OBJECTIVE To explore the potential mechanism by which drug-containing serum of Dianxianqing granules （DXQ） inhibits microglial ferroptosis. METHODS Male SD rats were given normal saline and Dianxianqing granules solution via intragastric administration to prepare normal serum and DXQ， respectively. Mice microglia BV2 cells were collected and successfully transfected with a negative control small interfering RNA （si-NC）， and then they were included in the si-NC group and cultured under normal conditions. Cells successfully transfected with small interfering RNA targeting glutathione peroxidase 4 （GPX4） （si-GPX4） were divided into the si-GPX4 group， the CsA group （treated with 1 μmol/L cyclosporine A）， and the DXQ- L， DXQ-M and DXQ-H groups （treated with 5%， 7% and 10% DXQ， respectively）. These groups were subsequently treated with their corresponding drug solutions and ferroptosis inducer Erastin （10 μmol/L）. The intracellular levels of total iron ions， glutathione （GSH）， reactive oxygen species （ROS）， and the expression of mitochondrial superoxide were determined in each group after 48 h of treatment. Additionally， mitochondrial membrane potential， the opening degree of mitochondrial permeability transition pore （MPTP）， and mRNA expressions of GPX4 and cyclophilin D （CypD） were detected. Furthermore， the expressions of ferroptosis-related proteins[GPX4， transferrin receptor 1 （TfR1） and ferritin heavy chain 1 （FTH1）]， as well as MPTP-related proteins [adenine nucleotide translocator （ANT）， cytochrome C （CytC）， mitochondrial calcium uniporter （MCU） and CypD] were assessed. RESULTS Compared with si-NC group， the levels of total iron ions and ROS， the expression level of mitochondrial superoxide， the opening degree of MPTP， protein and its mRNA expressions of CypD as well as protein expressions of TfR1 and MCU were increased or up-regulated significantly （P＜0.01）； however， GSH content， mitochondrial membrane potential， protein and mRNA expressions of GPX4， and protein expressions of FTH1， ANT and CytC were decreased or down-regulated significantly （P＜0.01）. Compared with the si-GPX4 group， the cells in the DXQ-M， DXQ-H groups showed a general improvement in the above quantitative indicators （P＜0.01 or P＜0.05）. CONCLUSIONS DXQ can enhance antioxidant capacity by activating the GSH/GPX4 pathway， regulate the expressions of TfR1 and FTH1 protein to correct iron ion homeostasis， inhibit excessive opening of MPTP to improve mitochondrial function， and ultimately suppress microglial ferroptosis.

The complete functional regeneration of periodontal tissues—specifically, the simultaneous reconstruction of alveolar bone, cementum, and periodontal ligament—represents a major challenge in oral regenerative medicine. Dental-derived mesenchymal stem cells (DMSCs) are regarded as ideal seed cells for achieving this goal due to their multi-lineage differentiation potential and immunomodulatory properties. As a cell carrier, hydrogels offer the key advantage of mimicking the extracellular matrix through precisely tunable physicochemical properties (e.g., matrix stiffness, topological structure, degradation kinetics), thereby constructing a mechanical and biochemical microenvironment that actively directs stem cell fate. This review summarizes the application and research progress of DMSC-laden hydrogels in periodontal tissue repair. We first analyze the material characteristics of different hydrogel systems, and then elaborate on the specific molecular mechanisms by which hydrogels regulate DMSCs’ differentiation through mechanical properties such as matrix stiffness: stiff hydrogels drive osteogenic differentiation by activating the integrin-focal adhesion kinase (FAK)-Akt/mechanistic target of rapamycin (mTOR) signaling axis; inducing cytoskeletal remodeling, and promoting dephosphorylation and nuclear translocation of Yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ) to initiate the transcription of osteogenesis-related genes; and stabilizing β-catenin and activating the Wnt/β-catenin signaling pathway, upregulating the expression of key osteogenic transcription factors including Runt-related transcription factor 2 (Runx2) and Osterix. Furthermore, as programmed controlled-release carriers for bioactive factors, hydrogels selectively activate Smad signaling subtypes—pro-osteogenic factors specifically activate the Smad1/5/8 pathway, whereas factors promoting periodontal ligament formation activate the Smad2/3 pathway—thereby achieving precise, directed differentiation of DMSCs toward osteogenic, cementogenic, or fibroblastic lineages. Current key scientific issues in this field include the dynamic adaptation of hydrogel properties during regeneration, stable control of the complex oral microenvironment (e.g., microbes, mechanical forces, inflammation), strategies for efficient directional differentiation of stem cells, and feasibility of clinical translation. Future research directions should focus on developing smart-responsive hydrogels, constructing personalized biomimetic scaffolds combined with three-dimensional bioprinting technology, and designing composite material systems with immunomodulatory functions, aiming ultimately to achieve integrated structural and functional regeneration of periodontal tissue.

Objective To explore the influence of cognitive-behavioral intervention on the anxiety and oral health-related quality of life in adult orthodontic patients.Methods 152 adult orthodontic patients whose MDAS scores were greater than 11 were divided into the intervention group and the control group according Multistage Grouping Process.The former were treated with MBT appliance combined with cognitive-behavioral intervention,and the latter were treated with MBT appliance only.The State-Trait Anxiety Inventory(STAI) was adopted to evaluate anxiety in all patients during orthodontic treatment,and the UK oral health-related quality of life questionnaire(OHRQoL-UK) was adopted to evaluate the oral health-related quality of life in all patients before and after orthodontic treatment,respectively.Results 1.After 3 and 6 months cognitive-behavioral intervention,the scores of SAI in the intervention group(50.37±9.18,35.65±8.92) were significantly reduced compared to the control group(56.62± 10.52,54.13± 10.03) (P＜0.01).After 6 months cognitive-behavioral intervention,the scores of TAI in the intervention group(47.92±6.82) were significantly reduced compared to the control group(51.52±7.41) (P ＜0.05).2.After the orthodontic treatment,the scores of OHRQoL-UK in the intervention group(58.27±13.43) were significantly improved compared to the control group (51.99± 11.69) (P＜ 0.01).3.The oral health-related quality of life after the orthodontic treatment were significantly related to post-treatment anxiety of adult orthodontic patients(r=-0.192 ～-0.459,P＜ 0.05).Conclusion Cognitive-behavioral intervention can effectively reduce anxiety and improve the oral health-related life quality in the adult orthodontic patients.

ObjectiveTo characterize the gene expression in acute phase of irradiated oligodendrocytes (OL) in vitro.Methods The total RNA was extracted from irradiated OLs with 10 Gy by 6 MV X-rays at 1 and 4 h.The Affymetrix RAT 230 2.0 microarray were used to evaluate and screen the gene expression profile.The quantitative real-time RT-PCR was performed to validate the microarray results of selected myelin basic protein (MBP) and neural cell adhesion molecule 1 ( NCAM-1 ) genes.Results Compared with un-irradiated OLs,there were 1079 different expressed genes in irradiated cells.Those genes were classified in 79 categories based on the functional classification.Some familiar genes associated with OL cellular physiological process,apoptosis,cell cycle control,metabolism,cell communication and receptor binding were included.Compared with the microarray results,the coincidence rate of real-time RT-PCR was 91.7%.The down-regulation of MBP and up-regulation of NCAM 1 gene expression were confirmed.Conclusions Radiation-induced changes in gene expression in OLs took place in acute phase and influenced by time-course.The changes of MBP and NCAM1 gene expression may play a key role in the pathogenesis of radiation-induced demyelination.