Changes of c-fos and c-jun mRNA Expression in Angiotensin Ⅱ-induced Cardiomyocyte Hypertrophy and Effects of Sodium Tanshinone ⅡA Sulfonate

The changes of proto-oncogene c-fos and c-jun mRNA expression in angiotensin Ⅱ （AngⅡ）-induced hypertrophy and effects of sodium tanshinone ⅡA sulfonate （STS） in the primary culture of neonatal rat cardiomyocytes were investigated. Twelve neonatal clean grade Wistar rats were selected. The cardiomyocytes were isolated, cultured and divided according to different treatments in the medium. The cardiomyocyte size was determined by phase contrast microscope, and the rate of protein synthesis was measured by [3H]-Leucine incorporation. The c-fos and c-jun mRNA expression in cardiomyocytes was detected by reverse transcription polymerase chain reaction （RT-PCR）. It was found after cardiomyocytes were treated with AngⅡ for 30 min, the c-fos and c-jun mRNA expression in cardiomyocytes was increased significantly （P〈0.01）. After treatment with AngⅡ for 24 h, the rate of protein synthesis in AngⅡ group was significantly increased as compared with control group （P〈0.01）. After treatment with AngⅡ for 7 days, the size of cardiomyocytes in AngⅡ group was increased obviously as compared with control group （P〈0.05）. After pretreatment with STS or Valsartan before AngⅡ treatment, both of them could inhibit the above effects of AngⅡ （P〈0.05 or P〈0.01）. It was suggested that STS could ameliorate AngⅡ-induced cardiomyocyte hy- pertrophy by inhibiting c-fos and c-jun mRNA expression and reducing protein synthesis rate of cardiomyocytes.

Protective Effect and Mechanism of Sodium Tanshinone ⅡA Sulfonate on Microcirculatory Disturbance of Small Intestine in Rats with Sepsis

To explore the protective effect of sodium tanshinone ⅡA sulfonate（STS） on microcirculatory disturbance of small intestine in rats with sepsis,and the possible mechanism,a rat model of sepsis was induced by cecal ligation and puncture（CLP）.Rats were randomly divided into 3 groups：sham operated group（S）,sepsis group（CLP） and STS treatment group（STS）.STS（1 mg/kg） was slowly injected through the right external jugular vein after CLP.The histopathologic changes in the intestinal tissue and changes of mesenteric microcirculation were observed.The levels of tumor necrosis factor-α（TNF-α） in the intestinal tissue were determined by using enzyme-linked immunoabsorbent assay（ELISA）.The expression of intercellular adhesion molecule-1（ICAM-1） in the intestinal tissue was detected by using immunohistochemisty and Western blot,that of nuclear factor κB（NF-κB） and tissue factor（TF） by using Western blot,and the levels of NF-κB mRNA expression by using RT-PCR respectively.The microcirculatory disturbance of the intestine was aggravated after CLP.The injury of the intestinal tissues was obviously aggravated in CLP group as compared with S group.The expression levels of NF-κB p65,ICAM-1,TF and TNF-α were upregulaed after CLP（P0.01）.STS post-treatment could ameliorate the microcirculatory disturbance,attenuate the injury of the intestinal tissues induced by CLP,and decrease the levels of NF-κB,ICAM-1,TF and TNF-α（P0.01）.It is suggested that STS can ameliorate the microcirculatory disturbance of the small intestine in rats with sepsis,and the mechanism may be associated with the inhibition of inflammatory responses and amelioration of coagulation abnormality.

Tanshinone ⅡA： an overview of its biological activity and the molecular mechanism

Danshen, the rhizome of Salvia miltiorrhiza Bunge, has been used in traditional Chinese medicine （TCM） for treatment of various diseases. Tanshinone IIA （TSA） is one of the main active components of Danshen, which has multiple bioactivities. This article reviews the research progress of TSA in the treatment of cardiovascular disease, anti-inflammatory and immune, anti-tumor, liver protection, neuroprotection. It provides more ideas for the clinical application of TSA and the development of drug resistance.

