Trained immunity represents a paradigm shift in immunology, wherein innate immune cells acquire antigen-agnostic memory through epigenetic and metabolic reprogramming, enabling enhanced responses to secondary challenges. However, conventional trained immunity inducers have limitations including poor targeting, transient efficacy and systemic toxicity. Engineered nanoformulations including polymeric nanoparticles, inorganic carriers and nanovesicles can enhance inducer bioavailability, and prolong tissue retention. And it can achieve precise delivery to hematopoietic organs (bone marrow, spleen) or specific immune cells (macrophages, dendritic cells), amplifying trained immunity while mitigating off-target effects. Therapeutically, nano-optimized inducers demonstrate significant efficacy across pathologies including oncology, sepsis, autoimmune diseases and so on. In this article, we review the latest progress of nanomaterials-mediated trained immunity and its application in disease treatment. We focus on different nanomaterials used as specific training immune inducers. Subsequently, we describe the applications of nanomaterials-based trained immunity in different diseases. Finally, we look forward to the key challenges faced by nanomaterials-based training immunity and the directions for future development.

Biofilms are the root of most chronic and persistent infections and pose a significant threat to human health. Reactive oxygen species (ROS) generation platforms have been used to combat biofilm‐associated infections. However, biofilm microenvironments (BME) such as hypoxia and overexpressed antioxidants restrict the efficacy of ROS‐based therapies. To address the problem, this study incorporates calcium peroxide (CaO 2 ) and berberine (BBR) into Fe and Zn containing bimetal metal–organic frameworks (FZ) to construct a composite ROS nanogenerator (CBFZ), which is able to remodel BME and further promotes ROS generation for enhance biofilm eradication. CBFZ degrades to release CaO 2 , Fe 3+ , Fe 2+, and BBR in biofilm, where CaO 2 decomposes into O 2 and H 2 O 2 to relieve hypoxia, and Fe 3+ consumes glutathione (GSH). Subsequently, the remodeled BME boosts the ROS production of the O 2 ‐dependent BBR‐mediated photodynamic therapy and H 2 O 2 ‐dependent Fe 2+ ‐based chemodynamic therapy, and the depleted GSH minimizes ROS scavenging in the meantime, ultimately maintaining a high level of ROS in biofilm. It is demonstrated that CBFZ can effectively eradicate biofilm by killing the embedded bacteria and dispersing the biofilm matrix. Moreover, CBFZ exhibits an outstanding therapeutic effect in a murine model with subcutaneous biofilm infection. Overall, this work offers a propagable strategy to enhance ROS‐based antibiofilm therapy.

Computer aided environment design technology, also known as Computer aided environment (CAE) technology, is a technology that utilizes computers for engineering design, analysis, and optimization. Simulation data refers to the data generated by simulating the real environment or system in a computer, with its core characteristics of simulation and predictability, used for performance evaluation. CAE technology simulates the state and behavior of buildings, facilities, or environments, evaluating the effectiveness of design solutions and predicting performance through simulation data. This article aims to conduct a technical analysis and practical case studies to evaluate the effectiveness, draw conclusions and suggestions from the technical analysis, in order to promote the development of computer-aided environmental design technology and improve the efficiency and quality of environmental design. Therefore, this article uses CAE technology to simulate the thermal performance, structural response, and fluid dynamics changes of buildings. This article simulates the temperature environment of rooms in buildings and the pedestrian density and traffic flow in traffic through experimental simulation and data comparison. It is found that the peak pedestrian density occurs at 16 and 17 minutes, and the lowest value is at 45 minutes. There is a certain similarity between the data results and the real data.

心电图显示ST段抬高的患者,结合典型临床症状及实验室检查,可诊断为心肌梗死,但仍有部分患者虽符合以上标准,冠状动脉(下称冠脉)造影或其他相关检查却不支持心肌梗死,如心室早复极、应激性心肌病、肥厚型心肌病、肺动脉栓塞、Brugada波、急性心包炎、重症心肌炎等.本研究收集 2021年11月至2023年9月义乌市中心医院非心肌梗死心电图ST段抬高患者6例,结合临床病史、超声心动图、冠脉造影、实验室检查等进行分析,探讨 6例患者心电图特征动态演变规律及ST段抬高的病因.临床医生应熟悉各种类型ST段抬高心电图改变,结合临床指标,仔细鉴别,减少误诊或漏诊.

