As a sub-discipline of field surgery,trauma surgery of naval warfare focuses on the treatment of marine casualties,which is the extension and application of field surgical theories and techniques in the context of naval warfare.Informatization and 3-dimension have been the basic features of modern naval warfare.With the extensive use of high-tech weapons,maritime combat styles and security needs have undergone profound changes.The complexity and diversity of marine trauma injuries have created new opportunities and challenges for the development of trauma surgery.This paper analyzes the marine trauma under the conditions of modern warfare,the characteristics of marine trauma surgical care,and the medical evacuation system of casualty care in naval battle,aiming to promote the research of naval medical support and the development of field surgery.

ObjectiveTo investigate the effects of ethoxysanguinarine （ETH） on angiotensin Ⅱ （Ang Ⅱ）-mediated cardiomyocyte apoptosis and its regulatory effects of inositol-requiring enzyme 1 （IRE1）/regulated IRE1-dependent decay （RIDD） signaling pathway and endoplasmic reticulum stress. MethodsWestern blot was used to detect the establishment of the H9c2 model via Ang Ⅱ stimulation， which was identified as a cardiomyocyte apoptosis model. Subsequently， the inhibitory effect of ETH on cell proliferation was assessed using the cell counting Kit-8 （CCK-8） to determine the optimal effective dose of ETH. H9c2 cardiomyocytes were divided into a blank group， a model group （Ang Ⅱ， 1 mmol·L^-1）， and low-， medium-， and high-dose ETH groups （1.25， 2.5， and 5 mmol·L^-1）. Morphological changes in cardiomyocytes induced by Ang Ⅱ were detected using phalloidin staining. Cardiomyocyte apoptosis was assessed using terminal deoxynucleotidyl transferase dUTP nick and labeling （TUNEL） staining. The apoptosis cycle was detected by Annexin V/PI flow cytometry. Western blot was used to detect the expression levels of apoptosis-related proteins， endoplasmic reticulum stress， and IRE1/RIDD pathway-related proteins. ResultsWestern blot results showed that 1 mmol/mL Ang Ⅱ stimulation significantly increased the protein expression levels of Bip， p-IRE1， and Bid in H9c2 cells （P<0.05， P<0.01）， indicating the induction of endoplasmic reticulum stress， activation of the IRE1/RIDD signaling pathway， and initiation of the apoptosis process. Compared with the blank group， the model group showed a significant increase in the surface area of H9c2 cells and the apoptosis rate of cardiomyocytes， as well as in both early and late apoptosis rates （P<0.01）. The expression levels of Bid， Bax， cleaved-Caspase-3， and cleaved-Caspase-8 proteins were significantly increased， while the expression level of Bcl-2 protein was significantly decreased （P<0.01）. The expression levels of Bip， p-IRE1， and p-RIDD proteins were significantly increased （P<0.05， P<0.01）. Compared with those in the model group， the surface area of cardiomyocytes and the apoptosis rate of cardiomyocytes in all ETH groups were significantly decreased after drug intervention. Both early and late apoptosis rates were significantly decreased. The expression level of cleaved-Caspase-8 was significantly decreased in the low-dose ETH group （P<0.05）. The expression levels of Bid， Bax， and cleaved-Caspase-8 were significantly decreased in the medium-dose ETH group （P<0.05， P<0.01）. The high-dose ETH group significantly reduced the expression levels of Bid， Bax， cleaved-Caspase-3， and cleaved-Caspase-8 （P<0.05， P<0.01） and significantly increased the expression level of Bcl-2 （P<0.05）. The level of p-IRE1 protein in the medium-dose ETH group was significantly decreased （P<0.01）. The expression levels of Bip， p-IRE1， and p-RIDD proteins in the high-dose ETH group were significantly decreased （P<0.05， P<0.01）. ConclusionETH can alleviate Ang Ⅱ-mediated cardiomyocyte apoptosis by inhibiting the IRE1/RIDD signaling pathway and further alleviate the cardiac injury caused by hypertension.

