Objective: To analyze the situation of blood return in medical institutions in Qingdao, and provide a reference basis for improving blood utilization efficiency. Methods: Data on whole blood donations, and the distribution and return of various blood components from 2022 to 2024 at the Qingdao Central Blood Station were collected. The overall trend of blood return, return situation of various blood components, main reasons for blood return, and related influencing factors were analyzed. Results: The average blood return rate from 2022 to 2024 was 1.43‰ (1 249/875 007), showing an overall downward trend (P<0.05). The return rate of red blood cell (RBC) components increased year by year over the three years, while those of plasma components and cryoprecipitated antihemophilic factors decreased. Regarding the reasons for blood return, the return rates due to direct antiglobulin test (DAT) positivity and unexpected antibody positivity increased year by year, whereas those due to leakage and other reasons decreased. Univariate analysis of the causes of RBC components return showed that DAT positivity rates differed significantly by sex, age, and blood type, but not by donation season; unexpected antibody positivity rate differed significantly by sex, but not by age, blood type, or donation season. Multivariate analysis indicated that female gender, age>30 years, and blood type A or AB were independent risk factors for DAT positivity, while female gender was an independent risk factor for unexpected antibody positivity. The return rate due to DAT positivity differed significantly among medical institutions of different levels, while that due to unexpected antibody positivity did not show a significant difference. Some donors who tested positive for DAT (76.92%, 60/78) or unexpected antibody (71.15%, 37/52) became antibody-negative upon subsequent donations. Comparing RBC donors with DAT positivity who became negative upon subsequent donations with those who remained positive, the difference in donation interval was statistically significant. Conclusion: Over the past three years, the overall blood return rate in Qingdao has declined, but the return rate of RBC components has increased. Further investigation and targeted interventions are needed to enhance the utilization of blood resources and ensure safe clinical blood transfusion.

Objective: To examine the impacts of chemotherapy/radiotherapy, targeted therapy, and combined treatment on the quality of life in patients with intermediate and advanced lung cancer. Methods: The patients with intermediate and advanced lung cancer undergoing chemotherapy/radiotherapy, targeted therapy, and combined treatment for the first time were recruited from a tertiary hospital in Weifang City, Shandong Province, using a quota sampling method in September 2023. Basic information was collected using a general information questionnaire, and the quality of life was assessed using the Chinese version of Functional Assessment of Cancer Therapy-General. The investigation started on the 7th day of treatment, and the follow-ups were conducted at 3 and 6 months. The quality of life in patients with different treatment regimens and at different treatment time were compared using repeated measure analysis of variance. Results: There were 26 chemotherapy/radiotherapy patients, 32 targeted therapy patients, and 95 combination therapy patients. There were no significant differences in age, gender, place of residence, education level, self-rated economic status, medical insurance, pathological type and disease stage among the three treatment regimens (all P>0.05). The repeated measure analysis of variance showed an interaction effect between time and group among patients receiving the three treatment regimens (P<0.05). The quality of life scores of patients receiving combination therapy decreased with extended treatment time (all P<0.05). The quality of life scores of patients receiving targeted therapy at 3 and 6 months were lower than those treated for 7 days (both P<0.05). No significant differences were observed in quality of life scores among chemotherapy/radiotherapy patients with different treatment durations (all P>0.05). At 3 and 6 months, patients receiving combination therapy had lower quality of life scores compared to those receiving chemotherapy/radiotherapy or targeted therapy (all P<0.05). Conclusion The decline in quality of life for patients with intermediate and advanced lung cancer undergoing chemotherapy/radiotherapy and targeted therapy is less than that for patients receiving combined therapy.