Altered Erythrocyte Membrane Calcium Binding in Hypertensive Rats and the Effects of Sodium Tanshinone Ⅱ-A Sulphonate on It

The calcium binding of erythrocyte membrane was determined in spontaneous hypertensiverats (SHR)and renovascular hypertensive rats (RVHR two-kidney, one-clip model) and the effect ofsodium tanshinone Ⅱ-A sulfonate(DS-201)on the calcium binding in SHRs was investigated. Ourresults show that the basal calcium binding was reduced in SHRs (P<0.01 vs WKY),while the maximalcalcium binding was not,but both typies calcium bindings had no significant change in RVHRs.Sodiumtanshinone Ⅱ-A sulfonate (125μ mol/L)have no effect on the calcium binding of ecythrocyte membraneof SHR in vitro.These data further support the hypothesis that there is a cell membrane abnormalitypresent in SHRs which may possibly serve as a marker genetics of in hypertension.

基于Meta分析的丹参酮Ⅱ_A磺酸钠注射液治疗急性脑梗死临床评价研究

目的:采用Meta分析方法评价丹参酮Ⅱ_A磺酸钠注射液治疗急性脑梗死的有效性及安全性。方法:计算机检索the Cochrane library、PubMed、Embase、SinoMed、中国知网、维普期刊数据库和万方数据库有关丹参酮Ⅱ_A磺酸钠注射液治疗急性脑梗死的随机对照试验,检索时限为各数据库建库至2016年10月。采用Cochrane风险评价表进行偏倚风险评价,提取资料通过Stata 13.1进行Meta分析。结果:最终共纳入13个随机对照试验,累计1 273名患者。Meta分析结果显示,对比西医常规治疗,丹参酮Ⅱ_A磺酸钠注射液辅助西医常规治疗急性脑梗死可提高临床总有效率(RR=1.22,95%CI:1.16~1.28,P<0.01),改善神经功能缺损(MD=-5.08,95%CI:-7.40^-2.77,P<0.01),降低炎性指标。在减少恶化情况方面,差异无统计学意义。有7篇文献明确无不良反应,2篇研究报道了共11例不良反应,其他文献均未对安全性做出说明,无严重不良反应。敏感性分析显示结果稳定性较好。结论:现有证据表明,丹参酮Ⅱ_A磺酸钠注射液治疗急性脑梗死在临床疗效、神经功能缺损改善及炎性指标减少等方面比单用西医常规疗效较好。但基于现有研究缺陷,所获得的支持证据强度有待提高,尚需要更多设计严谨、随访时间更长的临床研究予以证实。

Effects of Tanshinone Combined with Western Medicine on Clinical Symptoms and Cardiac Function in Patients with Acute Heart Failure

OBJECTIVE: To explore the effects of Tanshinone combined with western medicine on clinical symptoms and cardiac function in patients with acute heart failure. METHODS: The medical records of 96 patients with acute heart failure were randomly divided into 2 groups(48 cases in observation group and 48 cases in control group). The control group was treated with conventional western medicine, and the observation group was treated with Tanshinone IIA sulfonic acid natrium on the basis of western medicine. The traditional Chinese medicine(TCM) syndromes scores before and after treatment(after 28 d of treatment), clinical efficacy, and cardiac echocardiographic indexes and serum biochemical indicators before and after treatment were observed in the 2 groups. RESULTS: After treatment, the scores of TCM syndromes in the 2 groups were significantly decreased(P < 0.05), and the change in observation group was significantly greater than that in control group(P < 0.05). The total clinical effective rate in observation group was significantly higher than that in control group(91.67% vs 75.00%)(P < 0.05). After treatment, the echocardiographic indexes of left ventricular end-diastolic diameter(LVEDD) and left ventricular end-systolic diameter(LVESD) values were significantly reduced in the 2 groups while the left ventricular ejection fraction(LVEF) and stroke volume(SV) value were significantly increased, and the changes in observation group were significantly larger than those in control group(P < 0.05). After treatment, the levels of serum nuclear factor-kappaB(NF-KB), interleukin-1β(IL-1β) and N-terminal pro-brain natriuretic peptide(NT-proBNP) were significantly decreased in the 2 groups(P < 0.05), while the 6-keto-prostaglandin F1α(6-ketoPGF1α) level was significantly increased. And the changes in observation group were significantly greater than those in control group(P < 0.05). CONCLUSION: Tanshinone combined with western medicine can significantly improve the clinical symptoms of patients with acute heart failure, improve cardiac function, reduce the myocardial damage degree, and effectively reduce the risk of short-term recurrence and death, and it has exact clinical efficacy.