ObjectiveTo investigate the effects of ethoxysanguinarine （ETH） on angiotensin Ⅱ （Ang Ⅱ）-mediated cardiomyocyte apoptosis and its regulatory effects of inositol-requiring enzyme 1 （IRE1）/regulated IRE1-dependent decay （RIDD） signaling pathway and endoplasmic reticulum stress. MethodsWestern blot was used to detect the establishment of the H9c2 model via Ang Ⅱ stimulation， which was identified as a cardiomyocyte apoptosis model. Subsequently， the inhibitory effect of ETH on cell proliferation was assessed using the cell counting Kit-8 （CCK-8） to determine the optimal effective dose of ETH. H9c2 cardiomyocytes were divided into a blank group， a model group （Ang Ⅱ， 1 mmol·L^-1）， and low-， medium-， and high-dose ETH groups （1.25， 2.5， and 5 mmol·L^-1）. Morphological changes in cardiomyocytes induced by Ang Ⅱ were detected using phalloidin staining. Cardiomyocyte apoptosis was assessed using terminal deoxynucleotidyl transferase dUTP nick and labeling （TUNEL） staining. The apoptosis cycle was detected by Annexin V/PI flow cytometry. Western blot was used to detect the expression levels of apoptosis-related proteins， endoplasmic reticulum stress， and IRE1/RIDD pathway-related proteins. ResultsWestern blot results showed that 1 mmol/mL Ang Ⅱ stimulation significantly increased the protein expression levels of Bip， p-IRE1， and Bid in H9c2 cells （P<0.05， P<0.01）， indicating the induction of endoplasmic reticulum stress， activation of the IRE1/RIDD signaling pathway， and initiation of the apoptosis process. Compared with the blank group， the model group showed a significant increase in the surface area of H9c2 cells and the apoptosis rate of cardiomyocytes， as well as in both early and late apoptosis rates （P<0.01）. The expression levels of Bid， Bax， cleaved-Caspase-3， and cleaved-Caspase-8 proteins were significantly increased， while the expression level of Bcl-2 protein was significantly decreased （P<0.01）. The expression levels of Bip， p-IRE1， and p-RIDD proteins were significantly increased （P<0.05， P<0.01）. Compared with those in the model group， the surface area of cardiomyocytes and the apoptosis rate of cardiomyocytes in all ETH groups were significantly decreased after drug intervention. Both early and late apoptosis rates were significantly decreased. The expression level of cleaved-Caspase-8 was significantly decreased in the low-dose ETH group （P<0.05）. The expression levels of Bid， Bax， and cleaved-Caspase-8 were significantly decreased in the medium-dose ETH group （P<0.05， P<0.01）. The high-dose ETH group significantly reduced the expression levels of Bid， Bax， cleaved-Caspase-3， and cleaved-Caspase-8 （P<0.05， P<0.01） and significantly increased the expression level of Bcl-2 （P<0.05）. The level of p-IRE1 protein in the medium-dose ETH group was significantly decreased （P<0.01）. The expression levels of Bip， p-IRE1， and p-RIDD proteins in the high-dose ETH group were significantly decreased （P<0.05， P<0.01）. ConclusionETH can alleviate Ang Ⅱ-mediated cardiomyocyte apoptosis by inhibiting the IRE1/RIDD signaling pathway and further alleviate the cardiac injury caused by hypertension.

OBJECTIVE: To investigate whether auraptene (AUR) exerts a protective effect on acute diquat (DQ)-induced liver injury in mice and explore its underlying mechanisms. METHODS: Forty SPF-grade healthy male C57BL/6 mice were randomly divided into normal control group (Control group), DQ poisoning model group (DQ group), AUR treatment group (DQ+AUR group), and AUR control group (AUR group), with 10 mice in each group. The DQ poisoning model was established via a single intraperitoneal injection of 40 mg/kg DQ aqueous solution (0.5 mL); Control group and AUR group received an equal volume of pure water intraperitoneally. Four hours post-modeling, DQ+AUR group and AUR group were administered 0.5 mg/kg AUR aqueous solution (0.2 mL) by gavage once daily for 7 consecutive days, while Control group and DQ group received pure water. Blood and liver tissues were collected after anesthesia on day 7. Liver ultrastructure was observed by transmission electron microscopy. