Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a deadly disorder with poor therapeutic opportunities, driven by dysregulated immunity. Here we position monocyte-derived alveolar macrophages (Mo-AMs) as central mediators of ALI/ARDS pathogenesis, contrasting with homeostatic tissue-resident alveolar macrophages (TR-AMs). This review first traces the origin pathway of Mo-AMs, which differentiate from haematopoietic stem cells (HSCs) in the bone marrow and are recruited to the inflamed lung via a CCR2/CCL2-dependent pathway, ultimately differentiating into pathogenic effector cells within the alveolar microenvironment. Subsequently, we elucidate their primary pathogenic mechanisms: Mo-AMs mediate critical pathological injury by generating cytokine storms, depleting TR-AMs, disrupting the alveolar-capillary barrier and promoting fibrotic remodelling. Given their well-defined pathogenic role, Mo-AMs have emerged as a promising therapeutic target. Therefore, we conclude by reviewing recent advances in strategies targeting Mo-AMs, primarily encompassing the inhibition of their recruitment, induction of their apoptosis and reprogramming of their proinflammatory functions. These approaches collectively provide valuable insights for developing novel therapies for ALI/ARDS.

Objective:Severe hypothermia can precipitate acute lung injury(ALI)and may progress to acute respiratory distress syndrome(ARDS).Alveolar macrophage(AM)polarization plays a pivotal role in both the pathogenesis and resolution of ALI/ARDS.This study aimed to investigate alterations in AM polarization and to identify potential regulatory targets of macrophage polarization in severe hypothermia-induced ALI(SH-ALI).Methods:An SH-ALI rat model was established by immersion in 15 ℃ seawater for 5 h.Survival rate,inflammatory cytokine levels,lung histopathology,lung wet-to-dry weight ratio,and AM polarization status were assessed.RNA sequencing was performed to identify differentially expressed genes in bronchoalveolar lavage fluid-stimulated AMs from SH-ALI rats compared with normal AMs.Lipocalin-2(LCN2)was identified and validated as a differentially expressed gene in SH-ALI.The effects of LCN2 on macrophage polarization,survival rate,lung injury severity,and inflammatory factor levels were further evaluated.Results:SH-ALI was characterized by increased mortality,elevated inflammatory cytokine levels,marked inflammatory cell infiltration,aggravated pulmonary edema,and significant pulmonary parenchyma injury.An imbalance between M1 and M2 macrophage polarization was observed,with severe hypothermia promoting M1 polarization.LCN2 expression was significantly upregulated in SH-ALI rats.Downregulation of LCN2 suppressed M1 polarization and alleviated lung injury in SH-ALI in rats.Conclusion:Immersion in 15 ℃ seawater for 5 h successfully establishes an SH-ALI rat model.SH-ALI is associated with excessive M1 polarization,and LCN2 knockdown mitigates lung injury by inhibiting M1 polarization in SH-ALI rats.

This review aims to critically synthesize how Staphylococcus aureus (S. aureus) interacts with the vascular endothelium during invasive infection and to link endothelial pathogenic mechanisms with emerging therapeutic opportunities. We reviewed the literature on S. aureus virulence factors, endothelial barrier dysfunction, host immune amplification, complement modulation, immunothrombosis, antimicrobial resistance, and adjunctive therapeutic strategies. The evidence was organized according to functional virulence modules, biological stages of endothelial interaction, host-driven amplification pathways, and mechanism-linked therapeutic opportunities. S. aureus–induced endothelial injury arises from the convergence of bacterial virulence and host vascular responses. Adhesins and surface-associated proteins promote endothelial attachment and invasion; toxins disrupt membrane integrity, junctional stability, and immune homeostasis; and enzymes together with immune-evasion factors support dissemination and persistence. These bacterial mechanisms are amplified by complement activation and evasion, neutrophil extracellular traps, inflammasome signaling, immunothrombosis, and immunometabolic reprogramming, ultimately leading to vascular leakage, procoagulant conversion, impaired repair, and organ dysfunction. Evidence is strongest for selected adhesion pathways and α-haemolysin (Hla)-mediated endothelial barrier injury, whereas several host-amplification mechanisms are inferred from non-S. aureus inflammatory or sepsis models. Mechanistic understanding of S. aureus–endothelium interactions provides a rationale for adjunctive strategies beyond standard antimicrobial therapy, including anti-adhesion approaches, toxin neutralization, host-directed modulation of excessive inflammation and immunothrombosis, and candidate endothelial biomarker-guided risk stratification. However, most emerging strategies remain preclinical or lack prospective validation in well-defined S. aureus infection cohorts.

