Objective:To analyze the relationship between resistant hypertension (RH) and hypertension, diabetes mellitus, chronic kidney disease, sodium, calcium, magnesium, phosphorus. Methods:A total of 475 patients with hypertension admitted to Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine from January 2021 to December 2023 were divided into hypertension group (HT group) and resistant hypertension group (RH group). We compared the differences between these two groups, and analyzed the influencing factors of RH, as well as the correlation between RH and the course of hypertension, diabetes mellitus, chronic kidney disease, and levels of sodium, calcium, magnesium and phosphorus. Results:Compared with HT group, RH group had a significantly higher blood pressure (P < 0.05), longer duration of hypertension, diabetes mellitus, and chronic kidney disease (P < 0.01) and a higher proportion of combined chronic kidney disease (P = 0.006). The duration of hypertension, serum sodium ion concentration (≥142.00 mmol/L), calcium ion concentration (2.19 to < 2.30 mmol/L), and 24h urinary phosphorus ion level were independent influencing factors of RH (P < 0.05). Conclusion:For hypertension patients with diabetes mellitus or chronic kidney disease, the risk of RH is significantly higher. The risk of RH may be lower in patients with blood sodium <142.00 mmol/L, blood calcium >2.29 mmol/L, 24h urine sodium and magnesium ions of 116.52 and 2.69 mmol, respectively, and higher 24h urine phosphorus ions.

Abstract Background Dilated cardiomyopathy (DCM) is a severe condition characterized by cardiac enlargement and declining heart function, often leading to refractory heart failure and life-threatening outcomes. Globally, and particularly in China, a notable challenge arises from the insufficient availability of targeted therapies demonstrating significant efficacy for DCM. Additionally, the application of traditional anti-heart failure drugs in DCM is constrained, as many patients exhibit a propensity for hypotension or show limited improvement in their heart failure symptoms. Kuoxin Formula (KXF), an internally agreed-upon prescription at Longhua Hospital, is supported by clear biological evidence for improving cardiac function and myocardial remodeling. Previous clinical studies have also demonstrated its potential to improve patients' quality of life. This trial aims to further evaluate the safety and efficacy of KXF in treating DCM -related heart failure. Method This prospective, randomized, double-blind, placebo-controlled, multicenter trial recruits 230 patients diagnosed with DCM (Qi-Yin deficiency combined with blood stasis syndrome) from five centers. Participants will be randomly assigned in a 1:1 ratio to either the KXF treatment group or a placebo group. The treatment will span 12 weeks, during which key indicators and adverse events will be monitored. The primary outcome is the proportion of patients whose NT-proBNP decreased by more than 30%. The secondary outcomes include the NYHA functional classification, TCM syndrome scores, echocardiographic parameters, TGF-β, PICP, CITP, galectin-3, ST2 levels, 6MWT, Lee's heart failure score, and MLHFQ score. Discussion: This study will be the first multicentered research conducted in China that utilizes a randomized, double-blind, placebo-controlled design to investigate the use of TCM in the treatment of dilated cardiomyopathy. It seeks to develop new theoretical frameworks and provide solid clinical data to support the integration of TCM and modern medicine in treating heart failure in DCM patients. Trial Registration: China Clinical Trial Registry, ChiCTR2300068937. Registered on March 1, 2023.