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured via enzyme-linked immunosorbent assay (ELISA). Hepatic glutathione (GSH), superoxide dismutase (SOD), and malondialdehyde (MDA) levels were detected using WST-1, thiobarbituric acid (TBA), and enzymatic reaction methods, respectively. Protein expression of nuclear factor-erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), Kelch-like ECH-associated protein 1 (Keap1), and activated caspase-9 in liver tissues was analyzed by Western blotting. RESULTS: Transmission electron microscopy revealed that mitochondria in the Control group exhibited mild swelling, uneven distribution of matrix, and a small number of cristae fractures. In the AUR group, mitochondria showed mild swelling, with no obvious disruption of cristae structure. In the DQ group, mitochondria demonstrated marked swelling and increased volume, matrix dissolution, loss and fragmentation of cristae, and extensive vacuolization. In contrast, the DQ+AUR group showed significantly reduced mitochondrial swelling, volume increase, matrix dissolution, cristae loss and fragmentation, and vacuolization compared to the DQ group. Compared with the DQ group, the DQ+AUR group exhibited significantly lower serum AST levels (U/L: 173.45±23.60 vs. 255.33±41.51), ALT levels (U/L: 51.77±21.63 vs. 100.70±32.35), and hepatic MDA levels (μmol/g: 12.40±2.76 vs. 19.74±4.10), along with higher hepatic GSH levels (mmol/g: 37.65±14.95 vs. 20.58±8.52) and SOD levels (kU/g: 124.10±33.77 vs. 82.81±22.00), the differences were statistically significant (all P < 0.05). Western blotting showed upregulated Nrf2 expression (Nrf2/β-actin: 0.87±0.37 vs. 0.53±0.22) and HO-1 expression (HO-1/β-actin: 1.06±0.22 vs. 0.49±0.08), and downregulated Keap1 expression (Keap1/β-actin: 0.82±0.12 vs. 1.52±0.76) and activated caspase-9 expression (activated caspase-9/β-actin: 1.16±0.28 vs. 1.71±0.30) in the DQ+AUR group compared to the DQ group (all P < 0.05). CONCLUSION AUR attenuates DQ-induced acute liver injury in mice by activating the Keap1/Nrf2 signaling pathway.
Animals ; Male ; Mice ; Mice, Inbred C57BL ; Liver/pathology* ; Chemical and Drug Induced Liver Injury/drug therapy* ; Diquat/poisoning* ; NF-E2-Related Factor 2/metabolism* ; Oxidative Stress ; Apoptosis ; Coumarins

Objective:To evaluate the long-term outcomes and predictors of coronary atherosclerotic lesions deemed functionally non-ischemic (quantitative flow ratio(QFR)>0.80) and deferred from intervention.Methods:This study is a post-hoc analysis of the FAVOR Ⅲ China trial, which enrolled 3 825 patients with stable or unstable angina pectoris or with myocardial infarction occurring at least 72 hours prior to screening, between December 5, 2018 and January 9, 2020 from 26 research centers in China. Coronary vessels with QFR>0.80 and without interventional treatment were analyzed in this study. The primary endpoint was 3-year target vessel revascularization. Vessels with revascularization (revascularized group) during follow-up were matched 1∶1 using propensity score matching to comparable vessels without revascularization (non-revascularized group). Multivariate Cox regression analysis was used to identify the risk factors for target vessel revascularization (TVR).Results:A total of 6 212 functionally negative vessels with deferred intervention were included in the final analysis, among which 153 vessels (2.5%) underwent TVR during a 3-year follow-up. Prior to propensity score matching, 6 059 vessels comprised the non-revascularized group. At the vessel level, compared to the non-revascularized group, the revascularized group exhibited a significantly higher proportion of males (79.1% (121/153) vs. 70.2% (4 253/6 059), P=0.018), higher body mass index ((25.6±4.0) kg/m2 vs. (24.3±5.2) kg/m2, P=0.003), and a higher prevalence of hypertension (73.9% (113/153) vs. 65.1% (3 944/6 059), P=0.025). And 152 pairs of vessels were successfully matched. Multivariate Cox regression analysis identified in-stent restenosis lesions ( HR=2.59, 95% CI 1.28-5.23, P=0.008) as an independent risk factor for target vessel revascularization. Conclusions:Coronary lesions classified as functionally non-ischemic at baseline are not entirely stable and may progress to lesions that requiring revascularization over time. In-stent restenosis emerges as a critical independent predictor of revascularization.