Objective:To explore the role of curcumin (Cur) in improving IgA nephropathy (IgAN) and its related mechanisms.Methods:Fifty 7-month-old miR-23b knockout (miR-23b -/-) mice weighing (25±5) g were used to establish an IgAN disease model, and were randomly divided into IgAN group, IgAN+Cur (150 mg/kg) group and IgAN+Cur (300 mg/kg) group using simple randomisation. Sixteen healthy 7-month-old weighing (25±3) g C57BL/6J wild-type mice served as the normal control group. IgAN+Cur (150 mg/kg) and IgAN+Cur (300 mg/kg) groups were respectively gavaged continuously with 150 mg/kg Cur and 300 mg/kg Cur for 8 weeks, and the normal control and IgAN groups were gavaged continuously with an equal dose of 0.9% sodium chloride solution for 8 weeks. The samples of urine, serum, intestinal fluid, intestinal tissues, kidney tissues and liver tissues were collected from each group. In vitro experiments, human cloned colon adenocarcinoma (Caco-2) cells were divided into blank control (Ctrl), Ctrl+Cur (10 μmol/L), Ctrl+ Cur (60 μmol/L), tumor necrosis factor-α（TNF-α), TNF-α+Cur (10 μmol/L) and TNF-α+Cur (60 μmol/L) groups. Enzyme-linked immunosorbent assay was used to detect serum alanine transaminase, aspartate transaminase, secretory IgA (sIgA), creatinine, blood urea nitrogen, 24 h urine microalbumin, as well as sIgA, TNF-α, interleukin（IL)-6 and IL-1β in the intestinal fluids. HE staining was used to observe the effect of Cur on liver tissues, the hyperplasia of glomerular mesangial zone in kidney tissues and the morphological and structural changes of intestinal epithelial barrier, and the histopathological damage scores were performed respectively. PAS staining was used to observe the changes of glomerular basement membrane and mesangial matrix. Immunofluorescence was used to observe the deposition of immune complexes in the glomerular mesangial zone. Real-time quantitative PCR was used to detect the mRNA expression levels of B-cell activating factor ( BAFF) and a proliferation inducing ligand ( APRIL). Western blotting was used to detect the protein expression levels of tight junction proteins zonula occluden-1 (ZO-1) and occludin in the mouse intestinal tissues. The potential targets of Cur in IgAN were predicted. Western blotting was used to detect the protein expression levels of tight junction proteins, as well as Toll-like receptor 9 (TLR9), myeloid differentiation primary response protein (MyD88), nuclear factor-κB p65 (NF-κB p65) and p-NF-κB p65. Results:Genetic identification results revealed that all IgAN model mice exhibited the miR-23b -/- genotype, confirming successful model establishment. Seven-month-old mice were subsequently selected for Cur treatment. Histopathological analysis demonstrated no significant differences in hepatic tissue morphology across groups, with comparable liver histopathological injury scores and unaltered liver function parameters, thereby validating the safety of Cur administration. Compared with the normal control group, IgAN mice displayed elevated levels of serum sIgA, serum creatinine, blood urea nitrogen and 24 h urine microalbumin (all P<0.05). Renal pathological results revealed severe mesangial hypercellularity in glomeruli, higher glomerular injury scores, and notable glomerular mesangial deposits of IgA, IgG and complement C3 in IgAN mice (all P<0.05). Additionally, intestinal pathological alterations were observed, including structural changes in intestinal epithelium and Peyer's patches, accompanied by significantly higher intestinal histopathological injury scores in IgAN mice ( P<0.05). Intestinal epithelial expression levels of ZO-1 and occludin were significantly reduced, while sIgA, TNF-α, IL-1β and IL-6 in intestinal fluid were elevated (all P<0.05). Serum FITC fluorescence intensity was markedly increased, and intestinal tissue exhibited upregulated mRNA expression of BAFF and APRIL (all P<0.05). Following Cur treatment, serum sIgA level and renal function indices in mice showed partial recovery (all P<0.05). Renal pathological improvements included alleviated mesangial hypercellularity, reduced glomerular injury scores, and diminished glomerular immune complex deposition (all P<0.05). Intestinal pathologies, including epithelial and Peyer's patch lesions, were mitigated, with decreased intestinal histopathological injury scores ( P<0.05). Additionally, intestinal tight junction protein expression levels were upregulated, intestinal fluid sIgA level was reduced, inflammatory markers were attenuated, serum FITC fluorescence intensity was declined, and intestinal BAFF and APRIL mRNA expression levels were downregulated (all P<0.05). In vitro experiments demonstrated that TNF-α exposure reduced tight junction protein expression in Caco-2 cells, whereas Cur treatment reversed the effect (all P<0.05). Target prediction analysis revealed that Cur effectively bound to TLR9 structural domain in IgAN. Experimental validation confirmed that Cur treatment suppressed the upregulated protein expression levels of TLR9, MyD88, NF-κB p65 and p-NF-κB p65 in intestinal tissues of IgAN mice (all P<0.05). Conclusion:Cur has a significant effect in the treatment of IgAN and can regulate intestinal mucosal immunity by inhibiting the TLR9/MyD88/NF-κB signaling pathway, thereby reducing renal injury and protecting the kidneys.

