Schizandrin B exhibits prominent antioxidant and anti-inflammatory effects, and plays an important role in ameliorating myocardial ischemia/reperfusion injury. However, the underlying protective mechanisms remain to be elucidated. The aim of the present study was to explore the cardioprotective effects of schizandrin B against hypoxia/reoxygenation (H/R)-induced H9c2 cell injury, focusing on the role of the adenosine monophosphate-activated protein kinase (AMPK)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in this process. The results showed that schizandrin B attenuated the H/R-induced decrease in cell viability and the increase in lactate dehydrogenase release, as well as the apoptosis rate in H9c2 cells. Schizandrin B also mitigated H/R-induced oxidative stress, as illustrated by the decrease in intracellular reactive oxygen species generation, malondialdehyde content and NADPH oxidase 2 expression, and the increase in antioxidant enzyme superoxide dismutase and glutathione peroxidase activities. In addition, schizandrin B reversed the H/R-induced upregulation of pro-inflammatory cytokines [interleukin (IL)-1β (IL-1β) tumor necrosis factor-α, IL-6 and IL-8] and the downregulation of anti-inflammatory cytokines (transforming growth factor-β and IL-10) in the culture supernatant. Notably, schizandrin B increased the expression of Nrf2, NAD(P)H: Quinone oxidoreductase (NQO-1) and heme oxygenase-1 (HO-1) in H/R-treated H9c2 cells, activating the Nrf2 signaling pathway. The cardioprotection of schizandrin B against H/R injury was inhibited by Nrf2 knockdown induced byNrf-2-specific small interfering RNA (siRNA; si-Nrf2) transfection. Furthermore, schizandrin B enhanced phosphorylated (p)-AMPK expression, while AMPK knockdown induced by AMPK-specific siRNA(si-AMPK) transfection remarkably eliminated schizandrin B-induced cardioprotection and reduced Nrf2 expression in H/R-treated H9c2 cells. Taken together, these results suggested that schizandrin B exerts cardioprotection on H/R injury in H9c2 cells due to its antioxidant and anti-inflammatory activities via activation of the AMPK/Nrf2 pathway.

目的 探讨通心络胶囊对急性低压缺氧暴露大鼠认知功能损伤的神经保护作用及其相关机制.方法 64只雄性Sprague-Dawley大鼠随机均分为四组,包括正常组(C),通心络组(TXL),低压低氧组(HH),和低压低氧+通心络组(TXL+HH).在低压低氧暴露前,所有大鼠进行5 d水迷宫训练.然后在低压低氧环境下暴露7 d.7 d后,采用旷场实验,水迷宫实验测定认知功能,然后处死取海马组织,Western blot检测海马组织TLR-4、MyD88、IκB-α,NF-κB p65,AQP4,MMP-9的表达,ELISA检测血清和海马组织中IL-1β、TNF-α、IL-6的水平,HE染色观察海马组织病理学变化,并测定大鼠的脑水含量.结果(1)行为学实验:四组大鼠旷场实验结果无统计学差异(P>0.05);但在水迷宫空间探索实验中发现,与C组比较,HH组大鼠原平台所在象限停留时间及穿越平台次数明显降低(P<0.05);TXL干预后,大鼠原平台所在象限停留时间及穿越平台次数较低压低氧组明显升高,(P<0.05);(2)炎症指标比较:与C组比较,HH组大鼠血清及海马组织IL-1β、TNF-α、IL-6水平,海马TLR-4、MyD88、NF-κB p65蛋白水平明显升高(P<0.05),TXL干预后,炎症指标相关蛋白水平均下降(P<0.05);(3)海马组织损伤比较:HH组大鼠海马AQP4及MMP-9表达及脑水含量明显高于C组(P<0.05),海马区细胞排列紊乱,肿胀明显,边界模糊;而TXL干预后,AQP4,MMP-9表达及脑水含量均明显下降(P<0.05).结论 急性低压缺氧暴露可导致认知功能障碍和脑组织水肿,通心络干预可通过抑制TLR4/MyD88/NF-κB信号通路活化,减轻海马炎症,改善认知损伤和脑组织水肿.