Effect of Sodium Tanshinone ⅡA Sulfonate on Phosphorylation of Extracellular Signal-regulated Kinasel/2 in Angiotensin Ⅱ-induced Hypertrophy of Myocardial Cells

Objective： To observe the effects of sodium tanshinone ⅡA sulfonate （STS） on angiotensin Ⅱ （Ang Ⅱ）-induced hypertrophy of myocardial cells through the expression of phosphorylated extracellular signal-regulated kinase （p-ERK1/2）. Methods： In the primary culture of neonatal rat myocardial cells, the total protein content in myocardial cells was determined by coomassie brilliant blue and the protein synthesis rate was measured by [3H]-Leucine incorporation as indexes for hypertrophy of myocardial cells. The expression of p-ERK1/2 was determined using Western blot and immunofluorescence labeling. Results： （1） The total protein and protein synthesis rate increased significantly in contrast to the control group after the myocardial cells were stimulated by Ang Ⅱ （1 μ mol/L） for 24 h; STS markedly inhibited the increment of the total protein level induced by Ang Ⅱ and the syntheses of protein. （2） After pretreatment of myocardial cells with Ang Ⅱ （1 μmol/L） for 5 min, the p-ERK1/2 protein expression was increased, with the most obvious effect shown at about 10 min; pretreatment of myocardial cells with STS at different doses （2, 10, 50μmol/L） for 30 min resulted in obvious inhibition of the expression of p-ERK1/2 stimulated by Ang Ⅱ in a dose-dependent manner. （3） After the myocardial cells were stimulated by AngⅡ （1 μ mol/L）, the immunofluorescence of ERK1/2 rapidly appeared in the nucleus. The activation and translocation process of ERK1/2 induced by Ang Ⅱ was blocked distinctly by STS. （Conclusion： STS inhibited the myocardial cell hypertrophy induced by Ang Ⅱ, and the mechanism may be associated with the inhibition of p-ERK1/2 expression.

Effect of Sodium Tanshinone ⅡA Sulfonate on Cardiac Myocyte Hypertrophy and Its Underlying Mechanism

Objective： To investigate the effects of sodium tanshinone Ⅱ A sulfonate （STS） on the hypertrophy induced by angiotensin Ⅱ（Ang Ⅱ） in primary cultured neonatal rat cardiac myocytes. Methods： The effect of STS on cytotoxicity was evaluated using the 3-（4,5-dimethylthiazol-2-yl）-3,5- phenytetrazoliumromide （MTT） assay. As indexes for cardiocyte hypertrophy, cell size was determined by phase contrast microscopy and protein synthesis rate was measured by 3H-leucine incorporation. The proto-oncogene c-fos mRNA expression of cardiocytes was assessed using reverse transcription polymerase chain reaction （RT-PCR）. Results： STS could inhibit cardiocyte hypertrophy, increase the protein synthesis rate and enhance proto-oncogene c-fos mRNA expression in cardiocytes induced by Ang Ⅱ（P〈0.01）, with an effect similar to that of Valsartan, the Ang Ⅱ receptor antagonist. Conclusion： STS can prevent the hypertrophy of cardiac myocytes induced by Ang Ⅱ, which may be related to its inhibition of the expression of proto-oncogene c-fos mRNA.