Objective To analyze the academic literature on sepsis-related microRNA(miRNA)at worldwide,and to dentify thematic hotspots and future research trends.Methods A bibliometric analysis was employed to retrieve the literature on sepsis-related miRNA published in the core collection of China National Knowledge Infrastructure(CNKI),and Web of Science(WOS)databases from January 1,2010,to January 1,2025,which met the article inclusion criteria,and used CiteSpace 6.3.1 software to perform the co-occurrence analysis of keywords,keyword emergence analysis,and cluster analysison;on the basis of these analyses,the keywords were sorted according to time to generate clustering time line figure to explore the current status and hotspot evolution process of sepsis-related miRNA.Results A total of 135 and 1 278 articles were retrieved from CNKI and the core collection of WOS databases,respectively.The frequency and centrality of keywords such as sepsis,prognosis,microRNA,acute lung injury,acute kidney injury,etc.were high in 135 documents in CNKI;in 1 278 documents in WOS core collection,the frequency and centrality of keywords such as expression,sepsis,inflammation,cells,micrornas,etc.were high;The top 10 keywords in the CNKI database in terms of burst intensity were:microRNA,inflammatory response,inflammatory factor,interleukin-10,tumor necrosis factor-α,acute respiratory distress syndrome,interleukin-35,septic shock,rat,tiny microRNA-155(miR-155);the top 10 keywords in the core collection of the WOS database in terms of burst intensity were:expression,NF-κB,microRNA,cells,induction,pathway,mechanisms,septic shock,mortality,cancer.Representative clustering tags in the CNKI are#0 prognosis,#1 miRNA,#2 septic shock;The representative clustering labels in the core collection of WOS database are#0 acute lung injury,#1 cancer,#2 septic shock,and so on.In CNKI and WOS core databases,the early keywords mainly revolve around the study of inflammatory factors and related mechanisms of sepsis,and the research center gradually shifts to the clinical physiological injuries as well as complications and mortality in the later stage,miRNA-126,AMP-activated protein kinase,interleukin-35 and other keywords have emerged.Among the top 10 most-cited English literature,researchers have paid particular attention to studying various miRNA as potential biomarkers of sepsis,including miR-146a,miR-223 and miR-146.Conclusions There are similarities and differences in the direction and hotspots of sepsis-related miRNA research in China and abroad.The research paradigm of sepsis has gradually shifted from the early clinical observation focusing on the overall complications and prognosis of patients to the basic research centered on the molecular mechanisms of inflammatory factors and signaling pathways.In this context,the study of miRNA as novel biomarkers for sepsis has been increasingly emphasized,and miRNA represent a promising direction for sepsis research,with potential applications both in basic research and clinical treatment.

Objective To analyze the academic literature on sepsis-related microRNA(miRNA)at worldwide,and to dentify thematic hotspots and future research trends.Methods A bibliometric analysis was employed to retrieve the literature on sepsis-related miRNA published in the core collection of China National Knowledge Infrastructure(CNKI),and Web of Science(WOS)databases from January 1,2010,to January 1,2025,which met the article inclusion criteria,and used CiteSpace 6.3.1 software to perform the co-occurrence analysis of keywords,keyword emergence analysis,and cluster analysison;on the basis of these analyses,the keywords were sorted according to time to generate clustering time line figure to explore the current status and hotspot evolution process of sepsis-related miRNA.Results A total of 135 and 1 278 articles were retrieved from CNKI and the core collection of WOS databases,respectively.The frequency and centrality of keywords such as sepsis,prognosis,microRNA,acute lung injury,acute kidney injury,etc.were high in 135 documents in CNKI;in 1 278 documents in WOS core collection,the frequency and centrality of keywords such as expression,sepsis,inflammation,cells,micrornas,etc.were high;The top 10 keywords in the CNKI database in terms of burst intensity were:microRNA,inflammatory response,inflammatory factor,interleukin-10,tumor necrosis factor-α,acute respiratory distress syndrome,interleukin-35,septic shock,rat,tiny microRNA-155(miR-155);the top 10 keywords in the core collection of the WOS database in terms of burst intensity were:expression,NF-κB,microRNA,cells,induction,pathway,mechanisms,septic shock,mortality,cancer.Representative clustering tags in the CNKI are#0 prognosis,#1 miRNA,#2 septic shock;The representative clustering labels in the core collection of WOS database are#0 acute lung injury,#1 cancer,#2 septic shock,and so on.In CNKI and WOS core databases,the early keywords mainly revolve around the study of inflammatory factors and related mechanisms of sepsis,and the research center gradually shifts to the clinical physiological injuries as well as complications and mortality in the later stage,miRNA-126,AMP-activated protein kinase,interleukin-35 and other keywords have emerged.Among the top 10 most-cited English literature,researchers have paid particular attention to studying various miRNA as potential biomarkers of sepsis,including miR-146a,miR-223 and miR-146.Conclusions There are similarities and differences in the direction and hotspots of sepsis-related miRNA research in China and abroad.The research paradigm of sepsis has gradually shifted from the early clinical observation focusing on the overall complications and prognosis of patients to the basic research centered on the molecular mechanisms of inflammatory factors and signaling pathways.In this context,the study of miRNA as novel biomarkers for sepsis has been increasingly emphasized,and miRNA represent a promising direction for sepsis research,with potential applications both in basic research and clinical treatment.