Background:In China, Shen'ge formula (SGF), a Traditional Chinese Medicine blend crafted from ginseng and gecko, holds a revered place in the treatment of cardiovascular diseases. However, despite its prevalent use, the precise cardioprotective mechanisms of SGF remain largely uncharted. This study aims to fill this gap by delving deeper into SGF's therapeutic potential and underlying action mechanism, thus giving its traditional use a solid scientific grounding. Methods:In this study, rats were subjected to abdominal aortic constriction (AAC) to generate pressure overload. Following AAC, we administered SGF and bisoprolol intragastrically at specified doses for two distinct durations: 8 and 24 weeks. The cardiac function post-treatment was thoroughly analyzed using echocardiography and histological examinations, offering insights into SGF's influence on vital cardiovascular metrics, and signaling pathways central to cardiac health. Results:SGF exhibited promising results, significantly enhanced cardiac functions over both 8 and 24-week periods, evidenced by improved ejection fraction and fractional shortening while moderating left ventricular parameters. Noteworthy was SGF's role in the significant mitigation of myocardial hypertrophy and in fostering the expression of vital proteins essential for heart health by the 24-week mark. This intervention markedly altered the dynamics of the Akt/HIF-1α/p53 pathway, inhibiting detrimental processes while promoting protective mechanisms. Conclusion:Our research casts SGF in a promising light as a cardioprotective agent in heart failure conditions induced by pressure overload in rats. Central to this protective shield is the modulation of the Akt/HIF-1α/p53 pathway, pointing to a therapeutic trajectory that leverages HIF-1α promotion and p53 nuclear transport inhibition.

Although doxorubicin (DOX) is an efficient chemotherapeutic drug for human tumors, severe cardiotoxicity restricts its clinical use. Cinnamaldehyde (CA), a bioactive component isolated from Cinnamonum cassia, possesses potent anti-oxidative and anti-apoptotic potentials. The major aim of this study was to evaluate the protective role of CA against DOX-induced cardiotoxicity. To this end, cardiomyocyte injury models were developed using DOX-treated H9c2 cells and DOX-treated rats, respectively. Herein, we found that CA treatment increased cardiomyocyte viability and attenuated DOX-induced cardiomyocyte death in vitro. CA further protected rats against DOX-induced cardiotoxicity, as indicated by elevated creatine kinase (CK) and lactate dehydrogenase (LDH) levels, myocardium injury, and myocardial fibrosis. CA alleviated DOX-induced myocardial oxidative stress by regulating reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) levels. Mechanistically, CA markedly accelerated nuclear translocation of nuclear erythroid factor 2-related factor 2 (Nrf2) and increased heme oxygenase-1 (HO-1) expression. Consequently, CA decreased DOX-induced cardiomyocyte ferroptosis, while Erastin (a ferroptosis agonist) treatment destroyed the effect of CA on increasing cardiomyocyte viability. Taken together, the current results demonstrate that CA alleviates DOX-induced cardiotoxicity, providing a promising opportunity to increase the clinical application of DOX.

目的:分析参蛤散对斑马鱼血管生长的干预作用.方法:制备参蛤散水煎液,以转基因斑马鱼(Fli1:EGFP)为研究对象,建立斑马鱼正常的血管生长模型,采用不同浓度参蛤散水煎液干预后,观察斑马鱼肠下静脉血管直径、平均交叉数和平均出芽数.使用血管内皮生长因子酪氨酸酶抑制剂(VRI)建立斑马鱼血管损伤模型,观察不同浓度参蛤散水煎液干预后斑马鱼脊背节间血管完整型和缺损型血管数量.结果:参蛤散各浓度组肠下静脉平均出芽数、平均交叉数及血管直径与正常组比较,差异均无统计学意义(P>0.05).参蛤散各浓度组及 VRI组完整型血管较正常组减少,缺陷型血管较正常组增多(P<0.01);与 VRI组比较,参蛤散各浓度组完整型血管明显增多,缺陷型血管减少(P<0.01).当参蛤散浓度为 3 μg/mL时,斑马鱼完整型血管数最多,缺陷型血管数最少(P<0.01).结论:参蛤散作用于斑马鱼正常血管生长并无明显作用,但可抑制 VRI的血管损伤作用.

