Gorham-Stout disease(GSD) is a rare osteolytic disorder characterized by spontaneous and progressive osteolysis, along with abnormal angiogenesis and lymphangiogenesis, with no new bone formation. We present a case of a 15-year-old female admitted due to " recurrent right leg pain for 5 years, 11 months after undergoing right femoral fracture surgery". Through comprehensive integration of the patient's clinical phenotype, laboratory tests, imaging findings, pathological examinations, and molecular biological test results, GSD was considered highly likely. A multidisciplinary treatment approach was conducted, including a combination of zoledronic acid and sirolimus to inhibit osteolysis, along with rehabilitation training and orthopedic intervention, providing a personalized and comprehensive treatment strategy.

ObjectiveThis paper aims to conduct the feature analysis and correlation analysis on the ocular collateral features and differential metabolites in patients with chronic hepatitis B （CHB） complicated by glucose metabolism disorder （GMD），particularly those with the damp-heat syndrome type，by integrating shadowless scleral imaging and metabolomics technologies. MethodsA total of 313 patients were recruited from the Hepatology and Endocrinology Outpatient Departments of Public Health Clinical Center of Chengdu according to the inclusion/exclusion criteria，and they were divided into a CHB group and a CHB complicated by GMD groups （damp-heat syndrome group and non-damp-heat syndrome group）. All patients underwent high-definition ocular image acquisition and feature extraction using an intelligent analysis system for shadowless scleral imaging to analyze the differences in the counting of morphological feature scores of ocular collaterals among groups. By using a digital sampling method，24 patients from each group were randomly selected，along with 20 healthy volunteers，for untargeted metabolomic analysis of peripheral serum. Differential metabolites were identified，statistically analyzed，and subjected to potential biomarker analysis and pathway enrichment. Spearman method was performed to conduct the correlation analysis on the differential ocular collateral features and differential metabolites，followed by correlation network construction. ResultsCompared with those in the CHB group，patients with CHB complicated by GMD showed significant changes in ocular collateral feature scores such as "hillock"，"blood vessels"，and "pale dusky coloration" （P<0.05）. In comparison with those in the healthy group，metabolites including N-acetylglucosamine，acetylhomoserine，and myo-inositol （AUC>0.7） were identified as potential biomarkers for the disease. Compared with those in the CHB complicated by GMD group with non-damp-heat syndrome，patients with damp-heat syndrome exhibited significant changes in feature scores of "plaques"，"yellow coloration"，"spleen"，and "gallbladder" （P<0.05）. In comparison with those in the healthy group，metabolites such as O²′-4a-cyclic tetrahydrobiopterin，theobromine，xanthurenic acid，and L-glutamic acid 5-phosphate （AUC>0.7） were identified as potential biomarkers for the damp-heat syndrome type. The Spearman correlation analysis reveals weak to moderate linear correlations between the differential scleral collateral features and metabolites. By constructing a "disease-syndrome" network of ocular diagnosis and metabolites，"xanthurenic acid-gallbladder" and "theobromine-plaque/yellow coloration" were identified as specific molecular-phenotypic correlated biomarker clusters for CHB complicated by GMD with dampness-heat syndrome. ConclusionPatients with CHB complicated by GMD demonstrate differential ocular diagnostic features and serum metabolites corresponding to disease states and dampness-heat syndrome. These objective biomarkers can guide both clinical syndrome differentiation and medication. The macro-micro integration based on ocular feature clusters and potential metabolic biomarkers offers an innovative approach to a combined traditional Chinese and Western medicine diagnosis and treatment model for this disease.

