西洋参茎叶皂苷对脑缺血大鼠细胞凋亡及caspase-3表达的影响

目的：研究西洋参茎叶皂苷对大鼠局灶性脑缺血损伤的保护作用及其机制。方法：采用大鼠大脑中动脉内栓线阻断法制备局灶性脑缺血损伤模型，通过HE染色、TUNEL、免疫组化及RT—PCR等方法，观察西洋参茎叶皂苷对脑缺血损伤大鼠脑组织形态学改变，细胞凋亡及半胱氨酸天冬氨酸蛋白酶（caspase）-3mRNA和蛋白表达的影响。结果：西洋参茎叶皂苷（100、50mg／kg，ig）均可明显改善脑缺血损伤所致的大鼠脑组织病理形态学改变，抑制神经细胞凋亡，降低促凋亡基因caspase-3mRNA和caspase-3蛋白的表达。结论：西洋参茎叶皂苷对大鼠局灶性脑缺血损伤具有保护作用，其作用机制可能与抑制caspase-3表达有关。     

党参的亚临界水提取工艺优选

目的:优选党参的亚临界水提取工艺.方法:以党参炔苷和党参多糖提取率的综合评分为指标,采用单因素试验和正交试验考察料液比、提取时间和温度对党参亚临界水提取工艺的影响,并与传统提取工艺进行比较.结果:最佳亚临界水提取工艺为提取温度150℃,提取时间45 rain,料液比12 mL·g-1;党参炔苷和党参多糖的提取率分别达0.110 2,195.1mg·g-1.结论:与传统水煎煮工艺相比,优选的工艺可明显降低提取时间,并显著提高党参炔苷和党参多糖的提取率.     

浅谈“以气为主、以血为先”在伤科临床中的应用

上海石氏伤科肇始于清末石兰亭先生,19世纪70年代由江苏无锡迁至上海;其子晓山先生以理伤续断声誉日盛,至筱山、幼山先生昆仲则名震沪上,誉及江南。石氏伤科传人石印玉教授执诊于上海中医药大学附属曙光医院,带领学术团队,全面继承石氏伤科经验,并结合当代中医骨伤科学之特点,形成了系列石氏伤科学术理论。石氏伤科精于内治,“以气为主、以血为先”是石氏伤科重要的学术思想,学者同道也对此多有阐发。笔者有幸跟师学习,感悟良多,此结合l临床体会,对“以气为主、以血为先”的具体运用作一浅谈。     

阵发性睡眠性血红蛋白尿辨治探讨

阵发性睡眠性血红蛋白尿是一种慢性血管内溶血 ,以与睡眠有关的、间隙发作的血红蛋白尿为特征。临床论治分为虚实两型 ,并提出其治则为实者凉血利水 ,虚者扶正利水 ,同时不可偏废活血化瘀。     

HPLC法测定市售杭白菊中2种有机酸和2种黄酮的含量

摘 要 目的： 测定市售杭白菊中有效成分的含量,比较不同产地杭白菊质量。方法: 采用HPLC法测定绿原酸、3,5-O-双咖啡酰基奎宁酸2种有机酸成分以及木犀草苷、木犀草素2种黄酮成分的含量。结果: 收集杭白菊样品各有效成分差异较大,12批市售杭白菊绿原酸含量在0.22%～0.70%之间,木犀草苷含量在0.09%～0.25%之间,3,5-O-双咖啡酰基奎宁酸含量在0.84%～1.67%之间,木犀草素含量在0.008%～0.042%之间。结论: 市售杭白菊质量有较大差异,有必要进一步加强质量控制。     