目的 观察参蛤散对H9c2心肌细胞增殖的影响,为参蛤散后续研究提供依据.方法 采用H9c2心肌细胞株,制备参蛤散冻干粉进行干预,在24 h、48 h、72 h各时间点,用细胞计数试剂盒-8(CCK-8)法检测细胞吸光度值(OD值),细胞划痕实验检测细胞迁移率.结果 24 h参蛤散0.03 mg/mL、0.10 mg/mL、0.30 mg/mL、1.00 mg/mL组OD值高于对照组(P<0.05);48 h参蛤散各浓度组OD值均高于对照组(P<0.05);72 h参蛤散0.01 mg/mL组OD值高于对照组(P<0.05),其余组与对照组比较差异均无统计学意义(P>0.05).24 h参蛤散0.10 mg/mL、0.30 mg/mL、1.00 mg/mL组细胞迁移率大于对照组(P<0.05);48 h参蛤散0.01 mg/mL、0.10 mg/mL、0.30 mg/mL组细胞迁移率大于对照组(P<0.05);72 h参蛤散0.01 mg/mL、0.30 mg/mL组细胞迁移率大于对照组(P<0.05).结论 参蛤散可以促进H9c2心肌细胞增殖.

Heart failure (HF) is a worldwide health issue, and the application of Chinese medicine could provide new methods for the treatment of HF. Currently, there is no good medicine for diastolic heart failure (DHF) at present; therefore, we hope our study can confirm the effectiveness of Shen'ge formula (SGF) in the treatment of DHF and provide new strategies for patients with HF. To analyze the potential effect of SGF against HF, especially against DHF, we consult and summarize our previous researches on SGF. Our previous clinical studies demonstrated that SGF combined with conventional western medicine was able to improve ventricular contractility, heart function and reduce serum brain natriuretic peptide (BNP)/NT-proBNP levels of patients. The quality of life and clinical symptoms in HF patients were significantly improved after intervention. And basic researches also manifested that SGF was capable of preserving heart function, improving symptoms, and reducing cardiac hypertrophy and fibrosis in rats. Mechanisms involved in SGF ameliorating heart function probably were through downregulating AT1R, NADPH oxidase 2, 4, inhibiting TGF-β/smads pathway and RhoA/ROCK1 pathway. And SGF reducing serum metabolites accumulation was feasibly by up-regulating heart mRNA expressions of COX2, ATP6 and ATP8. In all, SGF exhibits many advantages in HF treatment according to the results of our previous researches, which indicates that SGF could be the potential beneficial strategy in DHF.

Doxorubicin, sold under the brand name Adriamycin among others, is an important drug for cancer therapy; however, its use is limited by its cardiotoxicity. Ginsenoside Rg2 is extracted from Panax ginseng C.A.Mey., Araliaceae, which is believed to have cardioprotective properties. However, to date, there have been no reports on whether ginsenoside Rg2 could protect cardiomyocytes against doxorubicin. In this study, we investigated the action and the underlying mechanisms of cardioprotection of ginsenoside Rg2 upon doxorubicin treatment. Cell counting kit-8 was used to determine cell viability; in addition, terminal deoxynucleotidyl transferase–mediated dUTP nick-end labeling staining was used to detect apoptotic cells. Western blotting was used to investigate the relevant pathways. LY294002, a phosphatidylinositol 3-kinase inhibitor, was also used in this study. Ginsenoside Rg2 significantly ( p < 0.01) neutralized cardiomyocyte apoptosis induced by doxorubicin in a dose-dependent manner, but this effect was blocked by LY294002. Furthermore, ginsenoside Rg2 upregulated protein kinase B phosphorylation through the phosphatidylinositol 3-kinase/protein kinase B pathway and inhibited p53 expression. These results suggest that ginsenoside Rg2 could attenuate doxorubicin-induced cardiomyocyte apoptosis via the phosphatidylinositol 3-kinase/protein kinase B pathway. Graphical abstract