Objective:To evaluate the long-term outcomes and predictors of coronary atherosclerotic lesions deemed functionally non-ischemic (quantitative flow ratio(QFR)>0.80) and deferred from intervention.Methods:This study is a post-hoc analysis of the FAVOR Ⅲ China trial, which enrolled 3 825 patients with stable or unstable angina pectoris or with myocardial infarction occurring at least 72 hours prior to screening, between December 5, 2018 and January 9, 2020 from 26 research centers in China. Coronary vessels with QFR>0.80 and without interventional treatment were analyzed in this study. The primary endpoint was 3-year target vessel revascularization. Vessels with revascularization (revascularized group) during follow-up were matched 1∶1 using propensity score matching to comparable vessels without revascularization (non-revascularized group). Multivariate Cox regression analysis was used to identify the risk factors for target vessel revascularization (TVR).Results:A total of 6 212 functionally negative vessels with deferred intervention were included in the final analysis, among which 153 vessels (2.5%) underwent TVR during a 3-year follow-up. Prior to propensity score matching, 6 059 vessels comprised the non-revascularized group. At the vessel level, compared to the non-revascularized group, the revascularized group exhibited a significantly higher proportion of males (79.1% (121/153) vs. 70.2% (4 253/6 059), P=0.018), higher body mass index ((25.6±4.0) kg/m2 vs. (24.3±5.2) kg/m2, P=0.003), and a higher prevalence of hypertension (73.9% (113/153) vs. 65.1% (3 944/6 059), P=0.025). And 152 pairs of vessels were successfully matched. Multivariate Cox regression analysis identified in-stent restenosis lesions ( HR=2.59, 95% CI 1.28-5.23, P=0.008) as an independent risk factor for target vessel revascularization. Conclusions:Coronary lesions classified as functionally non-ischemic at baseline are not entirely stable and may progress to lesions that requiring revascularization over time. In-stent restenosis emerges as a critical independent predictor of revascularization.

Infectious diarrhea is a gastrointestinal infectious disease caused by a wide range of pathogens and found throughout the world. It is one of the most important public health problems in the world and the second leading cause of death among children under five years of age. The pathogens of infectious diarrhea include viral diarrhea pathogens, bacterial diarrhea pathogens, and parasites. Viruses are the most frequent pathogens, mainly including norovirus, rotavirus, astrovirus and sapovirus. The most frequently identified organisms causing bacterial diarrhea are diarrheagenic Escherichia coli, Salmonella, Shigella, Vibrio parahaemolyticus and Campylobacter. This paper provides an overview of the epidemiological trends and changes in the pathogen spectrum of infectious diarrhea for better understanding the distribution and epidemiological features of infectious diarrhea in China, and hopes to provide reference for developing prevention and control strategies and reducing the disease burden.