Gentiopicroside(GPS)is the main active ingredient extracted from Gentiaceae.It has anti-inflammatory,antioxidant,analgesic,anti-fibrosis,inhibition of tumor cell proliferation and improvement of glucose and lipid metabolism.Gentiaceae shows a wide range of application prospects in the treatment of diabetes,liver diseases,bone and joint diseases and other diseases.This paper reviewed the pharmacokinetics of gentiopicrin,including its pharmacokinetic properties in different animal models,and its mechanism and targets in the treatment of diabetes mellitus and its complications,liver injury,bone and joint diseases.Studies have shown that gentiopictin exerts its therapeutic effects by regulating various signaling pathways,such as PI3K/AKT,FOXO1,PPAR-γ,NF-κB,etc.Although the current research has made some progress,there are still limitations,such as most studies focused on animal models and in vitro experiments,lack of high-quality clinical evidence-based trials support.Future studies should further explore the new targets and signal transduction pathways of gentiopicroside,improve its bioavailability,and strengthen the research of traditional Chinese medicine compounds,so as to give full play to the advantages of holistic treatment of traditional Chinese medicine.

AIM:To examine the impact of the transcription factor 7 analogue 2(TCF7L2)gene polymorphism on the hypoglycaemic effect of ex-enatide in patients with type 2 diabetes mellitus(T2DM).METHODS:A total of 100 newly diagnosed Han Chinese patients with T2DM who had not re-ceived any drug treatment were selected from the Affiliated Hospital of Xuzhou Medical University and treated with exenatide monotherapy for 6 months.The TCF7L2 rs290487 was genotyped by SnaPshot method,and blood glucose levels,lipids profiles and pancreatic function evaluation indica-tors were measured at baseline,3 months and 6 months after exenatide treatment.Multiple linear regression analysis was employed to assess the cor-relation between each indicator and the reduction in glycated hemoglobin(HbA1c)levels after 6 months of exenatide treatment.The expression of TCF7L2 protein in the plasma of T2DM patients was detected by enzyme-linked immunosorbent assay(ELISA)kit.Furthermore,western blotting was con-ducted to ascertain TCF7L2 expression in pancreat-ic tissues obtained from db/db mice and INS-1 cells cultured under high glucose conditions.Lentivirus transfection was used to overexpress or knock down TCF7L2 in insulinoma cell line(INS-1)cells,followed by measurement of KSIS activity and insu-lin content after a 24-hour intervention with exena-tide.RESULTS:The distribution pattern of TCF7L2 rs290487 was found to be in accordance with Har-dy-Weinberg equilibrium(P＞0.05).Following 6 months of exenatide treatment,there was a nota-ble reduction in blood glucose levels and an im-provement in lipid profiles when compared to base-line values.Additionally,there was a significant in-crease in the homeostasis model assessment of be-ta-cell function(HOMA-B)values.Patients with the TT genotype exhibited significantly lower postpran-dial plasma glucose(PPG)levels and HbA1c values compared to those with the CC or CT genotypes(P＜0.05).After adjusting for age,gender,body mass in-dex(BMI),and waist to hip ratio(WHR)in the mul-tiple linear regression model,a significant associa-tion was observed between the rs290487 TT geno-type,baseline HbA1c levels,and family history of diabetes with the reduction in HbA1c after six months of exenatide treatment(P＜0.05).Further-more,individuals with the rs290487 TT genotype demonstrated a notable elevation in TCF7L2 expres-sion in plasma among T2DM patients in comparison to those with the CC genotype(P＜0.05).In particu-lar,pancreatic tissue from db/db mice exhibited markedly elevated TCF7L2 expression compared to db/m mice.However,this up-regulation was re-versed by exenatide treatment.Similarly,INS-1 cells cultured under high glucose conditions dem-onstrated an increase in TCF7L2 expression,which was ameliorated upon exenatide administration.The knockdown of TCF7L2 using shRNA enhanced the KSIS function of pancreatic β cells and aug-mented the insulinotropic effect of exenatide.Con-versely,the upregulation of TCF7L2 impaired the KSIS function of pancreatic β cells and attenuated the insulinotropic effect of exenatide.CONCLU-SION:The TCF7L2 rs290487 gene polymorphism is closely associated with the hypoglycaemic efficacy of exenatide therapy.The risk allele C may diminish the effectiveness of exenatide by impacting the lev-els of PPG and HbA1c in T2DM patients.The muta-tion at TCF7L2 rs290487 site(C→T)influenced the expression of TCF7L2 protein.By exerting its regula-tory effect,exenatide may be capable of regulating the impact of TCF7L2 on the function of pancreaticβ cells.