肺炎鏈球菌會潛伏在人類鼻咽部並引起疾病，常見的感染包括中耳炎、鼻竇炎和肺炎。肺炎鏈球菌有時會造成侵襲性肺炎鏈球菌感染症，尤其是在高危險族群的病人。肺炎鏈球菌疫苗被認為是預防感染最有效的方法，目前台灣臨床上可供使用的有1種多醣體疫苗PPV 23和2種結合型疫苗PCV13及PCV15。高危險族群可依照疾病管制署之肺炎鏈球菌疫苗接種建議，接受預防注射以保護自己不受肺炎鏈球菌感染。除此之外，流感感染後的繼發性細菌感染，最常見的菌種之一即為肺炎鏈球菌，因此每年接種流感疫苗亦是重要的預防方法。 Streptococcus pneumoniae bacteria are common inhabitants of the respiratory tract and can cause various diseases, including otitis media, sinusitis, and pneumonia. S. pneumoniae bacteria also cause invasive pneumococcal disease, especially in high-risk groups, and vaccines are regarded as the most effective method for preventing pneumococcal infection. The pneumococcal vaccines currently available in Taiwan are PPV 23, which is a pneumococcal polysaccharide vaccine, and PCV13 and PCV15, which are pneumococcal conjugate vaccines. High-risk groups should follow the vaccine recommendations of the Taiwan Centers for Disease Control to obtain protection from pneumococcal infections. S. pneumoniae is the most identified pathogen in patients with secondary bacterial infection following a primary influenza virus infection. Consequently, annual influenza vaccination is crucial for preventing pneumococcal infections.

Abstract Background Inhibition of glutathione (GSH) synthesis in cancer cells considerably improves the efficacy of reactive oxygen species (ROS)‐related tumor therapy. Self‐assembled peptide derivatives can facilitate the efficient delivery and accumulation of small molecular drugs in cancer cells. Methods Self‐assembling modules were covalently linked to the GSH‐biosynthesis inhibitor l‐buthionine sulfoximine (BSO) by solid‐phase synthesis to form the self‐assembling peptide derivative Nap‐DFDFpY‐GG‐BSO (Nano‐BSO@ in situ). Subsequently, its enzyme‐instructed self‐assembly in vitro and on cell surfaces were confirmed, and its intracellular GSH depletion and radiotherapy‐sensitizing effects were determined. Results Nano‐BSO@ in situ successfully self‐assembles into a hydrogel with a nanofibrous microstructure upon incubation with alkaline phosphatase (ALP) at a critical concentration of 9.84 μM. Furthermore, it selectively self‐assembles in situ on HeLa cells with high ALP expression. At a concentration of 50 μM, Nano‐BSO@ in situ decreases intracellular GSH levels by 80%, ∼2.3 times more than free BSO. Meanwhile, pretreatment of HeLa cells with 50 μM Nano‐BSO@ in situ for 24 h results in a radiotherapy sensitization enhancement ratio to γ‐rays of 2.09. Conclusions A novel in situ self‐assembling peptide derivative for GSH depletion and selective enhancement of tumor radiotherapy was constructed. The excellent GSH‐depletion ability and remarkable radiotherapy‐enhancement performance indicate that Nano‐BSO@ in situ is a promising selective sensitizer for ROS‐related treatment of tumor cells with high ALP expression.

目的 研究丁苯酞修饰新型自组装短肽(NBP-SAP)对氧化低密度脂蛋白(ox-LDL)损伤血管内皮细胞的影响及与信号通路关系.方法 体外培养人脐静脉内皮细胞(HUVECs)并分为NBP-SAP+LY组、NBP-SAP组、ox-LDL组和对照组,分别给予NBP-SAP+LY450139+ox-LDL、NBP-SAP+ox-LDL、ox-LDL及对照处理.Realtime-qPCR法检测不同措施处理后HUVECs中血管内皮生长因子(VEGF)/血管内皮生长因子受体-2(VEGFR-2)-Notch1/DLL4通路相关基因表达,Western blot法检测VEGF/VEGFR2-Notch1、DLL4通路相关蛋白表达量,CCK-8法、Annexin-V/PI双染法、Transwell法分别检测各组细胞活力、细胞凋亡率及细胞侵袭力等.结果 NBP-SAP组较ox-LDL组48 h细胞活力及细胞侵袭力增强,细胞凋亡率下降(t分别=3.59、2.91、2.44,P均<0.05),VEGFR-2、B淋巴细胞瘤-2(Bcl-2)蛋白表达量上调(t分别=12.57、14.49,P均<0.05),Notch1、Bax蛋白表达量和DLL4、Notch1、Bax基因mRNA表达下调(t分别=11.30、12.41、13.08、13.16、6.96,P均<0.05).NBP-SAP+LY组较NBP-SAP组48 h时改善损伤细胞活力、侵袭力的作用减弱,细胞凋亡率升高(t分别=4.38、3.92、4.07,P均<0.05),Notch1、Bax的蛋白表达量上调(t分别=8.59、20.18,P均<0.05),VEGFR-2、Bcl-2蛋白表达量和VEGF、VEGFR-2、Bcl-2基因mRNA表达下调(t分别=14.18、11.23、12.96、19.93、20.33,P均<0.05).结论 NBP-SAP能够激活VEGF/VEGFR2-Notch1/DLL4信号通路,减轻ox-LDL损伤血管内皮细胞的作用.