Uncontrolled inflammation and excessive M1 macrophage polarization are key drivers of acute lung injury (ALI). Scutellarin (SCU), a natural flavonoid compound, possesses anti-inflammatory activity, but its precise mechanism remains unclear. This study aimed to investigate whether SCU alleviates ALI by targeting guanine nucleotide-binding protein 2 (GBP2) and regulating alveolar macrophage polarization. A lipopolysaccharide (LPS)-induced ALI mouse model was used to evaluate the therapeutic effects of SCU. Macrophage polarization and lung injury severity were assessed histologically and by cytokine analysis. Transcriptomic profiling (RNA-seq) identified GBP2 as a candidate target. GBP2 was knocked down or overexpressed in MH-S cells to evaluate its role in LPS-induced polarization. Co-immunoprecipitation, molecular docking, and immunofluorescence were performed to confirm the interaction between GBP2 and STAT3. SCU pre-treatment significantly alleviated lung injury, reduced inflammatory cytokine levels, and improved the wet-to-dry lung weight ratio. It modulated macrophage polarization by downregulating LPS-induced M1 polarization in alveolar macrophages. Mechanistically, SCU downregulated GBP2 expression and suppressed activation of the JAK2/STAT3 signaling pathway in LPS-stimulated models. SCU ameliorates LPS-induced ALI by modulating alveolar macrophage polarization through inhibition of the GBP2/JAK2/STAT3 pathway. These findings suggest that SCU may serve as a potential therapeutic agent for ALI.

Hypothermia can cause acute lung injury (ALI). The pathogenetic mechanism of hypothermic ALI involves various proteins. Cold-inducible RNA-binding protein (CIRP) is secreted by macrophages or damaged cells and enhances the inflammatory response, resulting in tissue and organ damage. However, it is unclear whether CIRP participates in the development of hypothermic ALI; moreover, the expression pattern of CIRP and its mechanism of action in hypothermic ALI remain unelucidated. To address this issue, we established a stable, long-term seawater immersion-induced hypothermic ALI rat model. CIRP expression in the rat lung tissue was downregulated by adeno-associated virus (AAV) to determine the correlation between the expression of CIRP as well as its related signaling pathway proteins Nuclear factor-κB (NF-κB) and Triggering Receptor Expressed on Myeloid Cells-1 (TREM-1)and lung injury in a low-temperature ALI model. A long-term, seawater immersion-induced hypothermic ALI rat model was established by immersing the rats in seawater at 18°C for 24 h. As the seawater immersion time increased, the intensity of ALI worsened. CIRP levels in the lung tissue and serum of rats with hypothermic ALI significantly increased in a time-dependent manner; the levels gradually increased within 24 h and were positively correlated with the expression of inflammatory factors. CIRP knockdown in the rat lung tissue by using AAV significantly decreased the lung coefficient and injury score, reduced the levels of inflammatory factors, and attenuated the expression levels of TREM-1 and NF-κB. This finding suggests that CIRP exacerbates the inflammatory response in hypothermic ALI through TREM-1 and NF-κB-related signaling pathways. The present study revealed that CIRP expression increased in the lung tissue and serum of rats with hypothermic ALI in a time-dependent manner and showed a positive correlation with inflammatory factor release. Knockdown of CIRP expression in the rat lung tissue might reduce inflammation and alleviate lung injury by inhibiting TREM-1 and NF-κB signaling pathway proteins.

Alveolar macrophage (AM) polarization plays a pivotal role in the inflammatory response during acute lung injury (ALI). As reported previously, vasodilator-stimulated phosphoprotein (VASP) may function as an anti-inflammatory agent in hepatic tissues. However, the specific role of VASP in ALI-induced macrophage polarization remains unclear. To elucidate the role of VASP in ALI, we established a lipopolysaccharide (LPS)-induced M1 polarization model of MH-S cells. RNA sequencing was performed to identify differentially expressed genes during macrophage polarization. The results revealed significant upregulation of the VASP gene. Subsequently, VASP gene knockdown in the lungs was achieved by intratracheal delivery of VASP-AAV6, and the resulting ALI symptoms and macrophage polarization were assessed. The VASP gene was also knocked down in MH-S cells; these cells were then stimulated with LPS for 24 h, and polarization-related markers of macrophages were analyzed. Finally, to validate the involvement of the PKG-VASP signaling pathway, experiments were conducted with a PKG agonist (8-Br-cGMP) and inhibitor (KT5823), and the effects of modulating the PKG-VASP pathway on macrophage polarization were investigated. VASP knockdown notably ameliorated ALI symptoms in these mice with LPS-induced ALI. Additionally, in vitro experiments showed that the PKG-VASP signaling pathway plays a pivotal role in macrophage polarization. VASP knockdown protected mice from LPS-induced ALI by inhibiting M1 polarization, and its protective effects were partially mediated by the cGMP-PKG signaling pathway.