Objective : To observe the brain tissue injury during hypoxia-ischemia, as well as the pathological changes and the expression of ferroptosis-related factors after the use of Shenfu injection(SFI), and to explore the protective effect of SFI on hypoxic-ischemic brain injury(HIBD) by inhibiting ferroptosis. Methods : An animal model of HIBD in SD rats was constructed and intervened with SFI. Pathologic changes in brain tissue were observed by HE staining methods. Nissen staining was used to observe neuron survival. Glutathione Peroxidase 4(GPX4) and Divalent Metal Transporter 1(DMT1) expression were detected in brain tissue by Western blot, immunohistochemistry and immunofluorescence. Reduced Glutathione(GSH), Lactate Dehydrogenase(LDH), Malondialdehyde(MDA), Superoxide Dismutase(SOD) and tissue iron content were determined with the kits. BV-2 microglial cell line(BV2) cells were culturedin vitroand divided into control group(Ctrl group), oxygen-glucose deprivation group(OGD group), iron ferroptosis-inducing group(Erastin group), iron ferroptosis-inhibiting group(Fer-1 group), Shenfu injection group(SFI group), and Erastin+Shenfu injection group(Erastin+SFI group). 2′,7′-Dichlorodihydrofluorescein diacetate(DCFH-DA) reactive oxygen species(ROS) fluorescent probe was used to detect the ROS release level; Immunofluorescence was used to observe intracellular GPX4, DMT1 expression. Results : Compared with the Sham group, rats in the HIBD group showed significant neuronal cell damage in brain tissue, decreased GPX4 expression(P<0.01), increased DMT1 expression(P<0.01), decreased GSH and SOD levels(P<0.01), and increased LDH, MDA and tissue iron levels(P<0.05,P<0.05,P<0.01). In contrast, after the intervention of SFI, GPX4 expression was elevated(P<0.01), DMT1 expression decreased(P<0.01), GSH and SOD levels were elevated(P<0.01), and LDH, MDA, and tissue iron levels decreased(P<0.05,P<0.05,P<0.01). The cells experiments showed that compared with the Ctrl group, the OGD group had a significantly higher ROS content and a decrease in the expression of GPX4 fluorescence intensity, and an increase in the fluorescence intensity of DMT1(P<0.01), compared with the OGD group, the ROS content was reduced in the SFI group, while the expression of GPX4 was elevated and the expression of DMT1 was reduced(P<0.01). Conclusion Hippocampal and cortical regions are severely damaged after HIBD in neonatal rats, and their brain tissues show decreased expression of GPX4 and increased expression of DMT1. The above suggests that ferroptosis is involved in HIBD brain injury in neonatal rats. In contrast, Shenfu injection has a protective effect on HIBD experimental animal model and BV2 cell injury model by reducing iron aggregation and ROS production.

The occurrence and development of tumors are determined by both intrinsic and microenvironmental factors. The components of the tumor microenvironment exhibit great heterogeneity resulting in either pro-tumor or anti-tumor effects. The deep exploration of tumor immune microenvironment gave birth to the hypothesis of cancer immunoediting, which is supported by more and more evidence. Cancer immunoediting is accomplished through the interactions among various cells and factors in the microenvironment. While many molecular mechanisms have been studied, the cellular mechanisms of cancer immunoediting have been paid attention. This article explores the roles of cellular mechanisms in the cancer immunoediting, including immunogenic cell death, cellular senescence and neutrophil extracellular trap. The elucidation of these mechanisms not only reveals the complexity of the pathogenesis and progression of tumors, but also provides new targets and prognostic indicators for the diagnosis and treatment of tumors.