Objective To investigate the protective effects of ferroptosis inhibitor ferrostatin-1(Fer-1)on high-altitude hypoxic lung injury and explore novel preventive strategies for high-altitude hypoxia-induced lung injury.Methods ①Eighteen SPF male Wistar rats(5～6 weeks old,210～230 g)were randomly divided into 3 groups(n=6):normoxic control,hypoxic lung injury,and Fer-1 pretreatment groups.A hypobaric chamber was used to establish a rat model of high-altitude hypoxic lung injury.Liquid chromatography-tandem mass spectrometry(LC-MS/MS)was employed to compare pulmonary protein profiles between normoxic and hypoxic groups,followed by bioinformatics analysis of pathways enriched with differentially expressed proteins(DEPs).Histopathological changes and lung injury scores were assessed with HE staining.ELISA was used to quantify the inflammatory cytokines,flow cytometry and immunofluorescence assay were employed to measure the production of reactive oxygen species(ROS),and spectrophotometry was utilized to determine the contents of Fe2?,glutathione(GSH),malondialdehyde(MDA),and superoxide dismutase(SOD)to evaluate oxidative stress and detect ferroptosis-related markers.② Human bronchial epithelial cells(bronchial epithelium transformed with Ad12-SV40,BEAS-2B)and macrophages induced by tumor human peripheral blood monocytes-1(THP-1)cells were placed in a low oxygen conditions for 48 h to establish a cellular model of hypoxic lung injury,on which Fer-1 was administered as a preventive group.Ferroptosis markers in BEAS-2B cells and inflammatory cytokine secretion in macrophages were analyzed.Results ①Proteomics identified 2 962 proteins,with 357 DEPs(199 up-regulated,158 down-regulated).Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analysis showed ferroptosis as the most enriched pathway.Hypoxic lung injury resulted in elevated ROS,MDA,Fe2?,and inflammatory cytokines(P<0.05),reduced SOD,GSH,solute carrier family 7 member 11(SLC7A11),glutathione peroxidase 4(GPX4),and ferritin heavy chain 1(FTH1),and increased acyl-coa synthetase long chain family member 4(ACSL4)(P<0.05).Fer-1 pretreatment significantly mitigated oxidative stress(ROS,MDA,SOD,GSH;P<0.05),up-regulated SLC7A11 and FTH1,down-regulated ACSL4(P<0.05),and reduced inflammation(P<0.05).②In cellular models,Fer-1 increased SLC7A11,GPX4,FTH1,GSH,and SOD(P<0.05),declined ROS(P<0.05),and suppressed macrophage inflammatory cytokines(P<0.05).Conclusion Fer-1 alleviates high-altitude hypoxic lung injury by inhibiting ferroptosis in pulmonary epithelial cells and attenuating macrophage-driven inflammation,providing experimental evidence for novel therapeutic strategies.

Objective To investigate the relationship of aberrant SMAD family member 7(SMAD7)signaling pathway and ferroptosis in myelodysplastic syndromes(MDS)and evaluate the effect of asiaticoside(AC)-modulating SMAD7 up-regulation to suppress ferroptosis in MDS cell lines.Methods Publicly available MDS-related datasets from the Gene Expression Omnibus(GEO)database were analyzed to identify differentially expressed genes(DEGs)between MDS patients and healthy controls.These DEGs were cross-referenced with ferroptosis-associated genes from the Ferroptosis Database(FerrDb)to identify potential ferroptosis-related targets in MDS.Bone marrow mononuclear cells(BMMNCs)were isolated from 18 MDS patients freshly diagnosed in the First Medical Center of Chinese PLA General Hospitaland and from 16 healthy donors during October 2022 and November 2024.RT-qPCR was employed to detect the expression of SMAD7 and ferroptosis-related genes.Immunomagnetic bead sorting was applied to purify CD33+cells,and then qPCR and Western blotting were utilized to measure the expression of SMAD7 and ferroptosis-related biomarkers at mRNA and protein levels.Human normal bone marrow cells(HS-5)and MDS cell lines(MUTZ-1,SKM-1)were treated with gradient concentrations of AC(SMAD7 activator)and ferrostatin-1(Fer-1,ferroptosis inhibitor),and SMAD7 overexpression plasmids were transfected into MDS cells.qPCR and Western blotting were utilized to measure the expression of SMAD7 and ferroptosis-related biomarkers at mRNA and protein levels,and the contents of glutathione(GSH),malondialdehyde(MDA),superoxide dismutase(SOD),and reactive oxygen species(ROS)were detected.Flow cytometry of CD11b+was performed to measure cellular differentiation.Results ①Bioinformatics analysis revealed significant down-regulation of SMAD7 in MDS patients,correlating with ferroptosis activation.Compared to the healthy controls,MDS patients exhibited decreased SMAD7 expression(P<0.05),reduced levels of negative regulators of ferroptosis,glutathione peroxidase 4(GPX4)and ferritin heavy chain(FTH1)(P<0.05),and elevated expression of its positive regulator transferrin receptor protein 1(TFRC)(P<0.05).Consistent with this,when compared with the normal human bone marrow stromal cell line HS-5,the MDS cell lines MUTZ-1 and SKM-1 exhibited declined expression of SMAD7,GPX4,and FTH1,alongside elevated expression of TFRC(P<0.05).