HPLC法测定金水愈消口服液中原儿茶醛的含量

金水愈消口服液(暂定名)是由人参、黄连、丹参、天花粉、荔枝核等八味中药制备而成的纯中药制剂,具有益气生津、清热解毒、活血祛瘀的功效,对2型糖尿病有良好治疗作用。丹参是处方中的主要组分之一,其中原儿茶醛是丹参中重要生理活性成分之一。为控制本品的内在质量和为制备工艺的进一步完善提供检测手段,对其重要活性成分原儿茶醛进行了定量分析研究。1 材料与方法1.1 仪器与试药 美国HP109M液相色谱仪;陈列检测仪;自动进样器。原儿茶醛对照品(中国药品生物制品检定     

高忠英治疗慢性胃炎学术思想及临证特色

高忠荚教授精通《内经》《脾胃论》等经典医籍有关论述脾胃病的理论,提出本虚标实、脾虚胃燥是慢性胃炎的基本病机。临证以辨证与辨病相结合,益气健脾治其本,润燥和胃治其标。擅用甘凉清润药物以治燥,选用川贝、花粉等养胃阴,修复胃黏膜,疗效显著。     

海水浸泡性体温过低症的病理生理学研究进展

海水浸泡性体温过低症是近年海战伤研究的重点内容,对其病理生理改变的研究进展进行总结有利于推进该领域的基础理论研究,最终提高低温伤员的救治水平。     

缺氧复氧对IEC-6肠上皮细胞膜电位的影响及紫芪方的保护作用

目的观察缺氧复氧对IEC-6肠上皮细胞线粒体膜电位的影响,探讨抗休克复方中药-紫芪方对IEC-6肠上皮细胞缺氧复氧损伤的保护作用机制。方法建立IEC-6细胞缺氧复氧损伤模型;采用血清药理学方法,在细胞培养液中加入不同给药剂量获取的“紫芪方”药物血清(分别以10、20g·kg-1分为1次给药和间隔1h、2次给药,DJ-1,SJ-2);参附药物血清(间隔1h,2次给药20g·kg-1SF)及生理氯化钠血清(S)。采用紫外分光光度分析法测定乳酸脱氢酶(LDH)漏出量,以及采用激光共聚焦显微镜测定线粒体膜电位(MMP)变化。结果IEC-6细胞缺氧复氧损伤后,可致细胞LDH的漏出量明显升高,线粒体膜电位明显降低。紫芪方药物血清明显减轻上述损伤,与对照组比较,SJ-2组制备的药物血清能明显减少IEC-6细胞LDH的漏出量(P<0.01);并具有保护IEC-6肠上皮细胞线粒体膜电位的作用(P<0.01)。结论缺氧复氧可导致IEC-6肠上皮细胞LDH漏出量升高和线粒体膜电位降低,“紫芪方”药物血清可减少细胞LDH漏出量及保护线粒体膜电位,从而发挥细胞的保护作用。     

紫芪方对失血性休克大鼠重要脏器血流量的影响

目的观察紫芪方对失血性休克模型Wistar大鼠重要器官血流量的影响。方法将30只Wistar大鼠随机分为休克组、复苏组、紫芪方组、参附组、蒸馏水组,采用改良wigger’s模型制备大鼠失血性休克模型、参照文献各组分别灌胃给药,采用激光多普勒微循环监测技术测定器官血流量的方法检测不同实验组大鼠的肠黏膜、肝脏、肾脏及颈动脉血流量。选择直径1 mm激光多普勒微循环监测仪光纤探头轻触脏器表面,取连续测得10个读数的平均值为即时测得的微循环血流量值,血流计每隔0.2 s取信号1次,由仪器数码管自动显示。结果紫芪方有效提高失血性休克导致的小肠黏膜、肝脏、肾脏及颈动脉微循环血流量下降,效应强于阳性对照药物参附汤(P<0.05)。结论紫芪方对失血性休克大鼠肠黏膜修复及肝肾功能的保护有重要作用,为紫芪方保护肠道屏障功能的有效性提供重要依据。     

康复新液治疗消化道溃疡随机对照试验的系统评价

目的对康复新液治疗消化道溃疡的疗效和安全性进行系统评价。方法计算机检索Pubmed数据库、中国学术期刊全文数据库(CNKI)、中文科技期刊全文数据库(VIP)、中国生物医学文献数据库(CBM)、中文生物医学期刊数据库(CMCI),检索日期为各数据建库时间起至2011年5月30日止。纳入的试验类型为随机对照试验,康复新液与三联疗法、抗菌药、抑制胃酸药比较的试验,或康复新液联合三联疗法、抗菌药、抑制胃酸药与后者比较的试验。采用Cochrane协作网的质量评价标准并用其提供的软件RevMan 5.1软件进行资料分析。结局的效应指标为胃镜下溃疡痊愈情况、临床症状痊愈情况、临床症状有效情况、幽门螺杆菌(HP)根除情况以及不良反应。结果共纳入22篇随机对照试验(2 224例患者)进行系统评价,所纳入的文献质量偏低。统计分析结果显示在溃疡痊愈、临床症状痊愈方面康复新液联合质子泵抑制剂或加用抗幽门螺杆菌药物与单用质子泵抑制剂或加用抗HP药物相比,结果均有统计学意义,单用康复新液与质子泵抑制剂或H2受体拮抗剂比较以及康复新液联合抗HP药物与抗HP药物比较,疗效相当,结果无统计学意义。结论康复新液可以更有效地促进消化道溃疡愈合以及改善临床各种症状,但方法学方面亟待提高。     

Systematic review of randomized controlled trials of traditional Chinese medicine treatment of non-acute bronchial asthma complicated by gastroesophageal reflux