We performed a meta-analysis to evaluate the effect of prophylactic sacral protective dressings on preventing pressure injury. A systematic literature search up to July 2021 was performed, and 11 studies included 5150 community or hospital-based adult subjects requiring care at the start of the study; 2832 of them were using sacral protective dressings and 2318 were given standard care with no sacral protective dressings. They were reporting relationships between the effects of prophylactic sacral protective dressings on preventing pressure injury. We calculated the odds ratio (OR) with 95% confidence intervals (CIs) to assess the effects of prophylactic sacral protective dressings on preventing pressure injury using the dichotomous method with a random or fixed-effect model. Sacral protective dressings had a significantly lower incidence of pressure injuries (OR, 0.39; 95% CI, 0.28-0.53, P < .001) compared with standard care with no sacral protective dressings in community- or hospital-based adult subjects requiring care. Sacral protective dressings had a significantly lower incidence of pressure injuries compared with standard care with no sacral protective dressings in community- or hospital-based adult subjects requiring care. Further studies are needed to confirm these findings.

Abstract In the current study, via applying the mixed-ligand method, a new metal-organic framework (MOF) containing Tb was hydrothermally synthesized and characterized; its chemical formula is {[Tb(dpc)(H2O)2]·(Hbibp)0.5} n (1, in which bibp = 4,4′-bis(imidazolyl) biphenyl and H4dpc = 2-(3′,4′-dicarboxylphenoxy) isophthalic acid). The as-produced 1 reveals significant sensitivity and remarkable selectivity for the detection of PO4 3– as a kind of easy-to-use fluorescent probe having extensive range of detection, rapid response, and low limit of detection. The Mycobacterium tuberculosis bacterial burdens were measured with the spread plate method. In addition to this, real time RT-PCR was implemented for the evaluation of the survival genes relative expression levels in the Mycobacterium tuberculosis. The carboxyl-rich metal complex was further evaluated by molecular docking simulation which confirmed that multiple binding interactions were formed with active sites from the target protein. GRAPHICAL ABSTRACT

In the current study, via applying the mixed-ligand method, a new metal-organic framework (MOF) containing Tb was hydrothermally synthesized and characterized; its chemical formula is {[Tb(dpc)(H2O)(2)]center dot(Hbibp)(0.5)}(n) (1, in which bibp = 4,4 '-bis(imidazolyl) biphenyl and H(4)dpc = 2-(3 ',4 '-dicarboxylphenoxy) isophthalic acid). The as-produced 1 reveals significant sensitivity and remarkable selectivity for the detection of PO43- as a kind of easy-to-use fluorescent probe having extensive range of detection, rapid response, and low limit of detection. The Mycobacterium tuberculosis bacterial burdens were measured with the spread plate method. In addition to this, real time RT-PCR was implemented for the evaluation of the survival genes relative expression levels in the Mycobacterium tuberculosis. The carboxyl-rich metal complex was further evaluated by molecular docking simulation which confirmed that multiple binding interactions were formed with active sites from the target protein.