② Treatment with gradient concentrations of the ferroptosis inhibitors ferrostatin-1(Fer-1),the expression levels of GPX4 and FTH1 in MDS cell lines were significantly upregulated in a concentration-dependent manner(P<0.05),while TFRC was markedly downregulated(P<0.05).Additionally,GSH content and SOD activity were enhanced,whereas ROS levels and MDA content were significantly reduced(P<0.05).These results suggest that Fer-1 effectively suppresses ferroptosis in MDS cells.③SMAD7 overexpression led to up-regulation of GPX4 and FTH1 ih MDS cell lines,while downregulation of TFRC,improved anti-oxidative ability and reduced ferroptosis,with enhanced CD11b+expression and myeloid differentiation.④ Following AC treatment,the expression levels of GPX4 and FTH1 in MDS cell lines were significantly upregulated in a concentration-dependent manner(P<0.05),whereas the downregulation of TFRC did not reach statistical significance.Additionally,AC treatment effectively enhanced the antioxidant capacity of the cells,increased the proportion of CD11b+cells(P<0.05),and facilitated cellular differentiation.Conclusion AC activates SMAD7 in MDS cell lines,up-regulating GPX4 and FTH1 while suppressing TFRC expression.This mechanism alleviates oxidative damage and lipid peroxidation,thereby inhibiting ferroptosis in MDS cells.Concurrently,SMAD7 activation promotes cellular differentiation.

Objective:To investigate the effect of nourishing yin and tonifying yang method on inflammatory response and bone metabolism in patients with T2DM complicated with osteoporosis (OP).Methods:A randomized controlled trial. From January 2022 to December 2023,80 patients with T2DM and OP in our hospital were selected as the observation objects, and they were divided into two groups by random number table method, with 40 cases in each group.On the basis of conventional treatment, the control group chewed vitamin D calcium chewable tablets, and the observation group added nourishing yin and tonifying yang Chinese medicine.Both groups were treated for 6 months. TCM syndrome scores were performed before and after treatment ;the levels of fasting blood glucose (FPG), 2 hPG and HbA1c were detected by intelligent blood glucose monitor;the levels of serum neutrophils and lymphocytes were detected by automatic blood analyzer, and the neutrophil/lymphocyte ratio (NLR) was calculated;the levels of serum IL-1β and TNF-α were detected by automatic chemiluminescence analyzer, the levels of type I procollagen amino terminal propeptide (PINP), type I collagen carboxy terminal peptide β special sequence (β-CTX) and 25-hydroxy vitamin D3 [25-(OH)D3] were detected by ELISA;Bone mineral density (BMD) was detected by bone mineral density detector. The adverse reactions during treatment were observed and recorded, and the clinical efficacy was evaluated.Results:The total effective rate was 92.5 %(37/40) in the observation group and 75.0 % (30/40) in the control group,the difference between the two groups was statistically significant ( &chi;2=4.50, P=0.034).After treatment, the scores of soreness and weakness of waist and knees, soreness and pain of waist and back, clear and long urine, pale tongue and white coating in the observation group were lower than those in the control group ( t=3.11, 3.75, 3.51, 3.74, P<0.01);the levels of serum FPG, 2 hPG and HbA1c in the observation group were lower than those in the control group ( t=3.11,3.20,3.39, P<0.01).The levels of serum NLR (2.63 ± 0.68 vs. 3.24 ± 0.79, t=3.70), IL-1β [(81.65 ± 8.30) ng/L vs. (89.03 ± 8.98) ng/L, t=3.82] and TNF-α [(35.14 ± 5.11) μg/L vs. (39.96 ± 5.38) μg/L, t=4.11] in the observation group were lower than those in the control group ( P<0.01). After treatment, the levels of PINP [(29.83 ± 3.92) ng/L vs. (34.02 ± 4.03) ng/L, t=4.71] and β-CTX [(21.30 ± 3.95 ) ng/L vs. (25.32 ± 4.18) ng/L, t=4.42] in the observation group were lower than those in the control group ( P<0.01), the levels of 25-(OH)D3 [(42.86 ± 5.12) μg/L vs. (38.08 ± 4.55) μg/L, t=4.41] and BMD [(0.90 ± 0.18) g/cm 3vs. (0.78 ± 0.16) g/cm 3, t=3.15] were higher than those in the control group ( P<0.01).During the treatment, the incidence of adverse reactions was 12.5% (5/40) in the observation group and 10.0 % (4/40) in the control group,there was no significant difference between the two groups ( &chi;2=0.13, P=0.723). Conclusion:The method of nourishing yin and tonifying yang can effectively improve the TCM syndromes of T2DM patients with OP, reduce the levels of blood glucose and inflammatory factors, improve bone metabolism, improve clinical efficacy and have good treatment safety.

