission protein 1, phosphorylated dynamin-related protein 1 expression, and apoptosis rate were significantly increased (P < 0.05). Compared with the model group, triptolide intervention reduced malondialdehyde levels, increased superoxide dismutase activity and mitochondrial membrane potential, promoted fusion protein expression, inhibited fission protein expression, increased oxidative phosphorylation complex protein levels, and decreased apoptosis rate (P < 0.05). These results confirm that triptolide can regulate mitochondrial dynamic imbalance to alleviate H₂O₂-induced apoptosis in SH-SY5Y cells.