目的 探讨在铁路职工中应用基于健康小站的“互联网+”高血压管理模式进行血压管理的效果.方法 选取2018年3～9月北京铁路某两处机务段的高血压患者601例,采取自身前后对照研究,应用基于健康小站的“互联网+”高血压管理模式进行血压管理,连续干预6个月后,比较干预前后血压(血压水平、血压达标率),用药依从性,代谢指标[BMI、空腹血糖(fasting plasma glucose,FPG)、TC],行为改变(戒烟、增加锻炼、低盐饮食)等情况.结果 6个月干预后共收集574例完整资料,患者血压水平较干预前降低(P＜0.05),血压达标率、用药依从性均较干预前有显著提高(P＜0.05),BMI、TC显著下降(P＜0.05),FPG有下降趋势,但差异无统计学意义(P＞0.05),戒烟、增加锻炼、低盐饮食等生活行为较干预前明显改善(P＜ 0.001).结论 基于健康小站的“互联网+”高血压管理模式可改善患者血压水平,提高血压达标率、用药依从性,改善部分代谢指标及生活行为.

To investigate the application of PG-SGA in nutritional assessment of elderly patients with chronic heart failure.Methods A continuous approach was used to screen a total of 125 elderly patients who were hospitalized in the Beijing Shijitan Hospital Capital Medical University and Rizhao Central Hospital from October 2017 to February 2019.According to the NYHA classification of heart failure the patients were divided into the clinical heart failure group grade Ⅱ～Ⅳ and the pre-clinical heart failure group grade I .Patients were evaluated for nutritional status using PG-SGA.The body mass index BMI albumin ALB pre-albumin PA hemoglobin Hb and NT-proBNP were measured.The correlation between each test index and PG-SGA was observed.The relationship between PG-SGA score and cardiac function classification was studied.Results The incidence of malnutrition in the clinical heart failure group was significantly higher than that in the pre-clinical heart failure group P<0.001 .Compared to the patients rated unmalnutrition the patients rated malnutrition got lower BMI ALB PA Hb levels and a higher NT-proBNP level P<0.05 .PG-SGA scores and PA levels have statistically significant differences between each cardiac function classification subgroups P<0.05 .Conclusions The incidence of malnutrition in elderly chronic heart failure patients is high and PG-SGA could be used for the nutritional assessment of these patients.PG-SGA scores might be used as an auxiliary index to evaluate cardiac function.

遗传与基因组医学的进展,催生了精准医疗学科的发展.高血压领域与高血压相关基因研究的进展非常快,主要在三个方面:(1)单基因高血压致病基因的发现,目前至少有17种单基因(或寡基因)高血压,能够找到致病基因,根据致病基因,进行靶向治疗.这一进展目前就可以在临床上推广使用.(2)药物基因组学指导的降压药选择,提高疗效,降低药物副反应,已经显示广阔的前景,如β-受体阻滞剂.但是药物基因组指导的降压药选择,缺乏大规模前瞻性研究,对临床后果影响的研究报告比较少.有待补充这方面的数据.(3)大多数高血压是原发性高血压,多基因,多因素疾病,通过人类全基因组关联分析(GWAS)研究,已经有一些高血压相关遗传变异被发现,但是,所能解释的血压变异非常少,有待进一步研究证明.

目的 在大鼠模型中探索通心络对高原性肺高血压的作用及其可能的TGF-β 1作用机制.方法 将30只健康雄性SD大鼠随机分为实验组、模型组和对照组,每组各10只.实验组与模型组大鼠置于全自动调节低压低氧舱内,持续暴露于模拟低压低氧环境(气压50 kPa,氧浓度10％),对照组大鼠置于同室,暴露于常压常氧环境.实验组每日每千克体重给予通心络超微粉1.2 g生药灌胃1次,模型组及对照组每日给予等量生理盐水灌胃1次.4周后采用右心导管检查测定各组大鼠平均肺动脉压(mPAP);用电子天平称量右心室(RV)、左心室(LV)、室间隔(S)重量,以RV/(LV+S)计算得出右心肥厚指数(RVH1);行苏木精-伊红(HE)染色,观察肺组织显微形态学;应用实时荧光定量PCR(RT-PCR)测定肺组织TGF-β 1 mRNA表达水平;应用Western blot测定肺组织TGF-β 1蛋白表达水平.结果 模型组大鼠的mPAP、RVHI均显著高于对照组和实验组(P＜0.05),模型组大鼠肺组织TGF-β 1在mRNA及蛋白水平表达均显著高于对照组和实验组(P＜0.05),差异具有统计学意义.结论 通心络对高原性肺高血压具有保护性调控作用,该作用可能与抑制TGF-β1表达有关.

目的 调查和分析某地区铁路职工高血压患病情况及影响因素,为健康宣教和干预管理提供基础支撑.方法 采用随机抽样的方法,选取某地区铁路部门部分机务系统、车辆系统和客运系统职工共2 008名,通过问卷调查收集其常见病、多发病情况,并用统计学方法对数据进行描述性分析、单因素分析和Logistic回归分析.结果 2 008名职工有13.2％患有高血压(该样本平均年龄35.5岁),其慢性疾病谱具有行业特点.结论 某地区铁路职工高血压患病情况与职业特点密切相关,应给予相应的健康宣教和干预管理.

