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| 1 | 高强度间歇训练对冠心病患者心肺功能、生活质量及miRNA表达谱的影响显示文摘目的研究高强度间歇训练对冠状动脉粥样硬化性心脏病(冠心病)患者的心肺功能及生活质量的影响并筛选鉴定与高强度间歇训练运动调控相关的差异化表达miRNA。方法选取2018年1月~12月于郑州中心医院进行规范治疗的冠心病患者80例为研究对象,随机分为对照组与高强度间歇训练组。对照组采用常规药物治疗,训练组则进一步联合高强度间歇训练,8周后再次评估两组患者的心功能、肺功能及生活质量变化,同时采用AffymetrixGeneChip miRNA芯片检测两组患者血清表达差异的miRNA并采用Realtime PCR进行验证。结果在治疗结束后发现,对照组和HIIT组患者6MWD、LVEF、LVEDD较治疗前均得到显著改善(P<0.05);而HIIT组患者的心功能改善显著优于对照组(P<0.05);同样治疗结束后HIIT组患者AT时氧脉搏、AT时分钟通气量、最高氧脉搏和最高每分钟通气量指标显著优于治疗前(P<0.05)和对照组患者(P<0.05);生活质量方面,经过8周干预治疗后,对照组和HIIT组患者生理功能、生理职能、躯体疼痛和总体健康较治疗前均得到显著改善(P<0.05);而HIIT组患者的生活质量改善显著优于Control组患者(P<0.05)。进一步两组患者的miRNA基因芯片筛选发现训练组患者血清miR-20a-5p,miR-93-5p和miR-1287-5p表达显著增加,而miR-7706,miR-28-5p和miR-125b-5p表达显著降低,可能参与了高强度间歇训练改善冠心病的进程。结论高强度间歇训练对于冠心病患者的心肺功能及生活质量都能够起到显著改善作用,其获益机理可能与调控miRNA差异化表达有关。 | 孙漾丽 顾迎春 李征艳 孙兵兵 马娟 侯亚敏 张友峰 赵智琛 胡大一 王东伟 | 2020 | 中国循证心血管医学杂志2020，12，10： | 9 |
| 2 | miRNA-368在糖尿病脑病中的表达水平变化及临床意义显示文摘目的探讨糖尿病脑病患者外周血血清和单核细胞中miRNA-368水平的表达变化及临床意义。方法 qRT-PCR检测糖尿病脑病中患者外周血血清的miRNA-368表达水平,并将miRNA-368转染到糖尿病脑患者外周血单核细胞中,然后通过qRT-PCR检测转染效率,采取CCK-8和克隆形成实验检测miRNA-368对糖尿病脑患者外周血单核细胞增殖的影响,流式细胞技术检测miRNA-368对糖尿病脑患者外周血单核细胞周期和凋亡率的影响。结果 27例糖尿病脑病患者外周血中miRNA-368的相对表达量为1.402,95%CI=0.363~0.595;miRNA-368相对表达水平与患者的一般资料如年龄、性别并不存在明显关系(P>0.05);糖尿病脑病患者的miRNA-368相对表达水平明显上调(P<0.05);qRT-PCR显示糖尿病脑病外周血单核细胞miRNA-368的表达水平明显上调;si-miRNA-368干预后糖尿病脑病患者外周血单核细胞增殖受到抑制,凋亡率增高。结论 miRNA-368在糖尿病脑病患者外周血血清和单核细胞中的表达水平明显上调,且miRNA-368能抑制单核细胞的凋亡,促进了糖尿病脑病的发生发展。 | 孟开顺 宋科秀 王小蕊 | 2019 | 卒中与神经疾病2019，26，6： | 3 |
| 3 | Exercise-mediated regulation of autophagy in the cardiovascular system显示文摘Cardiovascular disease is the leading cause of human death worldwide. Autophagy is an evolutionarily conserved degradation pathway,which is a highly conserved cellular degradation process in which lysosomes decompose their own organelles and recycle the resulting macromolecules.Autophagy is critical in maintaining cardiovascular homeostasis and function, and excessive or insufficient autophagy or autophagic flux can lead to cardiovascular disease. Enormous evidence indicates that exercise training plays a beneficial role in the prevention and treatment of cardiovascular diseases. The regulation of autophagy during exercise is a bidirectional process. For cardiovascular disease caused by either insufficient or excessive autophagy, exercise training restores normal autophagy function and delays the progression of cardiovascular disease.An in-depth exploration and discussion of exercise-mediated regulation of autophagy in the cardiovascular system can broaden our view about the prevention of various autophagy-related diseases through exercise training. In this article, we review autophagy and its related signaling pathways,as well as autophagy-dependent beneficial effects of exercise in cardiovascular system. | Lijun Wang Jiaqi Wang Dragos Cretoiu Guoping Li Junjie Xiao | 2020 | Journal of Sport and Health Science2020，9，3： | 3 |