Objective:To explore the effects and mechanism of annexin A1 ( ANXA1)-overexpressing human adipose-derived mesenchymal stem cells (AMSCs) in the treatment of mice with acute respiratory distress syndrome (ARDS). Methods:The experimental study method was adopted. After the adult AMSCs were identified by flow cytometry, the 3 rd passage cells were selected for the follow-up experiments. According to the random number table (the same grouping method below), the cells were divided into ANXA1-overexpressing group transfected with plasmid containing RNA sequences of ANXA1 gene and no-load control group transfected with the corresponding no-load plasmid. The other cells were divided into ANXA1-knockdown group transfected with plasmid containing small interfering RNA sequences of ANXA1 gene and no-load control group transfected with the corresponding no-load plasmid. At post transfection hour (PTH) 72, the fluorescence expression was observed under a fluorescence microscope imaging system, and the protein and mRNA expressions of ANXA1 were detected by Western blotting and real-time fluorescence quantitative reverse transcription polymerase chain reaction respectively (with the sample numbers being 3). Fifty male C57BL/6J mice aged 6-8 weeks were divided into sham injury group, ARDS alone group, normal cell group, ANXA1-overexpressing group, and ANXA1-knockdown group, with 10 mice in each group. Mice in the last 4 groups were treated with endotoxin/lipopolysaccharide to make ARDS lung injury model, and mice in sham injury group were simulated to cause false injury. Immediately after injury, mice in sham injury group and ARDS alone group were injected with normal saline through the tail vein, while mice in normal cell group, ANXA1-overexpressing group, and ANXA1-knockdown group were injected with normal AMSCs, ANXA1-overexpressing AMSCs, and ANXA1-knockdown AMSCs, correspondingly. At post injection hour (PIH) 24, 5 mice in each group were selected, the Evans blue staining was performed to observe the gross staining of the right lung tissue, and the absorbance value of bronchoalveolar lavage fluid (BALF) supernatant of left lung was detected by microplate reader to evaluate the pulmonary vascular permeability. Three days after injection, the remaining 5 mice in each group were taken, the right lung tissue was collected for hematoxylin-eosin staining to observe the pathological changes and immunohistochemical staining to observe the CD11b and F4/80 positive macrophages, and the levels of tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), and IL-1β in BALF supernatant of left lung were determined by enzyme-linked immunosorbent assay. Data were statistically analyzed with paired sample t test, one-way analysis of variance, and least significant difference test. Results:At PTH 72, AMSCs in both ANXA1-overexpressing group and ANXA1-knockdown group expressed higher fluorescence intensity than AMSCs in corresponding no-load control group, respectively. At PTH 72, compared with those in corresponding no-load control group, the protein and mRNA expressions of ANXA1 in ANXA1-overexpressing group were significantly increased (wth t values of 249.80 and 6.56, respectively, P<0.05), while the protein and mRNA expressions of ANXA1 in ANXA1-knockdown group were significantly decreased (wth t values of 176.50 and 18.18, respectively, P<0.05). At PIH 24, compared with those in sham injury group (with the absorbance value of BALF supernatant being 0.041±0.009), the lung tissue of mice in ARDS alone group was obviously blue-stained and the absorbance value of BALF supernatant (0.126±0.022) was significantly increased ( P<0.05). Compared with those in ARDS alone group, the degree of blue-staining in lung tissue of mice was significantly reduced in normal cell group or ANXA1-overexpressing group, and the absorbance values of BALF supernatant (0.095±0.020 and 0.069±0.015) were significantly decreased ( P<0.05), but the degree of blue-staining in lung tissue and the absorbance value of BALF supernatant (0.109±0.016, P>0.05) of mice in ANXA1-knockdown group had no significant change. Compared with that in normal cell group, the absorbance value of BALF supernatant of mice in ANXA1-overexpressing group was significantly decreased ( P<0.05). Three days after injection, the lung tissue structure of mice in ARDS alone group was significantly damaged compared with that in sham injury group. Compared with those in ARDS alone group, hemorrhage, infiltration of inflammatory cells, alveolar collapse, and interstitial widening in the lung tissue of mice were significantly alleviated in normal cell group and ANXA1-overexpressing group, while no significant improvement of above-mentioned lung tissue manifestation was observed in ANXA1-knockdown group. Three days after injection, the numbers of CD11b and F4/80 positive macrophages in the lung tissue of mice in ARDS alone group were significantly increased compared with those in sham injury group. Compared with those in ARDS alone group, the numbers of CD11b and F4/80 positive macrophages in lung tissue of mice in normal cell group, ANXA1-overexpressing group, and ANXA1-knockdown group reduced, with the most significant reduction in ANXA1-overexpressing group. Three days after injection, compared with those in sham injury group, the levels of TNF-α, IL-6, and IL-1β in BALF supernatant of mice in ARDS alone group were significantly increased ( P<0.05). Compared with those in ARDS alone group, the levels of TNF-α, IL-6, and IL-1β in BALF supernatant of mice in normal cell group and ANXA1-overexpressing group, as well as the level of IL-1β in BALF supernatant of mice in ANXA1-knockdown group were significantly decreased ( P<0.05). Compared with that in normal cell group, the level of TNF-α in BALF supernatant of mice was significantly decreased in ANXA1-overexpressing group ( P<0.05) but significantly increased in ANXA1-knockdown group ( P<0.05). Conclusions:Overexpression of ANXA1 can optimize the efficacy of AMSCs in treating ARDS and enhance the effects of these cells in inhibiting inflammatory response and improving pulmonary vascular permeability, thereby alleviating lung injury of mice with ARDS.