Objective:To investigate the protective effect of Tongxinluo pretreatment on pulmonary hypertension in rats and its possible NO mechanism.Methods:Thirty male SD rats were randomly divided into 3 groups (n =10):control group;model group and Tongxinluo pretreatment group.The control group used normal oxygen and normal pressure.The model group used low-pressure and low-oxygen and Tongxinluo group was in low-pressure and low oxygen.The auto-modulating hyobaric and hypoxic cabin was used to simulate 5000 m high altitude environment.Tongxinluo pretreatment group animals were pretreated with Tongxinluo[1.2 g/(kg · d)] by orogastric route 4 weeks.The other two groups pretreatment was normal CMC-Na in the same.4 weeks later,the mPAP,WT％ and WA％ were measured and the endothelial NOX (eNOS),inducible NOS (iNOS) activity and NO level were detected by ultraviolet spectrophotometer.The mRNA expression of myocardial eNOS and iNOS were detected by real-time fluorescence quantitative PCR (RTFQ-PCR).Results:The WT％ and WA％ of model group were higher than the those of Tongxinluo group and control group.But compared with the model group,the Tongxinluo group's serum NO,eNOS levels and intestinal tissue eNOS mRNA expression elevated (P ＜ 0.05),but the plasma iNOS of serum and lung iNOS mRNA expression decreased (P ＜ 0.05).Conclusion:Tongxingluo pretreatment has protective effects on pulmonary hypertension in rats.The mechanism may be related to inhibition of iNOS expression and increasing expression of eNOS,thereby increasing NO activity.

Objective To This study aims to investigate the potential role of tissue factor (TF) in hypercoagulable state of hypobaric hypoxia-induced pulmonary.Methods 16 healthy male SD rats were randomly divided into experiment group and control group,8 for each group.The experiment group was continuously housed in an automatic adjusting hypobaric hypoxia chamber (atmospheric pressure of about 50kPa,oxygen concentration 10％),the control group is housed under normobaric normoxic condition in the same room.After 4 weeks all rats were sacrificed.The mean pulmonary arterial pressure (mPAP) was measured by right-sided heart catheterization.The right heart hypertrophy index (RVHI) was calculated by the formula RV/(LV + S) to evaluate the degree of right ventricular hypertrophy.Lung tissue microstructure morphology was observed on hematoxylin-eosin (HE) staining sections and Verhoeff-Van Gieson elastic (EVG) staining sections.The expression of HIF-1α,VEGF,TF in plasma was analyzed by ELISA.Results The mPAP,RVHI of rats in experiment group were significantly higher than those of control group (P＜0.05).The pathological staining suggests obvious pulmonary arterial remodeling and situ thrombus in experimental group.The expression level of plasma HIF-1α,VEGF and TF in experimental group were significantly higher than those in control group (P＜0.05).Conclusions The elevation of TF may partly responsible for the situ pulmonary thrombosis and hypercoagulable state in hypobaric hypoxia-induced pulmonary hypertension.The extrinsic route of blood coagulation may be related to pulmonary hypertension hypercoagulability.

BACKGROUND The aim of this study was to explore the regulating effects of Substance P (SP) on the collagen synthesis of rat myocardial fibroblasts (CFBs) induced by angiotensin II (Ang II) and its potential mechanism. MATERIAL AND METHODS The CFBs of a neonatal SD rat were separately cultured and divided into the control group, Ang II treatment group, and treatment groups with different concentrations of SP, Ang II +; each group was given corresponding treatment respectively. RESULTS Ang II successfully induced the collagen synthesis of CFBs. Compared with the control group, the phosphorylation levels of TGF-β, erk, and smad2/3 were higher (p<0.05). Different concentrations of SP had an effect on Ang II-induced CFBs, reduced the collagen synthesis of CFBs, and increased the expressions of SP receptors, accompanied by lowering TGF-β protein, erk protein phosphorylation level, and smad2/3 protein phosphorylation level (p<0.05). Moreover, the higher the concentrations of SP, the more obvious of an effect it exerted. Treating the Ang II + SP group with aprepitant reduced the inhibiting effects of SP on collagen synthesis. The expression changes of collagen I and collagen III detected by immunocytochemistry were exactly in accordance with the results of qPCR and Western blotting. CONCLUSIONS SP can inhibit collagen synthesis of CFBs after Ang II inducing which may adjust the downstream signaling pathways associated protein including TGF-β, erk and smad2/3. SP can block the progress of myocardial fibrosis and is dose dependent, which is expected to be a promising target for the treatment of myocardial fibrosis.