Background Circular RNAs (circRNAs) play critical roles in the development of atherosclerosis (AS). This study investigated the role of circMTO1 in the progression of AS. Methods Serum samples from AS patients and healthy volunteers and vascular smooth muscle cells (VSMCs) were used as the study materials. The expressions of circMTO1 and miR-182-5p were measured by RT-qPCR. The effects of circMTO1, miR-182-5p, and RASA1 on VSMC proliferation and apoptosis were examined by MTT and BrdU assays and wound healing and flow cytometric analyses, respectively. Downstream target genes of circMTO1 and miR-182-5p were predicted using target gene prediction and screening and confirmed using a luciferase reporter assay. RASA1 expression was detected by RT-qPCR and Western blot. Results circMTO1 expression was decreased, while miR-182-5p expression was increased in human AS sera and oxidized low-density lipoprotein (ox-LDL)-stimulated VSMCs. CircMTO1 overexpression inhibited the proliferation and promoted the apoptosis of ox-LDL-stimulated VSMCs. CircMTO1 was found to be served as a sponge of miR-182-5p and RASA1 as a target of miR-182-5p. Moreover, circMTO1 acted as a ceRNA of miR-182-5p to enhance RASA1 expression. Furthermore, miR-182-5p overexpression and RASA1 knockdown reversed the effects of circMTO1 overexpression on the proliferation, migration, and apoptosis of ox-LDL-stimulated VSMCs. Conclusion CircMTO1 inhibited the proliferation and promoted the apoptosis of ox-LDL-stimulated VSMCs by regulating miR-182-5p/RASA1 axis. These results suggest that circMTO1 has potential in AS treatment.

目的 探讨他汀基团修饰的新型自组装短肽(statins-SAP)对氧化低密度脂蛋白(ox-LDL)诱导血管内皮细胞损伤的保护效应及分子机制.方法 将人脐静脉内皮细胞分为5组并给予含不同试剂的DMEM完全培养基培养:对照组(磷酸盐缓冲液)、ox-LDL组(200 mg/L ox-LDL)、洛伐他汀组(200 mg/L ox-LDL+10 mg/L洛伐他汀原料药)、statins-SAP组(200 mg/L ox-LDL+150 mg/L statins-SAP)、信号通路组(200 mg/L ox-LDL+150 mg/L statins-SAP+25μmol/L信号通路抑制剂LY450139).检测并比较各实验组细胞活力、细胞迁移能力、细胞凋亡率、血管内皮生长因子(VEGF)/Notch通路基因表达、凋亡基因蛋白表达等.结果 与洛伐他汀组比较,statins-SAP组能明显改善ox-LDL对细胞造成的损伤,细胞活力及细胞迁移能力均明显增强(均P<0.05).各实验组细胞中B淋巴细胞瘤-2(Bcl-2)、VEGF、血管内皮生长因子受体2(VEGFR-2)基因相对表达量和Bcl-2、VEGFR-2的蛋白相对表达量比较,ox-LDL组低于对照组(均P<0.05),statins-SAP组高于ox-LDL组和信号通路组(均P<0.05).各实验组细胞中Bax、Notch1、DLL4基因相对表达量和Bax、Notch1的蛋白相对表达量比较,ox-LDL组高于对照组(均P<0.05),statins-SAP组低于ox-LDL组和信号通路组(均P<0.05).结论 statins-SAP通过激活VEGF/Notch信号通路减轻ox-LDL诱导的血管内皮细胞损伤.

Studies have shown that long non-coding RNAs (lncRNA) play critical roles in coronary atherosclerotic heart disease (CAD). However, the function of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in CAD is unclear. In this study, we aimed to investigate the functions of lncRNA NEAT1 in CAD. RT-PCR and western blot analysis were carried out to examine the expressions of related RNAs. Colony formation assay, cell proliferation assay, apoptosis assay, and dual-luciferase reporter assay were conducted to investigate the abilities of colony migration, cell proliferation, apoptosis, and targeting. The results showed that NEAT1 was up-regulated in CAD blood samples and in human coronary endothelial cells (HCAECs). Transfection of pcNEAT1 significantly inhibited the survival rate of HCAECs and induced apoptosis of HCAECs. MiR-140-3p was down-regulated in HCAECs. NEAT1 directly targeted miR-140-3p, and the expression of miR-140-3p was inversely correlated with the expression of NEAT1 in CAD patients. In addition, co-transfection of NEAT1 with miR-140-3p mimic reversed the effect of pcNEAT1 on cell viability and apoptosis. mitogen-activated protein kinase 1 (MAPK1) was proved to be a target gene of miR-140-3p, and the miR-140-3p mimic was shown to reduce the expression of MAPK1 in HCAECs. pcNEAT1 significantly increased the expression level of MAPK1, while shNEAT1 significantly reduced the expression level of MAPK1. Our results revealed that lncRNA NEAT1 increased cell viability and inhibited CAD cell apoptosis possibly by activating the miR-140-3p/MAPK1 pathway, and lncRNA NEAT1 might serve as a potential therapeutic target for CAD.

