期刊：
GENERAL PHYSIOLOGY AND BIOPHYSICS,2020年39(2):123-134 ISSN：0231-5882
通讯作者：
Hu, Zhi-Xi;Liang, Hao
作者机构：
[Yang, Cheng-Long] Hunan Univ Chinese Med, Cardiovasc Dept, Hosp 1, Changsha, Hunan, Peoples R China.;[Yang, Cheng-Long] Hunan Univ Chinese Med, TCM Sch 1, Changsha, Hunan, Peoples R China.;[Hu, ZX; Liang, H; Hu, Zhi-Xi; Liang, Hao; Zeng, Yi-Di] Hunan Univ Chinese Med, Inst TCM Diagnost, Changsha 410208, Hunan, Peoples R China.;[Hu, ZX; Liang, H; Hu, Zhi-Xi; Liang, Hao; Zeng, Yi-Di] Hunan Univ Chinese Med, Hunan Prov Key Lab TCM Diagnost, Changsha 410208, Hunan, Peoples R China.
通讯机构：
[Hu, ZX; Liang, H] H;Hunan Univ Chinese Med, Inst TCM Diagnost, Changsha 410208, Hunan, Peoples R China.;Hunan Univ Chinese Med, Hunan Prov Key Lab TCM Diagnost, Changsha 410208, Hunan, Peoples R China.
关键词：
PCSK9;Cardiomyocytes;Macrophages;Pro-inflammatory cytokines;NF-kappa B signalling
摘要：
The upregulation of proprotein convertase subtilisin/kexin type 9 (PCSK9) was reported to be involved in regulating the levels of inflammatory markers and apoptosis in macrophages. This study aims to investigate the function and regulation of PCSK9 in myocardial ischaemia. The results of our study showed dramatically increased expression of PCSK9 induced by hypoxia/reoxygenation (H/R) stress rather than by apoptosis in primary murine cardiomyocytes and HL-1 cells. Moreover, PCSK9 promoted H/R-induced pro-inflammatory cytokine release from macrophages, while silencing of PCSK9 inhibited the expression of the pro-inflammatory cytokines TNF-alpha, IL-6 and IL-1 beta. Additionally, PCSK9 facilitated the release of pro-inflammatory cytokines from macrophages under H/R conditions, which decreased cardiomyocyte viability and promoted apoptosis of cardiomyocytes. For the underlying mechanisms, we identified PCSK9-induced NF-kappa B activation as being involved in the cardiomyocyte apoptosis, which was blocked by the NF-kappa B inhibitor BAY 11-7082. Collectively, this study provides new insights into the therapeutic possibility of regulating PCSK9 in cardiomyocytes for the treatment of ischaemic cardiomyopathy.
摘要：
Objective:To analyze the medication law of treating arrhythmia by software of Traditional Chinese Medicine Inheritance Support System(中医传承辅助平台).Methods:Through the collection of clinical cases in the cardiovascular department of the First Affiliated Hospital of Hu’nan University of Traditional Chinese Medicine from January 2015 to October 2019,after sorting out and screening,the data conforming to the inclusion criteria were entered into the software of the Chinese Medicine Inheritance Support System(v2.5),and the use of correlation mining analysis was used to study and summarize the medication rule of treating arrhythmia in clinical cases.Results:179 prescriptions were selected to treat arrhythmia,involving 203 TCM medicines.The association rules of frequency,medicinal properties,taste and tropism,association rules of medicine combinations.Conclsion:The pathogenesis of arrhythmia is mainly the Xu(虚),Tan(痰),Huo(火),Qizhi(气滞)and Yu(瘀).Therapeutic principles of dominated by Benxu(本虚)and taking into account Qingre Huatan(清热化痰),Jianpi Ningxin(健脾宁心)and Xingqi Huoxue Huayu(行气活血化瘀),etc.should were also noticed.