OBJECTIVE:To assess the effectiveness and safety of Traditional Chinese Medicine(TCM) treatment of non-acute bronchial asthma complicated by gastroesophageal reflux.METHODS:We searched databases from MEDLINE,Cochrane Library,CNKI,VIP,CBM,Wanfang Data,and TCM Database Systems.All randomized,controlled trials(RTCs) of TCM treatment of non-acute asthma complicated by gastroesophageal reflux were included.Data were independently collected by two reviewers.The standards for assessing quality described in the Cochrane Handbook for Systematic Reviews of Interventions were used to evaluate articles.Meta-analyses were conducted using RevMan 5.0.17 software.Heterogeneity was assessed,and a corresponding effects model was used to merge and analyze results.Indexes used to evalu-ate curative effects were:clinical efficacy,symptom scores,pulmonary function values,and adverse incidents.Effectiveness was indicated using risk ratio(RR) or mean difference(MD),and 95% confidence intervals(CIs) were calculated.RESULTS:Six RCTs were included,involving 304 patients with non-acute asthma complicated by gastroesophageal reflux.The treatment groups received Chinese drugs alone or TCM combined with standard Western medical treatment,and the control groups received standard Western medical treatment alone.Standard Western medical treatment included anti-inflammatory drugs and bronchodilators for asthma,and drugs to promote gastric peristalsis and inhibit gastric acid production for gastroesophageal reflux.Methodological quality was low in all six RCTs.Two RCTs showed that clinical efficacy was higher in the treatment group than in the control group(RR:1.43,95%CI:1.10 to 1.87 vs RR:1.51,95% CI:1.09 to 2.08).One RCT showed that the asthma score was lowered more effectively in the treatment group than in the control group(MD:-1.10,95% CI:-2.04 to-0.16).Two RCTs showed that the gastroesophageal reflux score was reduced more effectively in the treatment group than in the control group(RR:-3.70,95% CI:-4.30 to 3.10 vs RR:-5.30,95% CI:-6.32 to-4.28).One RCT showed that some pulmonary function values were improved more effectively in the treatment group than in the control group(P< 0.05).No differences were seen in the various indexes between groups in the other RCTs.No adverse reactions,dropout rates,or follow-up rates were reported in any of the RCTs.CONCLUSIONS:The clinical symptoms ofnon-acute asthma complicated by gastroesophageal reflux can be improved by some Chinese drugs.Curative effects can be increased by combining the use of TCM with Western medicine.Because of the small quantity and low quality of research reported to date,it is necessary to conduct further RCTs to confirm these results.The results of this systematic review indicate that the quality of future clinical trials should be improved by including larger patient numbers,correctly randomizing patients into study groups,using blinding methods to measure and assess outcomes,and using accepted indexes to evaluate curative effects.     

中药DNA分子标识鉴定研究进展

分子生物学技术在生药学中应用研究方兴未艾。综述了ＤＮＡ分子遗传标记技术在近缘易混淆生药鉴定、药材道地性研究、中药质量标准化、中医药古迹考证、药材种子种苗检测等方面的研究进展，并提出一些值得注意的问题以及偏隍可能的发展方向。     

紫芪方对缺氧复氧所致大鼠小肠上皮细胞损伤的保护作用

目的观察缺氧复氧对大鼠小肠上皮细胞（intestinal epithelial cell，IEC）-6培养液中超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量及细胞内Ca^2＋浓度和线粒体膜电位的影响，探讨复方中药-紫芪方对IEC-6肠上皮细胞缺氧复氧损伤的保护作用及机制。方法复制IEC-6细胞缺氧复氧损伤模型，采用紫外分光法测定缺氧复氧后及紫芪方血清治疗后细胞培养液中SOD活性及MDA含量；采用激光共聚焦显微镜测定细胞Ca^2＋浓度和线粒体膜电位变化。结果细胞缺氧复氧损伤后，可导致细胞培养液中SOD活性显著降低、MDA含量显著升高、线粒体膜电位明显降低及细胞内Ca^2＋浓度明显升高（P〈0．01）。紫芪方药物血清治疗后，可提高细胞培养液中SOD活性并降低其MDA含量，同时稳定了线粒体膜电位并降低细胞内Ca^2＋浓度（P〈0．05）。结论缺氧复氧可导致IEC-6肠上皮细胞损伤；紫芪方血清对IEC-6小肠上皮细胞缺氧复氧损伤具有显著的保护作用。     

Gene damages of mitochondrial DNA encoding cytochrome oxidase of intestinal epithelial cells in hemorrhagic shock rats

Objective: To investigate the detrimental effects of hemorrhagic shock on the structure and function of mitochondria DNA (mtDNA) encoding cytochrome oxidase genes in intestinal epithelial cells. Methods: Wistar rats were used and divided into two groups: hemorrhagic shock group and control group. Hemorrhagic shock model of rats was utilized in this experiment. The mtDNA was extracted from the intestinal epithelial cells and amplified by polymerase chain reaction (PCR) with different primers of cytochrome oxidase (COX I, COX II and COX III). The products of PCR were directly sequenced. Results: Hemorrhagic shock could result in the point mutagenesis in mitochondrial genome encoding cytochrome oxidase (COX I and COX II). There were 4, 4, 22, 16, 35 point mutations in COX I from 5545 to 6838 bp in 5 shocked rats. There were five point mutations in COX II from 7191 to 7542 bp at the site of t7191c, t7212c, a7386g, a7483g, c7542g in 1 shocked rat. There was no mutation found in COX III. Conclusions: Hemorrhagic shock could significantly induce the damage of the gene of cytochrome oxidase encoded by mtDNA.