Sodium Tanshinone Ⅱ A sulfonate for acute myocardial infarction:a systematic review and Meta-analysis

OBJECTIVE: To investigate the efficacy and safety of Sodium tanshinone ⅡA sulfonate(STS) plus the conventional treatment on acute myocardial infarction(AMI) patients.METHODS: We searched several electrical databases and hand searched several Chinese medical journals up to January 2019. Randomized controlled trials(RCTs) comparing STS plus conventional treatment with conventional treatment were retrieved.Study screening, data extraction, quality assessment, and data analysis were conducted in accordance with the Cochrane standards.RESULTS: Sixteen trials involving 1383 people were included. The Meta-analysis showed STS combined with conventional treatment was a better treatment option than conventional treatment alone in reducing the risk of mortality, heart failure, arrhythmia and shock. In addition, STS was associated with improvement in left ventricular ejection fraction(LVEF) and left ventricular end diastolic dimension(LVEDD). No significant difference of STS was found on recurrent angina and recurrent AMI. However,the safety of STS remained uncertain for limited data.CONCLUSION: Compared with conventional treatment alone, STS combined with conventional treatment may provide more benefits for patients with AMI. Due to the fact that the overall quality of all included trials is generally low, further large-scale high quality trials are warranted.

Sodium Tanshinone Ⅱ A Sulfonate Injection as Adjuvant Treatment for Unstable Angina Pectoris: A Meta-Analysis of 17 Randomized Controlled Trials

Objective： To systematically evaluate the effectiveness and safety of Sodium Tanshinone ⅡA Sulfonate Injection（STS） as one adjuvant therapy for treating unstable angina pectoris（UAP）. Methods： Randomized controlled trials（RCTs） of UAP treated by STS were searched in the China National Knowledge Infrastructure Database（CNKI）, VIP Database for Chinese Technical Periodicals（VIP）, Wanfang Database, the Chinese Biomedical Literature Database（CBM）, Web of Science, the Cochrane Library, Embase, and Pub Med, which from inception to January, 2016. The Cochrane Risk Assessment Tool was used to evaluate the methodological quality of the RCTs. The Review Manager 5.3 software was used to conduct the metaanalysis. Results： The results showed that 17 RCTs involving 1,372 patients were included. The meta-analysis indicated that the combined use of STS and Western medicine（WM） in the treatment of UAP can obviously improve the total effective rate [risk ratio（RR）=1.31, 95% confidence interval（CI）（1.24,1.39）, P〈0.0001], and the total effective rate of electrocardiogram [RR=1.43, 95% CI（1.30,1.56）, P〈0.0001], decrease the level of CRP [mean difference（MD）=–3.06, 95%CI（–3.85, –2.27）, P〈0.00001], fibrinogen [MD=–1.03, 95% CI（–1.16, –0.89）, P〈0.00001], and whole blood high shear viscosity [MD=–0.70, 95% CI（–0.92, –0.49）, P〈0.00001]. Additionally, the occurrence of adverse drug reaction of the experimental group was significantly higher than that of the control group [RR=3.57, 95% CI（1.28, 9.94）, P〈0.05]. Conclusions： Compared with WM, the combined use of STS was more effective.

丹参酮Ⅱ-A磺酸钠对纤维化人肾间质成纤维细胞体外增殖及cyclin E蛋白表达的影响

目的研究丹参酮Ⅱ-A磺酸钠(sodium tanshinoneⅡ-A sulfonate,DS-201)对人肾间质纤维化来源的成纤维细胞(human renal interstitial fibroblasts,hRIFs)体外增殖及细胞周期素E(cyclin E)基因表达的影响,探讨该药治疗肾间质纤维化的作用机制。方法体外培养并鉴定hRIFs;用四甲基偶氮唑(MTT)法检测对照组与不同DS-201浓度组hRIFs的增殖活性;用免疫细胞化学S-P法和图像分析技术检测对照组与不同DS-201浓度组hRIFs cyclin E基因的表达。结果随药物浓度的升高和作用时间的延长,抑制率逐渐升高,抑制作用逐渐增强,呈剂量依赖性和时间依赖性。用药组阳性细胞的平均光密度值在第3、5、7、9天显著低于对照组(P<0.05,P<0.01),第1天用药各组与对照组之间无统计学差异(P>0.05)。结论①DS-201对hRIFs体外增殖有显著抑制作用,可能是其治疗肾间质纤维化的机制之一。②DS-201抑制hRIFs体外增殖可能是通过抑制细胞中cyclin E基因的表达,阻滞细胞通过G1/S关卡,延长细胞周期实现的。