期刊：
Evidence-Based Complementary and Alternative Medicine,2020年2020 ISSN：1741-427X
通讯作者：
Hu, Zhixi
作者机构：
[Hu, Zhixi; Li, Lin] Hunan Univ Chinese Med, Domest Class Discipline Construct Project Chinese, Changsha, Hunan, Peoples R China.;[Hu, Zhixi; Li, Lin] Hunan Univ Chinese Med, Inst Tradit Chinese Med Diagnost, Changsha, Hunan, Peoples R China.;[Cheng, Bin; Zhong, Senjie; Qiu, Hong] Hunan Univ Chinese Med, Postgrad Sch, Changsha, Hunan, Peoples R China.
通讯机构：
[Hu, Zhixi] H;Hunan Univ Chinese Med, Domest Class Discipline Construct Project Chinese, Changsha, Hunan, Peoples R China.;Hunan Univ Chinese Med, Inst Tradit Chinese Med Diagnost, Changsha, Hunan, Peoples R China.
摘要：
目的 探讨急性脑卒中患者并发院内感染的特点及危险因素.方法 选取2018-01至2019-10湖南中医药大学第一附属医院神经内科收治的急性脑卒中患者110例为研究对象,分析患者发生院内感染的临床特点及危险因素.结果 110例患者总感染率为28.18％(31/110);下呼吸道感染率20.00％(22/110)明显高于其他部位,差异均有统计学意义(P<0.05).单因素分析显示,年龄≥60岁,出血性脑卒中,合并心脏病、肺疾病、吞咽功能障碍,有侵入性操作,使用质子泵抑制剂、镇静类药物,格拉斯哥昏迷评分(glasgow coma scale,GCS)≥8分,美国国立卫生研究院卒中量表(national institute of health stroke scale,NIHSS)评分≥15分,以及日常生活能力量表(activity of daily living scale,ADL)评分<50分与急性脑卒中患者发生感染呈正相关(P<0.05).多因素Logistic回归分析显示,年龄≥60岁,有侵入性操作,使用镇静类药物,合并吞咽功能障碍,NIHSS≥15分,以及ADL<50分为急性脑卒中患者发生感染的独立危险因素(P<0.05). 结论 急性脑卒中患者并发院内感染率较高,尤以下呼吸道感染多见,而年龄≥60岁,有侵入性操作,使用镇静类药物,合并吞咽功能障碍,NIHSS≥15分,以及ADL<50分均为急性脑卒中患者并发院内感染的独立危险因素.
摘要：
Objective To investigate the effects and possible mechanism of Shenmai Injection(参麦注射液)on hypertensive heart failure.Methods A total of 20 Dahl /SS salt-sensitive male rats were randomly divided into three groups: A normal group with 6 rats was given low-salt diet for 20 weeks;a model group(n = 7)and a Shenmai Injection group(n = 7)were given 20 g high-salt diets(8% sodium chloride)for 20 weeks to establish a rat model of hypertension heart failure.Left ventricular ejection fraction(LVEF)and left ventricular shortening fraction(LVFS)were detected by echocardiography.Serum amino-terminal brain natriuretic peptide(NT-proBNP)levels were measured.Rat urine was collected for liquid chromatography mass spectrometry(LC-MS)combined with technical analysis to screen differential metabolites and analyze related metabolic pathways.Results Compared with the normal group,LVEF and LVFS in the model group decreased,and serum NT-proBNP levels increased(P < 0.01).Compared with the model group,the LVEF and LVFS in the Shenmai Injection group increased,and the serum NTproBNP level decreased(P < 0.01).The urine metabolic profile of the 3 groups of rats showed a clear trend of separation.After intervention with Shenmai Injection,the 6 differential metabolites of 4-pyridoxine,kynuric acid,Larginine,creatine,inositol,5-L-glutamyl-bovine sulfonic acid had significant changes,and their metabolic pathways involve arginine and proline metabolism.Conclusion Shenmai Injection can normalize abnormal urine metabolism in hypertensive heart failure rats,and its mechanism may be related to regulating amino acid metabolism,energy metabolism and oxidative stress response.