| 4 | Animal exercise studies in cardiovascular research:Current knowledge and optimal design--A position paper of the Committee on Cardiac Rehabilitation,Chinese Medical Doctors’Association显示文摘Growing evidence has demonstrated exercise as an effective way to promote cardiovascular health and protect against cardiovascular diseases However,the underlying mechanisms of the beneficial effects of exercise have yet to be elucidated.Animal exercise studies are widely used to investigate the key mechanisms of exercise-induced cardiovascular protection.However,standardized procedures and well-established evaluation indicators for animal exercise models are needed to guide researchers in carrying out effective,high-quality animal studies using exercise to prevent and treat cardiovascular diseases.In our review,we present the commonly used animal exercise models in cardiovascular research and propose a set of standard procedures for exercise training,emphasizing the appropriate measurements and analysis in these chronic exercise models.We also provide recommendations for optimal design of animal exercise studies in cardiovascular research,including the choice of exercise models,control of exercise protocols,exercise at different stages of disease,and other considerations,such as age,sex,and genetic background.We hope that this position paper will promote basic research on exercise-induced cardiovascular protection and pave the way for successful translation of exercise studies from bench to bedside in the prevention and treatment of cardiovascular diseases. | Yihua Bei Lei Wang Rongjing Ding Lin Che Zhiqing Fan Wei Gao Qi Liang Shenghui Lin Suixin Liu Xiao Lu Yuqin Shen Guifu Wu Jian Yang Guolin Zhang Wei Zhao Lan Guo Junjie Xiao | 2021 | Journal of Sport and Health Science2021，10，6： | 2 |
| 5 | Human Serum-derived Extracellular Vesicles Protect A549 from PM_(2.5)-induced Cell Apoptosis显示文摘Objective Epidemiological studies reveal that exposure to fine particulate matter(aerodynamic diameter≤2.5μm,PM_(2.5))increases the morbidity and mortality of respiratory diseases.Emerging evidence suggests that human circulating extracellular vesicles(EVs)may offer protective effects against injury caused by particulate matter.Currently,however,whether EVs attenuate PM_(2.5)-induced A549 cell apoptosis is unknown.Methods EVs were isolated from the serum of healthy subjects,quantified via nanoparticle tracking analysis,and qualified by the marker protein CD63.PM_(2.5)-exposed(50μg/mL)A549 cells were pretreated with 10μg/mL EVs for 