背景 海上遇难者落水后常死于海水长时间浸泡后的低体温及相关并发症,肺是低体温损伤的重要器官之一,但目前针对低体温造成急性肺损伤(acute lung injury,ALI)的研究相对匮乏.目的 探讨冷诱导RNA结合蛋白(cold-inducible RNA-binding protein,CIRP)在低体温性ALI大鼠模型中的变化及其可能的作用机制.方法 将 40只雄性成年SD大鼠随机分为 0h组(0 h,8只)和实验组(32只).实验组分别用低温海水浸泡 12 h、16 h、20 h、24 h(每组 8只),构建低体温性ALI动物模型.ELISA检测白细胞介素-6(interleukin-6,IL-6)、IL-1β、细胞外CIRP的含量,对肺组织进行HE染色、TUNEL染色和CIRP免疫组织化学染色,qRT-PCR检测CIRP mRNA的表达.结果 与 0h组相比,实验组出现不同程度肺损伤,病理切片可见肺泡壁增厚或结构破坏,肺泡腔内出血,伴中性粒细胞和淋巴细胞浸润等;16 h、20 h、24 h实验组血清中IL-6的表达显著增加,20 h、24 h实验组血清中IL-1β表达显著增加,差异均有统计学意义(P＜0.01);各实验组大鼠血清中CIRP表达增加均有统计学差异(12 h、16 h、20 h组,P＜0.05;24 h组,P＜0.01).TUNEL结果显示,各实验组的大鼠肺组织出现不同程度的细胞凋亡现象(P＜0.01);通过炎症因子的表达水平、肺组织病理改变以及细胞凋亡情况选择低温海水浸泡 24h为最佳构建模型时间,免疫组织化学染色和qRT-PCR观察到 24h组肺组织内CIRP的表达增加.结论 肺组织和外周血清的CIRP在低体温性ALI大鼠模型中随时间延长而表达增高,提示其可能与低体温致ALI相关,同时与炎症因子IL-1β、IL-6水平呈现一致性趋势变化,因此推测CIRP可能通过促进炎症因子释放发挥作用,本研究初步证实了CIRP在肺组织区域和整体与低体温ALI的相关性.

背景 烟雾吸入性损伤后期研究较少,且后期是否发生肺纤维化仍存在争议,建立不同烟雾吸入性肺损伤动物模型,评估损伤后期肺纤维情况,对研究烟雾吸入致伤机制有重要意义.目的 建立重复烟雾吸入性肺损伤大鼠模型,探讨其肺纤维化情况.方法 将健康成年雄性SD大鼠随机分为4组,每组30只.其中A组为空白对照,B组烟雾吸入1次(1次/d×1 d,15 min/次),C组烟雾吸入3次(1次/d×3 d,15 min/次),D组烟雾吸入7次(1次/d×7 d,15 min/次).烟雾吸入各组分别于吸入完成后第1天、第7天和第28天采集大鼠肺组织标本,检测炎性指标、血气分析、湿干比和肺组织病理染色.结果 A组大鼠无死亡,B、C和D组烟雾吸入后分别死亡4只、7只和10只.与A组相比,B组第1天肺组织湿干比升高,白细胞介素-6和肿瘤坏死因子升高,碳氧血红蛋白(carboxyhemoglobin,COHb)升高,动脉血氧分压(PaO2)下降.B组病理染色示肺泡结构弥漫性破坏,肺泡腔内可见红细胞、白细胞浸润,肺泡间隔增厚,炎细胞浸润明显,第7天时各指标较第1天好转,第28天部分指标恢复正常,Masson染色无明显胶原纤维沉积.与B组相比,C组和D组湿干比、炎性指标、COHb有升高趋势,特别是第28天Masson染色出现明显蓝色胶原纤维沉积.结论 重复烟雾吸入可以导致肺组织更明显的炎性反应,肺损伤程度增加,特别是后期可出现更明显的肺组织纤维化.