丹参酮ⅡA磺酸钠和丹参素对猪冠状动脉平滑肌细胞钙激活钾通道的激活机制

目的研究丹参酮ⅡA磺酸钠(DS-201)和丹参素(DS-182)的冠状动脉舒张作用除了已知的机制外,是否还与钙激活钾通道(KCa)有关。方法猪冠脉平滑肌细胞贴附式和内面向外式膜片钳单通道电流记录技术。结果DS-201和DS-182均可激活冠脉平滑肌细胞KCa,但DS-201在内面向外膜片方式下激活KCa;而DS-182在细胞贴附膜片方式下激活KCa。结论DS-201和DS-182激活KCa的作用机制不同。DS-201能直接激活KCa,而DS-182则可能需要一系列胞内过程。这种差异可能与二者的结构和溶解性质不同有关。

丹参酮Ⅱ A 磺酸钠对脑缺血/ 再灌注模型大鼠脑梗死及神经功能评分影响的实验研究

目的 研究丹参酮Ⅱ A 磺酸钠对缺血/ 再灌注（I/R）模型大鼠脑梗死体积、脑含水量及神经功能 评分的影响.方法 40 只SD 大鼠按随机数字表法分成假手术组、模型组、丹参酮Ⅱ A 预处理组、丹参酮Ⅱ A 治 疗组，每组10 只。用改良Longa 栓线法复制大脑中动脉闭塞（MCAO）模型，2 h 后开放血流再灌注。24 h 处死 大鼠取脑。比较分析各组大鼠脑梗死体积（%）、脑含水量（%）及术后12 h 和24 h 神经功能评分. 结果 模型 组脑梗死体积明显高于丹参酮Ⅱ A 预处理组和治疗组〔（33.5±6.7）% 比（24.3±4.8）%、（25.3±4.6）%，均P ＜ 0.01〕；模型组脑含水量明显高于预处理组和治疗组〔（84.6±4.2）% 比（79.9±6.3）%、（80.1±6.0）%，均P ＜0.01〕； 模型组12 h、24 h 神经功能评分（分）高于预处理组和治疗组（12 h ：3.10±0.48 比2.30±0.59、2.50±0.50，24 h ： 3.30±0.62 比1.90±0.36、2.10±0.46，P ＜0.05 或P ＜0.01）.结论 丹参酮Ⅱ A 磺酸钠可以减少I/R 模型大鼠 的脑梗死体积，降低脑含水量，改善神经功能评分.

丹参酮ⅡA磺酸钠对高血压病病人血清Ⅰ型及Ⅲ型前胶原水平的影响

目的探讨丹参酮ⅡA磺酸钠注射液(诺新康)对高血压病病人血清Ⅰ型前胶原羧基端肽(PⅠCP)和Ⅲ型前胶原氨基端肽(PⅢNP)水平的影响。方法60例高血压病病人随机分为对照组和治疗组。对照组采用常规疗法,积极控制血压。治疗组在对照组治疗基础上予丹参酮ⅡA磺酸钠注射液治疗。采用放射免疫分析法测定两组病人治疗前后血清PⅠCP,PⅢNP浓度,彩色多普勒超声心动图测量左室质量指数(LVMI)。结果高血压病病人血清PⅠCP和PⅢNP水平与LVMI呈正相关(r=0.4286、0.5224,P<0.05),治疗后两组血清PⅠCP和PⅢNP水平较治疗前均有下降(P<0.05或P<0.01),但治疗组下降更明显(P<0.05)。结论PⅠCP,PⅢNP水平是反映高血压病病人心肌胶原合成活跃程度、左心室肥大的敏感指标。丹参酮ⅡA磺酸钠注射液能有效降低高血压病病人血清PⅠCP,PⅢNP水平,对逆转高血压病左室肥厚具有明确的作用。