目的 研究参蛤散对压力负荷型心力衰竭大鼠心脏的保护作用及机制.方法 采用腹主动脉缩窄术诱导大鼠压力负荷性心力衰竭.术后大鼠灌胃参蛤散[1.89g/(kg·d)]和比索洛尔[1 mg/(kg·d)],持续8周和12周.观察参蛤散和比索洛尔对大鼠心脏超声、血流动力学、病理形态以及凋亡相关分子的影响.结果 与模型组相比,参蛤散组射血分数和缩短分数升高(P＜0.01),左室舒张末期压(LVEDP)、左室压力最大上升/下 降速率(±dP/dtMax)和左室后壁(LVPW)降低(P＜0.05).参蛤散减少了心肌细胞凋亡,改善心肌肥厚,增加PECAM-1表达.与模型组相比,参蛤散能够下调p53、Bax、Caspase-3、β-MHC和NF-κB的mRNA表达.结论 参蛤散可改善压力负荷型心力衰竭大鼠的心功能,作用机制可能与抑制细胞凋亡、心肌肥厚和炎症等相关.

目的 观察扩心方对阿霉素诱导扩张型心肌病(DCM)大鼠心肌纤维化的改善作用并探究其作用机制.方法 选取Wistar大鼠68只,设8只为空白对照组(Con组),余60只以腹腔注射阿霉素建立DCM模型后随机分为模型组(Dox组),扩心方低(KXF-L组)、扩心方中(KXF-M组)、扩心方高(KXF-H组)剂量组、卡扩普利组(Cap组),每组12只,连续灌胃4周.治疗结束后,行心脏超声检查测左室结构及心功能变化;Masson染色观察心肌组织形态学改变;免疫组化观察心肌组织I型胶原(简称ColI)、III型胶原(简称ColIII)表达;蛋白芯片检测TGF-β1相关通路中各蛋白表达情况;蛋白印迹法(Western blot)测心肌TGF-β1、Smad2蛋白表达.结果 ①心超:与Con组相比,Dox组LVEDD、LVESD明显增加(P<0.01),LVEF、LVFS明显降低(P<0.01),IVS缩小(P<0.05),心肌重塑明显,而经过扩心方干预后,LVEDD、LVESD、LVEF、LVFS明显改善(P<0.01).②Masson染色:与Con组相比,Dox组心肌细胞肥大,间质增生,细胞排列紊乱,经扩心方干预后上述病理改变明显改善(P<0.01).③免疫组化:与Con组相比,Dox组ColI、ColIII表达明显增多(P<0.01).经扩心方治疗后有明显减少(P<0.05).④蛋白芯片:与Con组相比,Dox组TGF-β信号传导通路中有3种蛋白表达上调,分别为PP2A-alpha(上调1.42倍)、Smad2(上调1.5倍)、TGFBR2(上调1.44倍),而经扩心方干预后Smad2表达下调0.81倍、TGFBR2表达下调0.77倍,差异有统计学意义(P<0.01).⑤Western blot:与Con组相比,Dox组Smad2、TGF-β1蛋白表达明显增加(P<0.01),而经扩心方干预后,各剂量组TGF-β1表达均明显降低(P<0.01),KXF-H组Smad2蛋白明显降低(P<0.01).结论 扩心方可改善阿霉素诱导的DCM大鼠心肌纤维化,其机制可能与抑制TGF-β1/Smad2信号通路有关.