Atherosclerosis (AS) is a common vascular disease, which can cause apoptosis of vascular endothelial cells. Notoginsenoside R1 (NGR1) is considered an anti-AS drug. MicroRNAs (miRNAs) are believed to play a vital role in cell apoptosis and angiogenesis. This study aimed to explore the mechanism of NGR1 for treating AS through miRNAs. Flow cytometry was used to detect the apoptosis rate. The levels of inflammatory cytokines interleukin (IL)-6 and IL-1β were detected using ELISA. Reactive oxygen species (ROS) and malondialdehyde (MDA) levels were measured using corresponding assay kits. Quantitative real-time polymerase chain reaction (qRT-PCR) assay was performed to detect miR-221-3p expression. Dual-luciferase reporter and RNA immunoprecipitation assays were carried out to examine the relationship between miR-221-3p and toll-like receptors 4 (TLR4). Also, western blot analysis was performed to determine the levels of TLR4 and nuclear factor kappa B (NF-κB) signaling pathway-related proteins. Oxidized low-density lipoprotein (ox-LDL) induced human umbilical vein endothelial cells (HUVECs) apoptosis, inflammation, and oxidative stress. NGR1 alleviated the negative effect of ox-LDL through promoting the expression of miR-221-3p in HUVECs. TLR4 was a target of miR-221-3p, and its overexpression could reverse the inhibition effects of miR-221-3p on apoptosis, inflammation, and oxidative stress. NGR1 improved miR-221-3p expression to inhibit the activation of the TLR4/NF-κB pathway in ox-LDL-treated HUVECs. NGR1 decreased ox-LDL-induced HUVECs apoptosis, inflammation, and oxidative stress through increasing miR-221-3p expression, thereby inhibiting the activation of the TLR4/NF-κB pathway. This study of the mechanism of NGR1 provided a more theoretical basis for the treatment of AS.

目的 探讨双肺12区超声评分法对新生儿呼吸窘迫综合征(NRDS)临床诊断及病情评估的应用价值.方法 将2017年6月至2019年7月期间在本院新生儿重症监护室住院的65例NRDS患儿和同期收治的50例非肺病新生儿,采用前瞻性研究方法入组,分别为NRDS组和对照组.两组新生儿均接受肺超声检查,观察NRDS患儿的超声征象,并进行经腹肺超声分级和双肺12区域肺超声评分,与X线分级下的NRDS新生儿双肺征象进行比较,采用Spearman法分析其相关性,借助受试者工作特征(ROC)曲线分析双肺12区域肺超声评分评估不同病情程度的最佳截断点(Cut-off),并计算灵敏度、特异度和曲线下面积(AUC).结果 经腹肺超声分级 Ⅰ 级20例,Ⅱ 级26例,Ⅲ 级19例.X线分级 Ⅰ 级23例,Ⅱ 级19例,Ⅲ 级16例,Ⅳ 级7例.NRDS新生儿经腹超声和X线分级呈正相关(r=0.652,P<0.05).X线分级中Ⅰ级、Ⅱ级、Ⅲ级、Ⅳ级双肺12区肺超声评分分别为(32.97±5.90)分、(24.39±5.48)分、(18.95±4.27)分、(12.18±3.29)分.X线不同分级的双肺12区与超声评分比较,差异有统计学意义(F=35.287,P<0.05).NRDS新生儿双肺12区超声评分与X线分级呈显著负相关(r=-0.803,P<0.05).根据X线分级将65例NRDS组分为轻度(Ⅰ级,n=23)、中度(Ⅱ ～ Ⅲ级,n=35)和重度(Ⅳ级,n=7)3个亚组,ROC曲线分析显示:双肺12区超声评分评估轻度和中度NRDS、中度和重度NRDS的Cut-off分别为27.58分、14.70分,灵敏度分别为91.11％、92.00％,特异度分别为84.00％ 、95.55％,AUC分别为0.832、0.897.结论 双肺12区超声评分是临床诊断新生儿NRDS和定量评估病情程度的有效方法,值得深入研究和临床应用.

目的 探讨利格列汀联合阿卡波糖对2型糖尿病血糖控制及相关指标的影响.方法 将60例2型糖尿病患者随机分为2组,对照组30例采取口服利格列汀片治疗,观察组30例在对照组治疗基础上加服阿卡波糖.分别于治疗前后检测2组空腹血糖(FPG)、餐后2 h血糖(2 hPG)、糖化血红蛋白(HbAlc)、空腹血浆胰岛素(FINS)、肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、白细胞介素17A(IL-17A)、白细胞介素22(IL-22)、干扰素γ(IFN-γ)水平.并记录2组不良反应发生情况及胰岛素抵抗指数(HOAM-IR).结果 观察组治疗后FPG、2 hPG、HbAlc、FINS含量和HOMA-IR以及TNF-α、IL-6、IL-17A、IL-22、IFN-γ水平降低幅度优于对照组,差异有统计学意义(P<0.05);2组不良反应发生率比较差异无统计学意义(P>0.05).结论 利格列汀联合阿卡波糖治疗2型糖尿病有利于血糖控制及相关指标的改善,且未增加不良反应.