目的 探讨心房颤动(房颤)射频消融术是否通过对调控离子通道蛋白的微小RNA(microRNA,miRNA)的影响,实现心房离子流再平衡和逆重构,并试图发现有价值的调控miRNA.方法 选择行房颤射频消融术患者(阵发性、持续性和永久性房颤各10例)30例作为房颤组,健康体检者10例作为正常对照组.正常对照组体检时,房颤组射频消融术前和术后3个月分别取外周血,使用miRNA芯片(miRNA v18.0)进行全基因组miRNA表达谱微阵列分析,2组miRNA表达比值≥1.5倍为显著上调,实时定量PCR验证miRNA表达差异结果,并通过mirbase、miranda、targetscan数据库进行靶基因分析.结果 与正常对照组比较,房颤组射频消融术前主要参与离子通道蛋白调控的21个miRNA差异表达均有显著意义(P＜0.01);房颤组术后3个月与自身术前比较,上述21个miRNA表达亦有明显差异(P＜0.01).其中miR-1266等5个miRNA术前表达上调≥1.5倍,术后明显下调≥10倍;仅miR-3664-5p术前下调8.88倍,术后进一步下降46.06倍;其余15个miRNA均术前表达下调,术后显著上调.结论 房颤射频消融术通过影响调控离子通道蛋白的主要miRNA,实现了心房离子流逆重构.调控多个离子流的miR-1266,miR-377-5p,miR-101-5p和miR-151-3p有望成为房颤治疗新靶点.

Along with the completion of the Human Genome Project and the development of genome-wide association studies (GWAS), achievements of the genetic determinants of traits or diseases boost the development of personalized medicine,a model based on a patient's unique clinical, genetic, and environmental characteristics, which means that decisions for diagnosis, treatment and prevention are specific to the individual patient. The remaining obstacles to personalized medicine are certain to be overcome, and it is essential that all involved in the application of this new approach to patient care prepare themselves through education and develop system changes as needed.

Objective To discuss the influence factors related to exercise capacity in patients with hypertension accompanied by chest pain during treadmill exercise test. Methods The patients (n=136) with hypertension accompanied by chest pain were chosen and given symptom-limited treadmill exercise test. All patients were divided into group I (achieved exercise capacity≥predicted exercise capacity) and group II (achieved exercise capacity<predicted exercise capacity). The indexes of age, sex, body mass index (BMI), blood fat, fasting plasma glucose (FPG), fasting insulin (FINS) and homeostasis model assessment of insulin resistance (HOMA-IR) were compared between 2 groups. The influence factors related to exercise capacity were analyzed by using multiple linear regression analysis (MLR). Results In group II, resting heart rate (RHR), BMI, FINS and HOMA-IR were significantly higher than those in group I [(78.3±5.4) time/min vs. (72.1±6.0) time/min, P<0.001], [(26.4 ±2.8) kg/m2 vs. (24.1±2.6) kg/m2, P<0.001], [(12.9±4.8)μIU/ml vs. (8.6±2.6)μIU/ml, P<0.001] and [(3.82± 1.66) vs. (2.21±1.23), P<0.001]. MLR showed that sex (female), age, RHR, HOMA-IR were negatively correlated to exercise capacity (standard regression coefficientβwas, respectively,-0.547,-0.396,-0.336 and-0.438, all P<0.05). Conclusion In the patients with hypertension accompanied by chest pain, female, aging, RHR increasing and higher HOMA-IR are influence factors reducing exercise capacity.

Objective To discuss the risk factors related to coronary lesion progress in the patients with coronary heart disease (CHD). Methods The patients (n=122) with coronary angiography (CAG) examinations were chosen from Jan. 2008 to Dec. 2012, and all patients were diagnosed with CHD in the first CAG and they were given the second CAG. All patients were divided into progress group and non-progress group according to the outcomes of 2 times of CAG. The baseline risk factors related to CHD were compared between 2 groups including sex, age, smoking history, hypertension history, diabetes history, level of blood fat and features of coronary lesion. The independent predictors of coronary lesion progress were studied by using binary logistic regression analysis. Results The mean interval was (33.4±19.5) between 2 times of CAG. In the second CAG there were 71 patients (58.2%) with coronary lesion progress and 51 (41.8%) without coronary lesion progress. Compared with non-progress group, the percentage of baseline smoking patients was higher (59.2%vs. 39.2%, P=0.03), baseline level of high-density lipoprotein-cholesterol (HDL-C) was lower (0.97±0.25 mmoL/L vs. 1.18±0.25 mmoL/L, P=0.029), more patients had 3-vessel lesion during baseline CAG (38.0%vs. 15.7%, P=0.007), and more patients had percutaneous coronary intervention (PCI) during baseline CAG (88.7%vs. 70.6%, P=0.011) in progress group. The binary logistic regression analysis showed that baseline HDL-C level (OR=0.167, 95%CI: 0.033-0.854, P=0.032), PCI during baseline CAG (OR=3.281, 95%CI:1.268-8.491, P=0.014), 3-vessel lesion during baseline CAG (OR=4.289, 95%CI:1.447-12.712, P=0.009) and mean interval between 2 times of CAG (OR=1.029, 95%CI:1.007-1.052, P=0.01) were the independent predictors of coronary lesion progress. Conclusion The baseline HDL-C level, PCI during baseline CAG, 3-vessel lesion during baseline CAG and mean interval between 2 times of CAG are the independent predictors of coronary lesion progress.