Background: The genetic basis for hyperglycaemia in pregnancy remain unclear. This study aimed to uncover the genetic determinants of gestational diabetes mellitus (GDM) and investigate their applications. Methods: We performed a meta-analysis of genome-wide association studies (GWAS) for GDM in Chinese women (464 cases and 1,217 controls), followed by de novo replications in an independent Chinese cohort (564 cases and 572 controls) and in silico replication in European (12,332 cases and 131,109 controls) and multi-ethnic populations (5,485 cases and 347,856 controls). A polygenic risk score (PRS) was derived based on the identified variants. Results: Using the genome-wide scan and candidate gene approaches, we identified four susceptibility loci for GDM. These included three previously reported loci for GDM and type 2 diabetes mellitus (T2DM) at MTNR1B (rs7945617, odds ratio [OR], 1.64; 95% confidence interval [CI],1.38 to 1.96]), CDKAL1 (rs7754840, OR, 1.33; 95% CI, 1.13 to 1.58), and INS-IGF2-KCNQ1 (rs2237897, OR, 1.48; 95% CI, 1.23 to 1.79), as well as a novel genome-wide significant locus near TBR1-SLC4A10 (rs117781972, OR, 2.05; 95% CI, 1.61 to 2.62; Pmeta=7.6×10-9), which has not been previously reported in GWAS for T2DM or glycaemic traits. Moreover, we found that women with a high PRS (top quintile) had over threefold (95% CI, 2.30 to 4.09; Pmeta=3.1×10-14) and 71% (95% CI, 1.08 to 2.71; P=0.0220) higher risk for GDM and abnormal glucose tolerance post-pregnancy, respectively, compared to other individuals. Conclusion Our results indicate that the genetic architecture of glucose metabolism exhibits both similarities and differences between the pregnant and non-pregnant states. Integrating genetic information can facilitate identification of pregnant women at a higher risk of developing GDM or later diabetes.

6-gingerol, a bioactive compound from ginger, has demonstrated promising anticancer properties across various cancer models by inducing apoptosis and inhibiting cell proliferation and invasion. In this study, we explore its mechanisms against glioblastoma multiforme (GBM), a notably aggressive and treatment-resistant brain tumor. We found that 6-gingerol crosses the blood-brain barrier more effectively than curcumin, enhancing its potential as a therapeutic agent for brain tumors. Our experiments show that 6-gingerol reduces cell proliferation and triggers apoptosis in GBM cell lines by disrupting cellular energy homeostasis. This process involves an increase in mitochondrial reactive oxygen species (mtROS) and a decrease in mitochondrial membrane potential, primarily due to the downregulation of manganese superoxide dismutase (MnSOD). Additionally, 6-gingerol reduces ERK phosphorylation by inhibiting EGFR and RAF, leading to G1 phase cell cycle arrest. These findings indicate that 6-gingerol promotes cell death in GBM cells by modulating MnSOD and ROS levels and arresting the cell cycle through the ERFR-RAF-1/MEK/ ERK signaling pathway, highlighting its potential as a therapeutic agent for GBM and setting the stage for future clinical research.