Hand, foot and mouth disease was mainly caused by EV-A71 virus. The main antigen structure of VP1 region of EV-A71 was easily varied. Here, we investigated the seroprevalence of EV-A71 based on a large group of healthy individuals in Beijing, China, in order to study the effectiveness of EV-A71 vaccine in a real-world setting. BrCr and the clinical strain isolated from the Chinese mainland in 2008 ("vaccine strain:"CMU4232/BJ/CHN/2008), EV-A71 C4 epidemic strains isolated in 2010, 2013, and 2016, were tested for neutralizing antibodies (NtAb) in every year. Phylogenetic tree analysis of the EV-A71 strains above, as well as amino acid composition homologous sequence analysis were applied. The "vaccine strain" has 83.0% homology with FY23, H07 and FY7VP5. It belongs to the same branch of C4a as 10 C4, 13 C4 and 16 C4, and differs from the amino acid sites 283 and 293 of 16 C4. Compared with "vaccine strains," there was a significant difference between the 50-59 years old age group when the NtAb titer of 16 C4 strain was 1:512-1:1024. Our results suggest that changes in the functional epitopes of NtAb caused by amino acid 283 and 293 loci in EV-A71 strains may affect the production of neutralizing antibodies.

目的 了解基质辅助激光解吸电离飞行时间质谱(MALDI-TOF MS)联合HB&L微生物培养系统(简称HB&L系统)在人工关节置换术后病原菌快速鉴定中的价值.方法 收集104例人工关节置换术后患者关节液样本,分别接种于血培养瓶及常规培养琼脂平板,将阳性培养物分别进行2种直接MALDI-TOF MS鉴定、常规MALDI-TOF MS鉴定和平板培养鉴定,比较4种方法鉴定结果及鉴定时间.结果 直接和常规MALDI-TOF MS均检测到84.8％(84/99)的阳性结果,但平板培养仅检测到60.6％(60/99)的阳性结果.HB&L系统处理后直接MALDI-TOF MS鉴定革兰阳性菌和革兰阴性菌,检出率分别为86.9％和91.9％,高于分离胶富集细菌后直接MALDI-TOF MS(78.3％和83.8％)和平板培养(70.1％和67.6％).HB&L系统处理后直接MALDI-TOF MS鉴定的阳性结果中,金黄色葡萄球菌、表皮葡萄球菌、大肠埃希菌和肺炎克雷伯菌检出率较高.HB&L系统处理后直接MALDI-TOF MS的鉴定时间为5～14 h,低于常规MALDI-TOF MS(45.2 h)和平板培养(54.3 h).结论 与常规培养比较,HB&L系统处理后直接MALDI-TOF MS鉴定病原菌用时短,且具有一定的准确率,对人工关节置换术后病原菌的快速诊断有一定价值.

目的 评估一种新的快速检测血流感染革兰阳性球菌的方法,并评价其鉴定和药敏的准确性.方法 收集中国人民解放军总医院第六医学中心门诊及住院患者141例革兰阳性球菌血培养阳性样本,应用激光散射技术联合基质辅助激光解吸/电离飞行时间质谱(matrix assisted laser desorption ionization time of flight mass spectrom-etry,MALDI-TOF MS)对其进行快速直接鉴定,同时联合VITEK 2 Compact微生物仪进行直接快速药敏试验(简称快速直接法),并与常规方法比较,对快速直接法的鉴定率、药敏的分类一致性(categorical agreement,CA)和错误率进行分析.结果 快速直接法对革兰阳性球菌鉴定率为93.6％,其中葡萄球菌属91.8％,肠球菌属94.1％,链球菌属100.0％.金黄色葡萄球菌无错误,凝固酶阴性葡萄球菌在一般错误(minor errors,MIE)中3例、严重错误(major er-rors,ME)中5例和极严重错误(very major error,VME)中2例;屎肠球菌在MIE中3例,粪肠球菌在MIE中1例.在85株葡萄球菌中,快速直接法检测头孢西丁阴性一致率为100％(16/16),阳性一致率为97.1％(67/69),总体一致率为97.6％(83/85);检测诱导克林霉素耐药阴性一致率为92.2％(47/51),阳性一致率为94.1％(32/34),总体一致率为92.9％(79/85).结论 基于激光散射技术联合MALDI-TOF MS和VITEK 2 Compact,能够快速准确得到鉴定和药敏结果,有助于血流感染快速诊断.