扩张型心肌病(DCM)是以左心室扩张伴收缩功能障碍为特征的心脏疾病,常由遗传因素或环境因素(如感染、毒素或儿茶酚胺过量)引发.分子遗传检测可以发现有遗传性DCM危险因素的患者,而表观遗传和标记表型分期可以帮助发现需要干预治疗的高风险患者.表型分期包括临床和影像特征结合、转录组、更高层次的蛋白质组与代谢组的相互作用和流行病学资料.这些原理可以应用于DCM患者其他家族成员的基因检测和临床表型确定,使人们可以针对有相似危险因素的患者设计特异的干预方案,以改变DCM的自然进程,防止并发症[如心力衰竭(HF)/心律失常]的出现.本文综述了从DCM到HF的病因通路、遗传标志物和蛋白标志物的整合管理,也可为其他心血管疾病的基因和表型信息研究提供参照.

Objective To evaluate regional and global left ventricular systolic function after coronary artery bypass grafting (CABG) by speckle tracking imaging (STI).Methods Transthoracic echocardiography (TTE) was performed in 32 patients with coronary heart disease (CHD) preoperative and 3 months after CABG.The two-dimensional data were obtained in apical 4-chamble,2-chamble and long axis view.Peak systolic longitudinal strain (SLs),global longitudinal systolic strain (GLS) and average global strain(GLS-Avg) were measured using STI.30 healthy volunteers were involved as controls.Results SLs in the control group increased from the basal to the apical ventricular.SLs in the control group and CHD group apical segment were significantly higher than the basal and middle segments.Compared to the control group,SLs,GLS in part of myocardial ischemic segments were lower in CHD group before CABG (P ＜0.05).SLs and GSL in the corresponding segments showed significantly improving 3 months after CABG in CHD group (P ＜ 0.05).There was good relationship between GSL-Avg and left ventricular ejection fraction.Conclusions STI technology can be used to objectively and quantitatively evaluate the change of regional and global left ventricular systolic function.Therefore,it provide a non-invasive means for evaluation of curative effect and prognosis judgement of CHD after CABG.

Objective To assess the right ventricular (RV) performance in patients with type 2 diabetes mellitus (2-DM) by two-dimensional speckle tracking imaging (2D-STI),and to explore the clinical value of RV longitudinal strain and strain rate.Methods Thirty-seven patients with 2-DM only and thirtyone patients coexisting diabetes and hypertension (DM + HTN) were studied.Thirty-nine healthy age matched persons served as control subjects.In each patient a conventional two-dimensional echocardiography was performed and also an echocardiographic study with strain/strain rate imaging was studied.Analysis of RV longitudinal systolic strain were obtained in the apical four-chamber view of the RV for the assessment of the RV free wall(F-PLSS),interventricular septum (S-PLSS) and the global RV wall (G-PLSS).The entire RV longitudinal peak systolic strain rate (G-SRs),peak early-diastolic strain rate (G-SRe) and peak late-diastolic strain rate (G-SRa) were performed in the apical four-chamber view.Results Compared with controls,F-PLSS,S-PLSS,G-PLSS,G-SRs and G-SRe were decreased in 2-DM and DM + HTN (all P ＜0.01),with lower values in DM + HTN (P ＜0.05).In the patients coexisting diabetes and hypertension,G-SRa was significantly lower than those in the control group (P ＜ 0.05).Compared with 2-DM,this difference was not significant in controls and DM + HTN (P ＞0.05).Conclusions No matte the patients of 2-DM with or without hypertension,the early changes of RV dysfunction can be found by 2D-STI.Patients coexisting diabetes and hypertension may have worse RV dysfunction.