ObjectiveTo preliminarily explore the active components and target pathways of Angelicae Sinensis Radix-Polygonati Rhizoma （ASR-PR） herb pair in the treatment of simple obesity through network pharmacology and molecular docking， and to verify and investigate its mechanism of action via animal experiments. MethodsThe chemical constituents and targets of ASR and PR were predicted using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）. Targets related to simple obesity were identified by retrieving the GeneCards， Online Mendelian Inheritance in Man （OMIM）， Pharmacogenomics Knowledgebase （PharmGKB）， and DisGeNET databases. The intersection of drug and disease targets was used to construct an active component-target network using Cytoscape software. This network was imported into the STRING database to construct a protein-protein interaction （PPI） network， and topological analysis was conducted to identify core genes. Gene Ontology （GO） analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis and mapping were performed using the DAVID database and the Microbioinformatics platform. AutoDock 1.5.7 software was used to perform molecular docking between the top five active components and core targets. An animal model of simple obesity was established by feeding C57BL/6J mice a high-fat diet. The mice were administered ASR （2.06 g·kg^-1）， PR （2.06 g·kg^-1）， or ASR-PR （4.11 g·kg^-1） for 10 weeks， while the model group received an equal volume of purified water by gavage. After the administration period， the mice were sacrificed to measure body fat weight and serum levels of total cholesterol （TC）， triglycerides （TG）， high-density lipoprotein （HDL）， and low-density lipoprotein （LDL）. Hematoxylin-eosin （HE） staining was used to observe histopathological sections of liver and adipose tissue. Serum levels of leptin， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） were determined by enzyme-linked immunosorbent assay （ELISA）， and the mRNA expression levels of epidermal growth factor receptor （EGFR） and signal transducer and activator of transcription 3 （STAT3） in liver tissue were detected by real-time quantitative polymerase chain reaction （Real-time PCR）. ResultsNetwork pharmacology and molecular docking results indicated that the treatment of simple obesity by ASR-PR may involve the regulation of protein expression of core targets EGFR and STAT3 by its main components MOL009760 （Siberian glycoside A_qt）， MOL003889 （methyl protodioscin_qt）， MOL009766 （resveratrol）， MOL006331 （4′，5-dihydroxyflavone）， and MOL004941 （baicalin）， thereby modulating the PI3K/Akt and JAK/STAT signaling pathways. The animal experiment results showed that compared with the normal group， the model group had significantly increased body weight， body fat weight， and serum levels of TG， TC， TNF-α， IL-6， and leptin （P<0.01）. EGFR mRNA expression was significantly elevated （P<0.05）， while STAT3 mRNA expression was significantly decreased （P<0.01）. Histological analysis revealed disordered hepatic architecture in the model group， with pronounced lipid vacuoles， cytoplasmic loosening， lipid accumulation， and steatosis. Adipocytes in white adipose tissue （WAT） and brown adipose tissue （BAT） of the model group exhibited markedly increased diameters， reduced cell counts per unit area， and irregular morphology. Compared with the model group， the ASR-PR group significantly reduced body weight， body fat weight， serum TC， IL-6， TNF-α， leptin levels， and EGFR mRNA expression （P<0.01）. TG levels were also significantly decreased （P<0.05）， while STAT3 mRNA expression was significantly increased （P<0.01）. Histopathological improvements included reduced size and number of hepatic lipid vacuoles and restoration of liver cell morphology toward that of the normal group. The diameter of adipocytes significantly decreased， and the number of adipocytes per unit area increased. ConclusionASR-PR may regulate the expression of key target proteins such as EGFR and STAT3 via its core active components， modulate the PI3K/Akt and JAK/STAT signaling pathways， repair damaged liver and adipose tissues， and thereby alleviate the progression of obesity in mice.