目的 评价HB&L微生物培养体系对血培养阳性标本病原菌短期继代培养后,直接鉴定和药敏试验的准确性和时效性,为血流感染快速诊断提供新方法.方法 收集2020年1-12月解放军总医院第六医学中心经常规方法鉴定的113份单一细菌的革兰阴性菌,置于HB&L微生物培养体系继代培养并前处理后直接MALDI-TOF MS鉴定和Vitek-2 Compact系统药敏试验,结果以常规方法为参考.结果 在113株革兰阴性菌中,鉴定到菌种的肠杆菌科和非发酵菌科分别占76.99％ (87/113)和22.12％ (25/113).HB&L微生物培养体系增菌所需时间在6h之内,2～3 h居多.HB&L微生物培养体系药敏试验标准符合率为96.01％,错误率分别为0.06％VME(1/1578),0.95％ ME(15/1578),2.98％ MIE(47/1578),均在标准要求内.结论 HB&L微生物培养体系能短期继代培养后直接快速细菌鉴定和药敏,且操作简单,成本适当,能快速准确地诊断血流感染并提供药敏结果,为临床抢先治疗提供依据.

Objective:To evaluate the identification rate of separating gel or HB&L pretreatment methods of MALDI-TOF-MS, thereby to provide a new idea for the rapid and accurate identification of pathogens of bloodstream infections in daily clinic practice.Methods:A total of 149 alarmed positive blood culture samples of single bacterial infection by routine laboratory methods were collected between January to December 2020 from the Sixth Medical Center, Chinese PLA General Hospital. Samples were pretreated with the separation gel accelerating tube method or the HB&L microbial culture system, followed by direct MALDI-TOF MS bacterial identification, the identification rates of the two pretreatment methods were compared and results from the traditional method were used as the standard control.Results:Among the 149 positive blood culture samples, 47.0% (70/149) were gram-negative (G -) bacteria and 53.0% (79/149) were gram-positive (G +) bacteria. Identification rate of G -strain level was 78.6% (55/70) by serum separation gel coagulation tube method and 91.4% (64/70) by HB&L microbial culture system, the difference was statistically significant ( P=0.033). Identification rate of G +strain levels was 73.4% (58/79) by serum separation gel coagulation tube method and 87.3% (69/79) by HB&L microbial culture system, the difference was statistically significant ( P=0.028). For G -bacteria in the range of 3.000-2.300, the identification rate was 22.9% (16/70) by serum separation gel accelerating tube method and 38.6% (27/70) by the HB&L microbial culture system, the difference was statistically significant ( P=0.044). For G +bacteria in the range of 3.000-2.300, the identification rate was 19.0% (15/79) by serum separation gel accelerating tube method and 34.2% (27/79) by the HB&L microbial culture system, the difference was statistically significant ( P=0.031). Conclusion:The identification rate of HB&L microbial culture system is higher than that of serum separation gel coagulation tube method. Direct MALDI-TOF MS identification of pathogenic bacteria in positive blood culture samples after pretreatment is feasible in daily clinical practice.

Objective To compare the consistency and accuracy between rapid direct detection method (rapid method) and traditional detection method (traditional method) for bacterial identification and drug sensitivity test of positive blood culture specimens. Methods The bloodstream infection specimens of the outpatients, emergency patients and inpatients of the Chinese PLA General Hospital from 2019 to 2020 were collected and placed in a blood culture apparatus. After the blood culture alarm, positive blood culture specimens were collected. At the same time, the rapid method and the traditional method were used for culture. After culture, bacteria identification and drug susceptibility test were conducted respectively, and the consistency of bacteria identification and drug susceptibility test between the two methods was recorded and compared. Results Among the 149 positive blood specimens from patients with bloodstream infection, 79 strains of Gram-positive cocci and 70 strains of Gram-negative bacilli were identified by traditional method; 75 strains of Gram-positive cocci and 67 strains of Gram-negative bacilli were identified by the rapid method. Compared with the traditional method, the overall coincidence rate of the rapid method in identify bacteria was 95.3%(142/149), among which the coincidence rate of Gram-positive cocci was 94.9%(75/79), and that of Gram-negative bacilli was 95.7%(67/70). In the traditional method, 76 strains (96.2%) of Gram-positive cocci and 66 strains (94.3%) of Gram-negative bacteria can effectively identify their species; 3 strains (3.8%) of Gram-positive cocci and 4 strains (5.7%) of Gram-negative bacilli could effectively identify their genera. In the rapid method, 52 strains (69.3%) of Gram-positive cocci and 63 strains (94.0%) of Gram-negative bacilli could effectively identify their species, 20 strains (26.7%) of Gram-positive cocci and 3 strains (4.5%) of Gram-negative bacilli could effectively identify their genera. According to the criteria of drug sensitivity test results, the coincidence rates between the rapid method and the traditional method for drug sensitivity test of Gram-positive cocci and Gram-negative bacilli were more than or equal to 90.0%, the general error rates were less than 10.0%, the serious error rates were less than 3.0% except compound sulfamethoxazole, and the extremely serious error rates were less than 1.5%. Conclusion The rapid method can effectively shorten the time of identification and drug sensitivity test, and the identification results are accurate. It is helpful for clinicians to make a clear diagnosis and adjust the treatment plan in time, quickly shift from empirical use of broad-spectrum antibiotics to targeted treatment, and provide more effective treatment plan for patients. DOI: 10.11855/j.issn.0577-7402.2021.05.07