丹参酮Ⅱa磺酸钠抑制巨噬细胞源性生长因子刺激平滑肌细胞c－myc基因表达

本实验采用原位杂交技术，探讨丹参酮Ⅱａ磺酸钠对血管平滑肌细胞增殖相关基因ｃ－ｍｙｃ表达的影响。观察到巨噬细胞源性生长因子可明显促进平滑肌细胞ｃ－ｍｙｃ高表达；丹参酮Ⅱａ磺酸钠能阻止巨噬细胞源性生长因子刺激平滑肌细胞的作用，使ｃ－ｍｙｃ表达水平下降，提示丹参酮Ⅱａ磺酸钠可能在动脉粥样硬化疾病中阻止平滑肌细胞增殖起重要作用。

丹参酮ⅡA磺酸钠对AngⅡ诱导的心肌细胞肥大反应中磷酸化细胞外信号调节激酶1／2的作用

目的从细胞外信号调节激酶1/2(ERK1/2)激活角度研究丹参酮ⅡA磺酸钠(sodium tanshinoneⅡ Asulfonate,STS)对血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)诱导的心肌肥大反应中的作用。方法培养新生大鼠心肌细胞,考马斯亮蓝法测定心肌细胞蛋白含量、[3H]-亮氨酸参入法测定蛋白合成速率作为心肌肥大指标;用免疫荧光标记法和Western blot测定磷酸化ERK1/2蛋白(p-ERK1/2)表达。结果(1)AngⅡ(1μmol·L-1)处理24h,心肌细胞[3H]-亮氨酸参入率、蛋白含量明显增加,STS能明显抑制AngⅡ介导心肌细胞[3H]-亮氨酸参入率、蛋白含量的增加;(2)AngⅡ刺激心肌细胞可见胞核内出现磷酸化ERK1/2荧光染色,丹参酮ⅡA可阻断AngⅡ引起的ERK1/2活化、入核过程;(3)用AngⅡ(1μmol·L-1)处理心肌细胞5min,磷酸化ERK1/2蛋白(p-ERK1/2)表达即开始增加,10min左右时最明显。以AngⅡ(1μmol·L-1)处理心肌细胞10min,磷酸化ERK1/2蛋白(p-ERK1/2)表达为标准,预先以STS(2,10,50μmol·L-1)处理心肌细胞30min,发现STS可明显抑制AngⅡ诱导的心肌细胞磷酸化ERK1/2蛋白表达;(4)预先以不同浓度STS处理心肌细胞30min,发现STS对AngⅡ诱导的心肌细胞磷酸化ERK1/2蛋白表达的抑制作用存在剂量依赖性。结论STS可以抑制AngⅡ诱导的心肌肥厚,其机制与抑制磷酸化ERK1/2表达有关。

丹参酮ⅡA磺酸钠对AngⅡ诱导的心肌细胞肥大反应中磷酸化MAPK的作用

目的 主要从丝裂原活化蛋白激酶（MAPK）激活及失活的角度研究丹参酮ⅡA磺酸钠（STS）对血管紧张肽Ⅱ（AngⅡ）诱导的心肌肥大反应中的作用。方法 培养新生大鼠心肌细胞，考马斯亮蓝法测定心肌细胞蛋白含量、[^3H]-亮氨酸掺入法测定蛋白合成速率作为心肌肥大指标；用Western blot测定磷酸化MAPK蛋白（p44MAPK、p42MAPK）表达。结果 ①AngⅡ（1μmol／L）处理24h，心肌细胞[^3H]-亮氨酸掺入率、蛋白含量明显增加，STS能明显抑制AngⅡ介导心肌细胞[^3H]-亮氨酸掺入率、蛋白含量的增加。②用AngⅡ（1μmol／L）处理心肌细胞5min，磷酸化MAPK蛋白（p44MAPK、p42MAPK）表达即开始增加，10min左右时最明显。以AngⅡ（1μmol／L）处理心肌细胞10min，磷酸化MAPK蛋白（p44MAPK、p42MAPK）表达为标准，预先以STS（2、10、50μmol／L）处理心肌细胞30min。发现STS可明显抑制Angi诱导的心肌细胞磷酸化MAPK蛋白表达。③预先以不同浓度STS处理心肌细胞30min，发现STS对AngⅡ诱导的心肌细胞磷酸化MAPK蛋白表达的抑制作用存在剂量依赖性。结论 STS可以抑制AngⅡ诱导的心肌肥厚，其机制与抑制磷酸化MAPK表达有关。