创伤后应激障碍(PTSD)是由异常威胁性或灾难性事件导致的一类心理障碍,是21世纪迫切需要关注的公共卫生事件之一.探讨PTSD潜在的脑机制可为PTSD的早期干预、心理护理及追踪治疗提供理论基础.现有的研究从静息态和任务态两个方面对PTSD脑功能磁共振成像进行分析,结果表明PTSD患者的杏仁核反应增强、海马体积变小、前扣带回及内侧前额叶皮质反应减弱.未来的研究应关注控制组的选择,尤其是有无共病障碍的PTSD群体.

目的:探讨针刺联合穴位自血疗法治疗慢性湿疹的临床疗效.方法:随机从我院2016年5月～2018年6月收治的慢性湿疹患者中抽取80例进行讨论,用随机数表法分组,40例接受糖酸莫米松乳膏和氯雷他定片治疗(对照组),另40例接受针刺联合穴位自血疗法治疗(研究组),观察比较疗效.结果:研究组疗效高于对照组,差异有统计学意义(P＜0.05).比较EASI评分:治疗后1周、治疗后2周,研究组EASI评分低于对照组,数据差异较大(P＜0.05).研究组复发率5.00％低于对照组的32.50％,差异较大(P＜0.05).结论:慢性湿疹采用针刺联合穴位自血疗法治疗,可显著缓解瘙痒程度、皮损症状,降低复发率,提升疗效.

目的:观察益气养阴汤、二甲双胍片联合治疗2型糖尿病临床效果.方法:随机选取2016年1月～2018年1月我院收治的2型糖尿病患者72例,对照组36例予以二甲双胍片治疗,观察组36例加用益气养阴汤治疗,比较两组临床治疗效果.结果:观察组总有效率91.67％,明显高于对照组的77.78％,差异具有统计学意义(P＜0.05).两组治疗前血糖、血脂各项指标比较,差异无统计学意义(P＞0.05);两组治疗后血糖、血脂各项指标与治疗前比较,差异具有统计学意义(P＜0.05);观察组治疗后血糖、血脂各项指标与对照组治疗后比较,差异具有统计学意义(P＜0.05).结论:应用益气养阴汤、二甲双胍片联合治疗2型糖尿病,效果显著,可有效改善临床症状,控制血糖、血脂水平.

Background and Objectives: Appropriate inflammatory response is necessary for cardiac repairing after acute myocardial infarction (MI). Three-Bromo-4,5-dihydroxybenzaldehyde (BDB) is a potent antioxidant and natural bromophenol compound derived from red algae. Although BDB has been shown to have an anti-inflammatory effect, it remains unclear whether BDB affects cardiac remolding after MI. The aim of this study was to investigate the potential role of BDB on cardiac function recovery after MI in mice. Methods: Mice were intraperitoneally injected with BDB (100 mg/kg) or vehicle control respectively 1 hour before MI and then treated every other day. Cardiac function was monitored by transthoracic echocardiography at day 7 after MI. The survival of mice was observed for 2 weeks and hematoxylin and eosin (H&E) staining was used to determine the infarct size. Macrophages infiltration was examined by immunofluorescence staining. Enzyme-linked immunosorbent assay (ELISA) was used to test the production of cytokines associated with macrophages. The phosphorylation status of nuclear factor (NF)-kappa B was determined by western blot. Results: BDB administration dramatically improved cardiac function recovery, and decreased mortality and infarcted size after MI. Treatment with BDB reduced CD68' macrophages, M1 and M2 macrophages infiltration post-MI, and suppressed the secretion of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, monocyte chemoattractant protein (MCP)-1, and IL-6 in the injured hearts. Furthermore, BDB inhibited the phosphorylation of NF-kappa B in the infarcted hearts. Conclusions: These data demonstrate, for the first time, that BDB treatment facilitated cardiac healing by suppressing pro-inflammatory cytokine secretion, and indicate that BDB may serve as a therapeutic agent for acute MI.