目的 探讨荧光染色法在真菌镜检中的应用价值.方法 收集350例不同来源的临床标本,直接涂片后分别进行革兰染色和荧光染色镜检,同时接种沙保罗培养基进行真菌培养鉴定,3种方法任意一种为阳性,则认为该标本为真菌检测阳性,并以此为标准来计算3种方法的检出率、灵敏度和阴性预测值,应用χ2检验评价3种方法的差异.结果 350例临床标本应用荧光染色法、革兰染色法和真菌培养鉴定法的检出率分别为53.4％、11.4％和43.4％,灵敏度分别为86.6％、18.5％和70.4％,阴性预测值分别为82.2％,43.2％和67.7％,各组数据比较,差异均有统计学意义(P<0.05).结论 荧光染色法在真菌检测中显示出一定的优势,值得推广应用.

目的 建立海洋细菌基质辅助激光解吸电离飞行时间质谱鉴定数据库,为海洋细菌引起各类感染的病原快速鉴定提供支持.方法 本中心课题组2006-2016年收集国内外6个海域158个采样点海洋细菌530株,分离培养后进行细菌16srDNA扩增测序,应用FlexControl软件收集蛋白谱图,Biotyper软件构建评价数据库.分别用仪器商品化数据库、自建数据库和扩展数据库进行菌种鉴定,比较各数据库的鉴定差异.结果 自建本地化海洋细菌鉴定数据库包含32个菌属,82个菌种,共计421株海洋细菌谱图.以16srDNA测序鉴定结果 为金标准,验证菌株用商品化数据库鉴定时正确80株,鉴定正确率80.8％,用扩展数据库鉴定时正确97株,鉴定正确率98.0％,差异有统计学意义(P<0.001).结论 自建海洋细菌鉴定数据库菌株的鉴定能力较商品化数据库更强,有助于海洋细菌引起相关感染的诊断和治疗.

Objective To investigate the effects of the transplantation of autologous and allogeneic adipose-derived mesenchymal stem cells (ADMSCs) on the cardiac function in rats with acute myocardial infarction (AMI). Methods Firstly, ADMSCs were isolated from BN and Lewis rats, and the third generation were labeled with CM-DiI. Then 45 male Lewis rats were randomly divided into 3 groups (control group, autologous cell transplantation group, and allogeneic cell transplantation group). The AMI model was established by ligating the rats' left anterior descending artery, and then the infarcted myocardium as well as the peripheral parts was injected by the labeled ADMSCs via the endocardium. At 7 days after ADMSC transplantation, the infiltration of CD4+ T lymphocytes, CD8+ T lymphocytes and CD68+ macrophages were detected by immunofluorescence technique. At 7, 14 and 28 days after transplantation, survival rate of the transplanted cells was compared. Then echocardiography was used to detect the rats' cardiac function at 28 days after transplantation. And the expression of α-smooth muscle actin (α-SMA) was detected by immunofluorescence technique for determining the angiogenesis near the transplanted cells. Results The positive rate of the cells labeled with CM-DiI was nearly 100%. At 7 days after transplantation, lymphocyte infiltration and macrophages were observed around the transplanted cells in the allogeneic cell transplantation group. No lymphocyte infiltration and macrophages were observed in the autologous cell transplantation group. Compared with allogeneic cell transplantation, the survival rate of the transplanted cells increased significantly. Moreover, the left ventricular short axis shortening rate (LVFS) and the diastolic left ventricular anterior wall thickness (LVAWTd) increased at 7, 14 and 28 days after transplantation. Meanwhile, the number of angiogenesis around the infarcted myocardium also significantly increased. Conclusion Autologous ADMSC transplantation is significantly better at improving cardiac function in AMI rats than allogeneic ADMSC transplantation.