ObjectiveTo explore the effect of serum containing Zhenwutang on myocardial mast cell apoptosis induced by angiotensin Ⅱ （AngⅡ） and the mechanism of the correlation between apoptosis and mitochondrial autophagy. MethodsIn this experiment， AngⅡ and serum containing Zhenwutang with different concentrations were used to interfere with H9C2 cardiomyocytes for 24 h， and the survival rate of H9C2 cardiomyocytes was detected by cell counting kit-8 （CCK-8） to screen the optimal concentration for the experiment. Enzyme-linked immunosorbent assay （ELISA） was used to detect the content of B-type natriuretic peptide （BNP） in cell culture supernatant， and immunofluorescence was used to detect the cell surface area to verify the construction of the myocardial mast cell model. Subsequently， the experiment was divided into a blank group （20% blank serum）， a model group （20% blank serum + 5×10^-5 mol·L^-1 AngⅡ）， low-， medium-， and high-dose （5%， 10% and 20%） serum containing Zhenwutang groups， an autophagy inhibitor group （1×10^-4 mol·L^-1 3-MA）， and autophagy inducer group （1×10^-7 mol·L^-1 rapamycin）. The apoptosis level of H9C2 cells and the changes of mitochondrial membrane potential were detected by flow cytometry. The lysosomal probe （Lyso Tracker） and mitochondrial probe （Mito Tracker） co-localization was employed to detect autophagy. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect Caspase-3， Caspase-9， B-cell lymphoma 2 （Bcl-2）， Bcl-2-related X protein （Bax）， and cytochrome C （Cyt C） in apoptosis-related pathways and the relative mRNA expression of ubiquitin ligase （Parkin）， phosphatase and tensin homolog （PTEN）-induced kinase 1 （PINK1）， and p62 protein in mitochondrial autophagy-related pathways. Western blot was used to detect cleaved Caspase-3， cleaved Caspase-9， Bax， Bcl-2， and Cyt C in apoptosis-related pathways， phosphorylated ubiquitin ligase （p-Parkin）， phosphorylated PTEN-induced kinase 1 （p-PINK1）， p62， and Bcl-2 homology domain protein Beclin1 in mitochondrial autophagy-related pathways， and the change of microtubule-associated protein 1 light chain 3 （LC3） Ⅱ/Ⅰ ratio. ResultsCCK-8 showed that when the concentration of AngⅡ was 5×10^-5 mol·L^-1， the cell activity was the lowest， and there was no cytotoxicity. At this concentration， the surface area of cardiomyocytes was significantly increased （P<0.01）， and the content of BNP in the supernatant of culture medium was significantly increased （P<0.05）. Therefore， AngⅡ with a concentration of 5×10^-5 mol·L^-1 was selected for the subsequent modeling of myocardial mast cells. Compared with the blank group， the model group and the autophagy inhibitor 3-MA group had a significantly increased apoptosis rate （P<0.01） and significantly decreased mitochondrial membrane potential （P<0.01）. The results of immunofluorescence co-localization showed that compared with the blank group， the model group had a significantly decreased number of red and green fluorescence spots. The results of Real-time PCR showed that compared with that in the blank group， the relative mRNA expression of Bax， Caspase-3， Caspase-9， Cyt C， and p62 in the model group was significantly up-regulated （P<0.01）， while the relative mRNA expression of Bcl-2， Parkin， and PINK1 was significantly down-regulated （P<0.01）. In addition， the relative protein expression of Bax， cleaved Caspase-3， cleaved Caspase-9， Cyt C， and p62 was significantly up-regulated （P<0.01）. The LC3Ⅱ/Ⅰ was significantly decreased， and the relative protein expression of Bcl-2， p-Parkin， p-PINK1， and Beclin1 was significantly down-regulated （P<0.01）. Compared with the model group， the serum containing Zhenwutang groups and the autophagy inducer group had significantly decreased apoptosis rate （P<0.01）， and the decrease ratio of mitochondrial membrane potential is significantly lowered （P<0.01） in a dose-dependent manner. Additionally， both red and green fluorescence spots became more in these groups. In the 3-MA group， the number of red and green fluorescence spots decreased significantly. The relative mRNA expression of Bax， Caspase-3， Caspase-9， Cyt C， and p62 was significantly down-regulated （P<0.05， P<0.01）， while that of Bcl-2， Parkin， and PINK1 was significantly up-regulated （P<0.01）. In the serum containing Zhenwutang groups， the relative protein expression levels of Bax， cleaved Caspase-3， cleaved Caspase-9， Cyt C， and p62 were significantly down-regulated （P<0.05，P<0.01）. The LC3Ⅱ/Ⅰ was significantly increased， and the relative protein expression levels of Bcl-2， p-Parkin， p-PINK1， and Beclin1 were significantly up-regulated （P<0.01）. ConclusionThe serum containing Zhenwutang can reduce the apoptosis of myocardial mast cells and increase mitochondrial autophagy. This is related to the inhibition of intracellular Bax/Bcl-2/Caspase-3 apoptosis pathway and regulation of Parkin/PINK1 mitochondrial autophagy pathway.