OBJECTIVE:To investigate whether peroxisome proliferator-activated receptor γ-coactivator-1α/nuclear respiratory factor 1 (PGC-1α/NRF1) activity can protect mitochondrial function in the setting of cardiac hypertrophy and improve cardiomyocyte energy metabolism.METHODS:Cardiac hypertrophy was modeled in H9c2 cells treated with isoproterenol (ISO) to assess the effects of Shenge San (, SGS) on cell viability and mitochondrial membrane potential. We assessed mitochondrial complex mRNA levels and mitochondrial oxidative phosphorylation factor mRNA and protein levels.RESULTS:Compared with the 100 μM ISO group, cell size was significantly decreased in the 0.3 mg/mL SGS and 20 μM ZLN005 (PGC-1α activator) groups ( < 0.01). Compared with the SGS (0.3) +ISO group, we observed lower phosphorylated adenosine monophosphate-activated kinase (AMPK) protein levels in the ISO and ZLN005+SGS+ISO groups ( < 0.01). Compared with the compound C group, SGS significantly increased PGC-1α expression in ISO-induced cardiac hypertrophy cells ( < 0.01), and this was inhibited by compound C pretreatment ( < 0.05). Compared with the ISO group, the mitochondrial red-green fluorescence ratio increased in the 0.3 mg/mL SGS group ( < 0.05). mRNA levels of cytochrome c oxidase subunit 1 (CO1) in the ISO and compound C groups were lower than those in control group ( 0.01), and the mRNA levels of CO1 and ATP8 were significantly lower in the ISO and compound C groups versus control ( 0.01). Compared with the SGS (0.3) +ISO group, ATP synthetase subunit 8 (ATP8) mRNA was significantly decreased in the ISO group ( < 0.01) and compound C+SGS+ISO group ( < 0.05). Compared with the SGS (0.3) +ISO group, NRF1 mRNA levels were significantly decreased ( < 0.05) in the ISO and compound C+SGS+ISO groups.CONCLUSIONS:SGS can attenuate ISO-induced cardiomyocyte hypertrophy, restore the decrease in mitochondrial membrane potential, and upregulate PGC-1α/NRF1 levels. Notably, these effects can be blocked by AMPK inhibitor-compound C.

目的 观察益气养阴方联合阿胶治疗气阴两虚型慢性心力衰竭的临床疗效.方法 选取2016年7月—2018年6月上海中医药大学附属龙华医院心病科收治的气阴两虚型慢性心力衰竭病人105例,随机分为对照组、治疗A组和治疗B组,每组35例.对照组予常规西药抗心力衰竭治疗,治疗A组在对照组基础上加用益气养阴方,治疗B组在治疗A组基础上加阿胶,3组均治疗8周.观察两组治疗前后中医证候积分、6 min步行距离、心脏射血分数(EF)、每搏输出量(SV)变化.结果 治疗后,3组中医证候积分、6 min步行距离、EF、SV均较治疗前改善(P<0.01);与对照组比较,治疗A组和治疗B组中医证候积分、6 min步行距离、EF、SV改善均更明显(P<0.01);与治疗A组比较,治疗B组中医证候积分、6 min步行距离改善更明显(P<0.05).结论 益气养阴方可以改善慢性心力衰竭病人中医证候积分、6 min步行距离、EF、SV,联合阿胶可进一步增强其疗效.

Introduction: Diastolic heart failure (DHF) is an important pathological type of heart failure, that involves multiple organ dysfunction and multiple complications. The prevalence of DHF is high, and effective treatments are lacking. Chinese herbs are an alternative therapy for DHF. Shen'ge formula (SGF) is a classical formula from which patients can benefit, but convincing evidence of its efficacy is lacking. Therefore, we designed this randomized controlled trial protocol. Methods/design: This randomized, double-blind, placebo-controlled clinical trial will evaluate the efficacy and safety of SGF in the treatment of DHF. A total of 130 patients with DHF will be enrolled in the trial and treated with SGF granules or placebo for 12 weeks and followed up for 12 weeks. The primary outcome measurement will be to changes in plasma N-terminal brain natriuretic peptide precursor before versus after treatment, while the second primary outcome measurement will be changes in heart function before versus after treatment and the 12-week follow-up period. It will also include echocardiography, a cardiopulmonary exercise test, cardiac function grading, traditional Chinese medicine syndrome score, and the Minnesota Heart Failure Quality of Life Scale. Adverse events will be evaluated throughout the trial. Discussion: The results of this trial will demonstrate whether SGF could alleviate symptoms, improve cardiac function, reduce readmission rates, and improve quality of life of patients with DHF.