丹参酮ⅡA磺酸钠合成工艺研究

为改善丹参酮的水溶性,在其分子中引入水溶性官能团磺酸基。以不同的磺化剂与之发生磺化反应,结果表明,冰醋酸-浓硫酸的混合液是合成丹参酮水溶性衍生物的合适磺化剂。通过薄层色谱法、紫外吸收和红外吸收光谱法对其结构进行鉴定,证实了产物是丹参酮ⅡA磺酸钠。对以冰醋酸-浓硫酸为磺化剂合成丹参酮ⅡA磺酸钠进行了正交试验研究,得出其最佳工艺条件为:冰醋酸-浓硫酸(1∶1,v/v),反应温度15℃,反应时间1h,产品得率38.7%。

丹参酮ⅡA磺酸钠注射液治疗冠心病心绞痛有效性及安全性的Meta分析

目的通过Meta分析方法分析丹参酮ⅡA磺酸钠注射液治疗冠心病心绞痛的有效性及安全性。方法计算机检索Cochrane图书馆临床对照试验资料库、Embase、Pubmed、中文科技期刊数据库、万方数字化期刊库、中国(CNKI)学术文献总库,按纳入与排除标准选择随机对照试验、评价质量,提取资料,并用RevMan5.2软件对数据进行Meta分析。结果共初检出182篇文献,经筛选最终纳入7篇关于丹参酮ⅡA磺酸钠注射液治疗冠心病心绞痛的随机对照研究。以心绞痛缓解为疗效尺度:χ2=2.24,df=6,P=0.90,合并OR=3.08,95%CI[1.95,4.87],Z=4.83(P<0.00001);以心电图为疗效尺度:χ2=2.74,df=6,P=0.84,合并OR=3.20,95%CI[2.10,4.88],Z=5.39(P=0.00001)。结论丹参酮ⅡA磺酸钠注射液治疗冠心病心绞痛安全有效。

丹参酮ⅡA磺酸钠对血管紧张素Ⅱ诱导的大鼠心肌细胞外信号调节激酶1/2的作用

目的研究丹参酮ⅡA磺酸钠(STS)对血管紧张素Ⅱ(AngⅡ)诱导的心肌肥大反应中细胞外信号调节激酶1/2(ERK1/2)是否有抑制作用。方法培养新生大鼠心肌细胞,考马斯亮蓝法测定心肌细胞蛋白含量、[3H]-亮氨酸掺入法测定蛋白合成速率作为心肌肥大指标;用免疫荧光标记法和Western-blot测定磷酸化ERK1/2蛋白(p-ERK1/2)表达。结果1)AngⅡ(1μmol/L)处理24h,心肌细胞[3H]-亮氨酸掺入率、蛋白含量明显增加,STS能明显抑制AngⅡ介导心肌细胞[3H]-亮氨酸掺入率、蛋白含量的增加;2)AngⅡ刺激心肌细胞可见胞核内出现磷酸化ERK1/2荧光染色,丹参酮ⅡA可阻断AngⅡ引起的ERK1/2活化、入核过程。3)用AngⅡ(1μmol/L)处理心肌细胞5min,磷酸化ERK1/2蛋白(p-ERK1/2)表达即开始增加,10min左右时最明显。4)STS剂量依赖性抑制AngⅡ诱导的心肌细胞磷酸化ERK1/2蛋白表达。结论STS可以抑制AngⅡ诱导的心肌肥厚,其机制与抑制磷酸化ERK1/2表达有关。