ObjectiveTo observe the clinical efficacy and safety of Sizi Powder （四子散， SP） orientation osmotherapy in the treatment of stroke patients with hemiplegia. MethodsIn this study， 94 patients with post-stroke hemiplegia were randomly divided into a control group and a treatment group with 47 patients in each group. The control group received conventional treatment， nursing and rehabilitation training， while the treatment group was treated with SP orientation osmotherapy in addition to the treatments in the control group. The treatment consisted of 20 minutes per session， once daily， 5 times a week， 2 weeks per course， with a total of 2 courses. Before the intervention， after 2 weeks intervention and after 4 weeks intervention， the upper limb motor function was evaluated by using the Fugl-Meyer Assessment （U-FMA）. The modified Ashworth Scale （MAS） was used to assess upper limb spasticity， and joint range of motion was measured for shoulder flexion， extension， abduction， internal rotation， external rotation， elbow flexion， wrist palmar flexion， dorsiflexion， ulnar deviation， and radial deviation. Clinical efficacy for spasticity was evaluated after 2 and 4 weeks of treatment. Skin conditions， including burns， allergic reactions， and blisters， were monitored during the treatment process. ResultsA total of 44 patients in the treatment group and 45 patients in the control group completed the study. The results showed that after 2 and 4 weeks of intervention， the U-FMA scores of both groups increased， with the treatment group showing higher scores than the control group （P＜0.05）. After 4 weeks of treatment， the MAS score distribution improved significantly in both groups （P＜0.05）， although no significant difference was found between the groups after 2 and 4 weeks treatment（P＞0.05）. The total effective rate of spasticity clinical efficacy in the treatment group after 2 and 4 weeks was 15.91% （7/44） and 40.91% （18/44）， respectively， while in the control group， it was 11.11% （5/45） and 22.22% （10/45）. There was no significant difference after 2 weeks treatment （P＞0.05）， but the treatment group showed a significantly higher total effective rate after 4 weeks treatment （P＜0.05）. After 2 and 4 weeks of treatment， the joint range of motion in the upper limbs was greater in both groups （P＜0.05）. After 2 weeks of intervention， the treatment group showed greater range of motion in shoulder flexion， extension， and abduction than the control group， and after 4 weeks of intervention， the treatment group demonstrated greater range of motion in shoulder flexion， extension， abduction， internal rotation， external rotation， and elbow flexion compared to the control group （P＜0.05）. During the treatment， one patient in the treatment group experienced mild skin allergy， while no other severe adverse reactions， such as intense pain， itching， blisters， or infection， were observed in any patients. ConclusionSP orientation osmotherapy can effectively improve upper limb motor function and joint range of motion in stroke patients with hemiplegia. After 4 weeks of treatment， it can reduce upper limb spasticity and improve clinical efficacy， with good safety.

Objective To prepare a thermosensitive hydrogel scaffold loaded with bone marrow mesenchymal stem cells（BMSCs） and resveratrol liposomes （RSV-LIP） to form a therapeutic unit and evaluate its treatment efficacy for traumatic brain injury （TBI）. Methods BMSCs were extracted from rats, and RSV-LIP was prepared and characterized. Cell models were constructed to investigate the pharmacological effects of BMSCs combined with RSV-LIP. BMSCs and RSV-LIP were then loaded into the hydrogel, and a TBI mouse model was established to evaluate the therapeutic effects of the hydrogel. Results The RSV-LIP had a particle size of 127.8 nm, a Zeta potential of −4.9 mV, an encapsulation efficiency of 78.50%, and a drug loading content of 2.37%. Live-dead staining indicated good biocompatibility of the hydrogel. The combination of BMSCs and RSV-LIP significantly inhibited TNF-α and reduced ROS levels, promoting cell migration in scratch assays. Compared to the control group, the hydrogel group showed significantly lower mNSS scores （P<0.01）, higher hanging scores （P<0.001）, and reduced stepping errors （P<0.001）. Conclusion The combination of BMSCs and RSV-LIP exhibited antioxidative stress, anti-inflammatory, and neurogenic cell migration-promoting effects. When loaded into a hydrogel scaffold and locally implanted, it could improve the motor and sensory functions in TBI mice.