目的 观察红参水煎液干预斑马鱼血管生长的作用,为红参的临床应用提供依据.方法 建立斑马鱼正常血管生长模型,加入不同浓度的红参水煎液,观察对斑马鱼肠下静脉情况.采用血管内皮生长因子酪氨酸酶抑制剂Ⅱ(VRI)建立斑马鱼血管损伤模型,采用不同浓度红参水煎液干预,观察斑马鱼脊背节间血管情况.结果 红参水煎液各浓度组平均交叉数与空白对照组比较差异均无统计学意义(P>0.05);红参水煎液3μg/mL组、30μg/mL组、100μg/mL组出芽数多于空白对照组(P<0.01);红参水煎液10μg/mL组血管直径较空白对照组明显增加(P<0.05).在斑马鱼血管损伤模型中,与空白对照组比较,VRI组及红参水煎液各浓度组完整血管个数明显减少(P<0.01),缺陷血管明显增多(P<0.01);与VRI组比较,红参水煎液1μg/mL组完整血管数增多(P<0.05),红参水煎液3μg/mL组、10μg/mL组、30μg/mL组、100μg/mL组完整血管明显增多(P<0.01),红参水煎液10μg/mL组、100μg/mL组缺陷血管数明显减少(P<0.01).结论 红参水煎液有一定促进斑马鱼血管生长的作用,并能够抑制VRI诱导的血管损伤.

心衰是当今社会严重危害人类健康的一种复杂的临床综合征,其致病原因和作用机制复杂,为了更加深入地探索其发病机制和干预途径,需要选择和建立适合的动物模型.通过查阅近几年国内外文献,本文综述了常见的心衰动物模型建模方法及优缺点比较.各种模型有其自身的特点和优势,为今后在心衰模型选择方面提供参考.

目的 观察益气养阴方联合阿胶对慢性心力衰竭患者心功能及生活质量的作用.方法 将105例气阴两虚型心力衰竭患者随机分到对照组、治疗A组和治疗B组,治疗8周.对照组予西药常规抗心衰治疗,治疗A组在常规治疗基础上加用益气养阴方,治疗B组在治疗A组基础上加用阿胶(6 g/d).治疗前后分别观察患者纽约心功能分级(NY-HA)、明尼苏达心力衰竭生活量表(MLHF)评分及血浆BNP,观察益气养阴方联合阿胶的抗心衰作用.结果 治疗8周后,与治疗前比较,3组MLHF评分、血浆BNP均明显下降(P＜0.01);与对照组比较,两治疗组血浆BNP下降更明显(P＜0.05),且两治疗组差异无统计学意义(P＞0.05),MLHF评分治疗A组与治疗B组均较对照组下降明显(P＜0.05,P＜0.01),且治疗B组更优(P＜0.05).在改善NYHA心功能方面,治疗A组与对照组差异无统计学意义(P＞0.05),治疗B组优于对照组(P＜0.01).结论 益气养阴方可改善慢性心力衰竭患者心功能及生活质量,联合阿胶可增强临床疗效.

周端教授认为,高血压病病位在头窍,与肝、肾、心、脾四脏密切相关,阴虚是其病理核心,贯穿疾病始终.高血压病总属阴虚阳亢,虚者多而实者少,可分为初期、中期、晚期,在高血压病初期、中期应用膏方较为适宜.周老师运用膏方调治高血压病时,注重辨证与辨病、辨体质相结合,注重情志调节.在开具膏方时,重视滋补肝肾、调气活血,以平肝熄风治其标,更注重补肝肾之阴治其本,常用熟地黄、黄精、枸杞子、山萸肉等补肾填精,滋水涵木,以阴制阳;重视脾胃功能,将培元顾胃法作为膏方治疗高血压病的重要治则,以白术、茯苓、薏苡仁、六神曲、山药等培元健脾;善加活血之品,治疗"血瘀"之标实之证;根据患者气之升降,酌加陈皮、香附、川楝子、枳壳等使其顺"苍天之气",使各脏"阴密阳固".