ObjectiveTo preliminarily explore the active components and target pathways of Angelicae Sinensis Radix-Polygonati Rhizoma （ASR-PR） herb pair in the treatment of simple obesity through network pharmacology and molecular docking， and to verify and investigate its mechanism of action via animal experiments. MethodsThe chemical constituents and targets of ASR and PR were predicted using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）. Targets related to simple obesity were identified by retrieving the GeneCards， Online Mendelian Inheritance in Man （OMIM）， Pharmacogenomics Knowledgebase （PharmGKB）， and DisGeNET databases. The intersection of drug and disease targets was used to construct an active component-target network using Cytoscape software. This network was imported into the STRING database to construct a protein-protein interaction （PPI） network， and topological analysis was conducted to identify core genes. Gene Ontology （GO） analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis and mapping were performed using the DAVID database and the Microbioinformatics platform. AutoDock 1.5.7 software was used to perform molecular docking between the top five active components and core targets. An animal model of simple obesity was established by feeding C57BL/6J mice a high-fat diet. The mice were administered ASR （2.06 g·kg^-1）， PR （2.06 g·kg^-1）， or ASR-PR （4.11 g·kg^-1） for 10 weeks， while the model group received an equal volume of purified water by gavage. After the administration period， the mice were sacrificed to measure body fat weight and serum levels of total cholesterol （TC）， triglycerides （TG）， high-density lipoprotein （HDL）， and low-density lipoprotein （LDL）. Hematoxylin-eosin （HE） staining was used to observe histopathological sections of liver and adipose tissue. Serum levels of leptin， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） were determined by enzyme-linked immunosorbent assay （ELISA）， and the mRNA expression levels of epidermal growth factor receptor （EGFR） and signal transducer and activator of transcription 3 （STAT3） in liver tissue were detected by real-time quantitative polymerase chain reaction （Real-time PCR）. ResultsNetwork pharmacology and molecular docking results indicated that the treatment of simple obesity by ASR-PR may involve the regulation of protein expression of core targets EGFR and STAT3 by its main components MOL009760 （Siberian glycoside A_qt）， MOL003889 （methyl protodioscin_qt）， MOL009766 （resveratrol）， MOL006331 （4′，5-dihydroxyflavone）， and MOL004941 （baicalin）， thereby modulating the PI3K/Akt and JAK/STAT signaling pathways. The animal experiment results showed that compared with the normal group， the model group had significantly increased body weight， body fat weight， and serum levels of TG， TC， TNF-α， IL-6， and leptin （P<0.01）. EGFR mRNA expression was significantly elevated （P<0.05）， while STAT3 mRNA expression was significantly decreased （P<0.01）. Histological analysis revealed disordered hepatic architecture in the model group， with pronounced lipid vacuoles， cytoplasmic loosening， lipid accumulation， and steatosis. Adipocytes in white adipose tissue （WAT） and brown adipose tissue （BAT） of the model group exhibited markedly increased diameters， reduced cell counts per unit area， and irregular morphology. Compared with the model group， the ASR-PR group significantly reduced body weight， body fat weight， serum TC， IL-6， TNF-α， leptin levels， and EGFR mRNA expression （P<0.01）. TG levels were also significantly decreased （P<0.05）， while STAT3 mRNA expression was significantly increased （P<0.01）. Histopathological improvements included reduced size and number of hepatic lipid vacuoles and restoration of liver cell morphology toward that of the normal group. The diameter of adipocytes significantly decreased， and the number of adipocytes per unit area increased. ConclusionASR-PR may regulate the expression of key target proteins such as EGFR and STAT3 via its core active components， modulate the PI3K/Akt and JAK/STAT signaling pathways， repair damaged liver and adipose tissues， and thereby alleviate the progression of obesity in mice.

Although a single nucleotide polymorphism for N-acetyltransferase 10 (NAT10) has been identified in patients with early-onset stroke, the role of NAT10 in ischemic injury and the related underlying mechanisms remains elusive. Here, we provide evidence that NAT10, the only known RNA N4-acetylcytidine (ac4C) modification "writer", is increased in the damaged cortex of patients with acute ischemic stroke and the peri-infarct cortex of mice subjected to photothrombotic (PT) stroke. Pharmacological inhibition of NAT10 with remodelin on Days 3-7 post-stroke or astrocytic depletion of NAT10 via targeted virus attenuates ischemia-induced infarction and improves functional recovery in PT mice. Mechanistically, NAT10 enhances ac4C acetylation of the inflammatory cytokine tissue inhibitor of metalloproteinase 1 (Timp1) mRNA transcript, which increases TIMP1 expression and results in the accumulation of microtubule-associated protein 1 light chain 3 (LC3) and progression of astrocyte autophagy. These findings demonstrate that NAT10 regulates astrocyte autophagy by targeting Timp1 ac4C after stroke. This study highlights the critical role of ac4C in the regulation of astrocyte autophagy and proposes a promising strategy to improve post-stroke outcomes via NAT10 inhibition.