24 h.Cell viability,cell apoptosis,and AKT activation were assessed via Cell Counting Kit-8,flow cytometry,and Western blot,respectively.A rescue experiment was also performed using MK2206,an AKT inhibitor.Results PM_(2.5)exposure caused a 100%in crease in cell apoptosis.EVs treatme nt reduced cell apoptosis by 10%,promoted cell survival,and inhibited the PM_(2.5)-induced upregulation of Bax/Bcl2 and cleaved caspase 3/caspase 3 in PM_(2.5)-exposed A549 cells.Moreover,EVs treatment reversed PM_(2.5)-induced reductions in p-AKT^(Thr308)and p-AKT^(Ser473).A KT inhibition attenuated the anti-apoptotic effect of EVs treatment on PM_(2.5)-exposed A549 cells.Conclusions EVs treatment promotes cell survival and attenuates PM_(2.5)-induced cell apoptosis via AKT phosphorylation.Human serum-derived EVs may be an efficacious novel therapeutic strategy in PM_(2.5)-induced lung injury. | ZHOU Qiu Lian BAI Yu Zheng GAO Juan DUAN Yi LYU Yi Cheng GUAN Long Fei ELKIN Kenneth XIE Yu Ling JIAO Zheng WANG Hong Yun | 2021 | Biomedical and Environmental Sciences2021，34，1： | 0 |
| 6 | 原发性高血压患者血清miR-192表达水平与左室肥厚的关系显示文摘目的 探讨原发性高血压患者血清中miR-192表达与左心室肥厚的相关性。方法 收集2018年6月至2019年12月期间治疗的187例原发性高血压患者临床资料,行超声心动图检查获得LVPWd、IVST、LVEDD、LVESD、LVEDV、LVESV、LAD、LVEF和LVMI等指标,并根据超声心动图检查结果将患者分为肥厚组和对照组。实时荧光定量PCR检测血清中miR-192表达,ELISA法测定TGF-β1、Ⅰ型前胶原羧基末端肽(PⅠCP)和Ⅲ型前胶原氨基端肽(PⅢNP)水平。结果 经超声心动图检查,187例原发性高血压患者中,76例出现左心室肥厚(肥厚组),111例未发现左心室肥厚(对照组);肥厚组患者LVPWT、IVST、LVEDD、LVESD、LVEDV、LVESV、LAD、LVMI和hs-CRP均较对照组升高(P <0.05);肥厚组患者血清中miR-192、TGF-β1、PⅢNP和PⅠCP水平较对照组升高(P <0.05);Pearson相关分析结果显示,原发性高血压患者血清中miR-192水平与LVPWT、IVST、LVEDD、LVESD、LVEDV、LVESV、LAD、LVMI、TGF-β1、PⅠCP和PⅢNP呈正相关(P <0.05);多元线性回归分析结果显示,LVPWT、IVST、LVEDD、LVESV、TGF-β1、PⅠCP和PⅢNP是影响原发性高血压患者血清中miR-192水平的相关因素(P <0.05)。结论 血清miR-192水平在原发性高血压左心室肥厚患者中升高,且与左心室肥厚程度及心肌纤维化有关。 | 杜高波 贾小凤 余强 李晓鹃 | 2023 | 昆明医科大学学报2023，44，2： | 0 |
| 7 | 运动诱导的生理性心肌肥大中miR-497-3p的表达变化及作用显示文摘目的:探讨miR-497-3p、Beclin1在运动性心肌肥大大鼠心肌中的表达变化,及其对运动性心肌肥大发生和发展的影响。方法:选取Sprague-Dawley纯系6周龄雄性大鼠24只,随机分为安静对照组(Con组,n=12)和运动性心肌肥大模型组(Ex组,n=12)。运动性心肌肥大模型组大鼠参照Femandes和Oliveria等制定10周游泳运动训练方案,建立大鼠运动性心肌肥大模型。采用RT-qPCR检测miR-497-3p、心钠素(ANP)、心肌肌球蛋白重链α和β(α-MHC、β-MHC)、α-肌动蛋白(α-actin)、肌浆网钙ATP酶(SERCA2α)及Beclin1的mRNA表达水平,用Western blotting检测自噬相关基因Beclin1的蛋白表达水平。分别用过表达及干扰表达miR-497-3p腺病毒感染H9C2细胞,观察Beclin1的mRNA及蛋白表达水平。通过双荧光素酶报告基因实验验证Beclin1与miR-497-3p的靶向关系。结果:(1)10周游泳运动干预后,Ex组较Con组miR-497-3p表达量显著下降(P<0.01)。(2)10周游泳运动干预后,Ex组较Con组自噬相关蛋白Beclin1的mRNA、蛋白表达水平均显著升高(均P<0.01)。(3)过表达miR-497-3p抑制了自噬相关基因Beclin1的表达(P<0.01),引起心肌自噬水平降低。(4)干扰表达miR-497-3p后,Beclin1 mRNA和蛋白的水平显著上调(均P<0.01)。(5)Beclin1是miR-497-3p的靶基因。结论:10周游泳训练可以通过降低心肌中miR-497-3p的表达,靶向上调Beclin1表达水平,进而引起心肌自噬水平增强,从而诱导运动性心肌肥大形成。 | 张波 齐洁 张钧 | 2020 | 中国运动医学杂志2020，39，10： | 0 |
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