目的 观察人参皂苷Rg1对斑马鱼血管生长的影响.方法 使用转基因斑马鱼(Fli-1:EGFP),建立正常血管生长模型,人参皂苷Rg1(1、3、10、30、100 μmol/L)干预48 h后,观察斑马鱼肠下血管的直径、出芽和交叉情况;VRI诱导24 h建立血管损伤模型,人参皂苷Rg1干预24 h后,观察斑马鱼节间血管生长情况.结果 正常血管生长模型中,与正常组比较,人参皂苷Rg1的3μmol/L组交叉数有所增多(P＜0.05),人参皂苷Rg1各组出芽数均明显增多(P＜0.01),人参皂苷Rg1的3、100 μmol/L组直径明显增粗(P＜0.01),10 μmol/L组直径有所增粗(P＜0.05);血管损伤模型中,与正常组相比,VRI组及人参皂苷Rg1各浓度组的完整血管明显减少,缺陷血管明显增多(P＜0.01);与VRI组相比,人参皂苷Rg1的10、30、100μmol/L的完整型血管明显增多(P＜0.01),3μmol/L组的完整血管有所增多(P＜0.05),人参皂苷Rg1各组缺陷型血管明显减少(P＜0.01).结论 人参皂苷Rg1在一定浓度时可以促进斑马鱼血管生长,并能抑制VRI诱导的血管损伤.

目的 探讨参蛤散对离体大鼠胸主动脉的舒张作用及其机制.方法 采用离体大鼠血管功能实验装置,观察累积浓度的参蛤散对U46619预收缩的大鼠离体胸主动脉环张力的影响;使用参蛤散预处理血管环后,观察累积浓度的CaCl2对苯肾上腺素(Phe)和氯化钾(KCL)预收缩的大鼠离体胸主动脉环张力的影响;采用不同钙离子拮抗剂预处理血管环后,分别观察累积浓度参蛤散对血管环张力变化的影响.结果 参蛤散对U46619预收缩的离体大鼠胸主动脉环有浓度依赖性的舒张作用(P＜0.01);使用参蛤散预处理血管环后,累积浓度的CaCl2对血管环的收缩幅度明显下降(P＜0.01);使用钙离子拮抗剂预处理血管环后,均可明显增加参蛤散的血管舒张效应,且维拉帕米的效果更加明显(P＜0.01).结论 参蛤散能够呈剂量依赖性的产生血管舒张作用,其舒张作用可能与钙离子通道的抑制有关.

目的 观察人参皂苷Rb3对过氧化氢(H2 O2)诱导的心肌细胞损伤模型中缺氧诱导因子1α(HIF-1α)、血管内皮生长因子(VEGF)的调节作用,并探讨其作用机制.方法 采用心肌细胞株H9c2细胞,人参皂苷Rb3(25μmol/L)预处理24 h后,加入H2 O2(400μmol/L)分别诱导1 h和2 h,并使用磷酯酰激醇3-激酶(PI3K)抑制剂LY294002(LY294),通过荧光定量逆转录-聚合酶链式反应法测定细胞中HIF-1α、VEGF的mRNA表达水平.结果 与空白对照组相比,H2 O2增强了HIF-1α和VEGF的mRNA表达(P<0.01);与H2 O2组相比,人参皂苷Rb3可提高HIF-1α、VEGF的mRNA水平(P<0.01);与H2 O2+Rb3组相比,LY294降低了H2 O2作用2 h后HIF-1α的mRNA表达水平(P<0.01).结论 人参皂苷Rb3可以促进H2 O2诱导的心肌细胞损伤模型中HIF-1α和VEGF的mRNA表达,且前者可能与PI3K/蛋白激酶B(Akt)信号通路有关.