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| 1 | Molecular Mechanisms of Ventilator-Induced Lung Injury显示文摘 | Lin Chen Hai-Fa Xia You Shang Shang-Long Yao | 2018 | Chinese Medical Journal2018，，10： | 12 |
| 2 | Atorvastatin protects cardiac progenitor cells from hypoxia-induced cell growth inhibition via MEG3/miR-22/HMGB1 pathway显示文摘Heart failure (HF)induced by ischemia myocardial infarction (MI)is one of the major causes of morbidity and mortality all around the world.Atorvastatin,a hydroxyrnethylglutaryl coenzyme A reductase inhibitor,has been demonstrated to benefit patients with ischemic or non-ischemicinduced HF,but the mechanism is still poorly understood.Increasing evidence indicates that IncRNAs play important role in variety of human disease.However,the role and underlying molecular mechanisms remain largely unclear.In our work,we applied 0.5%02 to generate a hypoxia cardiac progenitor cell (CPC)model.Then,CCK8 and EdU assays were employed to investigate the role of atorvastatin in hypoxia CPC cell model.We found that hypoxia inhibits CPC viability and proliferation through modulating MEG3 expression,while atorvastatin application can protect CPCs from hypoxia-induced injury through inhibiting MEG3 expression.Then,we demonstrated that repression of MEG3 inhibited the hypoxia-induced injury of CPCs and overexpression of MEG3 inhibited the protective effect of atorvastatin in the hypoxia-induced injury of CPCs.Furthermore,our study illustrated that atorvastatin played its role in CPC viability and proliferation by modulating the expression of HMGB1 through the MEG3/miR-22 pathway.Our study, for the first time,uncovered the molecular mechanism of atorvastatin's protective role in cardiomyocytes under hypoxia condition,which may provide an exploitable target in developing effective therapy drugs for MI patients. | Jinwen Su Ming Fang Bei Tian Jun Luo Can Jin Xuejun Wang Zhongping Ning Xinming Li | 2018 | Acta Biochimica et Biophysica Sinica2018，50，12： | 6 |
| 3 | Validation of novel hub genes and molecular mechanisms in acute lung injury using an integrative bioinformatics approach显示文摘Acute lung injury(ALI)is an inflammatory pulmonary disease that can easily develop into serious acute respiratory distress syndrome,which has high morbidity and mortality.However,the molecular mechanism of ALI remains unclear,and few molecular biomarkers for diagnosis and treatment have been identified.In this study,we aimed to identify novel molecular biomarkers using a bioinformatics approach.Gene expression data were obtained from the Gene Expression Omnibus database,co-expressed differentially expressed genes(CoDEGs)were identified using R software,and further functional enrichment analyses were conducted using the online tool Database for Annotation,Visualization,and Integrated Discovery.A protein-protein interaction network was established using the STRING database and Cytoscape software.Lipopolysaccharide(LPS)-induced ALI mouse model was constructed and verified.The hub genes were screened and validated in vivo.The transcription factors(TFs)and miRNAs associated with the hub genes were predicted using the NetworkAnalyst database.In total,71 CoDEGs were screened and found to be mainly involved in the cytokine-cytokine receptor interactions,and the tumor necrosis factor and malaria signaling pathways.Animal experiments showed that the lung injury score,bronchoalveolar lavage fluid protein concentration,and wet-to-dry weight ratio were higher in the LPS group than those in the control group.Real-time polymerase chain reaction analysis indicated that most of the hub genes such as colony-stimulating factor 2(Csf2)were overexpressed in the LPS group.A total of 20 TFs including nuclear respiratory factor 1(NRF1)and two miRNAs were predicted to be regulators of the hub genes.In summary,Csf2 may serve as a novel diagnostic and therapeutic target for ALI.NRF1 and mmu-mir-122-5p may be key regulators in the development of ALI. | Qingchun Liang Qin Zhou Jinhe Li Zhugui Chen Zhihao Zhang Ruimeng Liu Haicheng Huang Zhiyong Peng Youtan Liu | 2021 | Acta Biochimica et Biophysica Sinica2021，53，3： | 1 |
| 4 | 依达拉奉预处理对单肺通气患者HGMB1的影响显示文摘目的评估依达拉奉预处理对单肺通气(OLV)患者高迁移率族蛋白B1(HMGB1)的影响。方法选择需OLV患者50例,年龄62-75岁,ASA分级Ⅰ-Ⅱ级,按随机数字表法分为2组(n=25):对照组(生理盐水)、观察组(依达拉奉),每组25例。观察组麻醉前微量泵静脉注射依达拉奉5mg/kg,30min内注射完成,对照组注射等容积生理盐水。2组分别在依达拉奉注射前(T1)、OLV3h(T2)、术后24h(T3)、术后48h(Td)检测HMGB1,并记录血氧饱和度(SaO2),在麻醉后OLV前、T2时点记录患者呼气末二氧化碳分压(PETCO2)、气道平台压(Ppean)、气道峰压(Ppeak);记录术后48h内发生急性肺损伤(Au)、急性呼吸窘迫综合征(ARDS)例数。结果观察组T2-T4时点HMGB1、SaO2均高于对照组;观察组T2时点PETCO2、Ppean、Ppeak低于对照组;观察组术后48h内发生ALI/ARDS例数低于对照组(P均〈0.05)。结论依达拉奉可以通过降低HMGB1表达减轻肺损伤,保护肺功能。 | 庞雪 程丹 崔旭 齐敦益 | 2018 | 徐州医科大学学报2018，38，9： | 0 |
| 5 | COPD患者HMGB1、免疫细胞和纤维蛋白原联合检测的临床意义显示文摘目的:探讨高迁移率蛋白1(HMGB1)、免疫细胞联合纤维蛋白原(FIB)、中性粒细胞/淋巴细胞水平(NLR)在COPD病情严重程度及预后中的作用.方法:选取2012-10/2016-04江苏省宜兴市人民医院呼吸内科收治的COPD患者80例作为研究对象,按照治疗效果分为COPD缓解组(n=40)及非缓解组(n=40),依据肺功能分轻-中度组(n=30),重-极重度组(n=25),以健康体检者共40例作为对照组.观察相关血清学指标与COPD治疗效果、肺功能指标的关系,并对患者进行3年随访,观察其与预后的关系.结果:COPD患者HMGB1、FIB和NLR水平明显高于健康体检者,差异具有统计学意义(P<0.05);COPD缓解组HMGB1、FIB和NLR水平低于非缓解组,差异具有统计学意义(P<0.05);COPD患者肺功能重-极重度组HMGB1、FIB和NLR表达较高,差异具有统计学意义(P<0.05);HMGB1、FIB和NLR高水平的COPD患者死亡率较高,差异具有统计学意义(P<0.05).结论:HMGB1、FIB和NLR联合检测对判断COPD疾病严重程度、肺功能分级和病情预后具有重要临床意义. | 周广辉 冯艳 陈如华 丁辉 | 2017 | 转化医学电子杂志2017，4，12： | 0 |
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