天麻糖复合物对大鼠缺血/再灌注模型视网膜的影响

目的观察天麻糖复合物(polysaccharides from Gastro-d ia elata B lum e,GEP)对大鼠视网膜缺血/再灌注(retinal is-chem ia reperfusion,R IR)后视网膜超氧化物歧化酶(superox-ide d ismutase,SOD)、丙二醛(m alond ialdehyde,MDA)、一氧化氮(n itric oxide,NO)含量及视网膜形态的影响。方法采用前房灌注液体形成16 kPa高眼压而建立R IR模型。SD大鼠随机分为:GEP小剂量组、中剂量组、大剂量组、维生素E组、阴性对照组,缺血60 m in后恢复血流,分别于再灌注60 m in,24 h和72 h检测视网膜组织中MDA(比色法),SOD(比色法)、NO(硝酸还原酶法)含量及视网膜光学显微镜的组织学观察。结果GEP干预后,再灌注60 m in,24 h和72h后中、大剂量干预组视网膜中MDA含量均明显低于阴性对照组(P<0.05);SOD含量均明显高于阴性对照组(P<0.05);NO含量在再灌注24~72 h时间段内明显低于阴性对照组(P<0.05),GEP干预组视网膜组织形态学损害较阴性对照组明显减轻。结论GEP对缺血/再灌注的视网膜具有保护作用。     

以药养医机制对医院合理用药的影响及对策

本文综述了以药养医机制对医院合理用药的影响,通过数据深入分析当前医药卫生体制改革亟需解决的问题,提出了建立健全更加合理的药品价格形成机制、政府财政投入机制、补偿机制,逐步推行医药分业制度等措施,建议用更加合理的新机制取代以药养医的旧机制,促进医院合理用药。     

蝎毒多肽提取物体外抑制胰腺癌细胞侵袭转移及相关机制

目的研究蝎毒多肽提取物PESV对人高转移胰腺癌细胞MIA-PaCa2-3转移相关能力的影响及其作用的机制。为PESV在临床上治疗胰腺肿瘤提供理论根据。方法以高转移的人胰腺癌细胞系MIA-PaCa2-3为研究对象,通过细胞增殖实验(MTT法)观察在PESV影响下肿瘤细胞活性及增殖情况,通过细胞黏附实验、细胞划痕实验及Transwell体外侵袭实验检测PESV干预后细胞的黏附、侵袭及运动能力变化。免疫细胞化学实验及Western blot检测胰腺癌细胞的E-钙粘蛋白、纤粘蛋白和基质金属蛋白酶-9的表达。结果细胞增殖实验结果显示,PESV对胰腺癌细胞呈明显剂量及时间效应关系的增殖抑制作用,与对照组比较细胞增殖抑制作用明显(P<0.05);黏附实验表明PESV可降低胰腺癌细胞的黏附力,侵袭实验及划痕实验的结果表明PESV可以使细胞的侵袭力和运动能力下降,PESV(40mg.L-1)干预8h后,黏附力、侵袭力和运动能力的抑制率分别为(30.3±4.7)%、(42.1±3.7)%、(47.6±3.3)%,与对照组比较差异均有显著性(P<0.05);免疫细胞化学及Western blot实验检测均显示,PESV干预后,胰腺癌细胞E-钙粘蛋白阳性表达细胞数量上升,灰度值明显上调(P<0.05),FN及MMP-9蛋白阳性表达数量减少,灰度值明显下调(P<0.05)。结论PESV能够明显抑制胰腺癌细胞的增殖、黏附力、侵袭及运动能力,其机制可能是通过提高E-cad表达、降低FN和MMP-9表达而实现的。     

牡荆子脂质对实验动物气道平滑肌的影响

观察牡荆子脂质对实验动物气道平滑肌的影响,结果表明;①牡荆子脂质可使通过小鼠肺支气管的灌流液流速明显增加,其增加程度与牡荆子脂质剂量呈依赖关系.此外,牡荆子脂质对ACh介导的小鼠气道平滑肌收缩有拮抗作用②给豚鼠牡荆子脂质(100～300 mg·kg~(-1)iP,可使由ACh+组胺喷雾引起的喘息潜伏期明显延长.牡荆子脂质对小鼠气道平滑肌的最佳扩张效果是其中油酸、亚油酸、棕榈酸和硬脂酸协同作用的结果.     

Purinoceptor-mediated modulation by endogenous and exogenous agonists of stimulation-evoked [3H]noradrenaline release on rat iris

Summary To investigate whether endogenous purinoceptor agonists affect the sympathetic neurotransmission in the rat isolated iris, and to classify the purinoceptors modulating exocytotic [³H]-noradrenaline release, we have determined the effect of adenosine receptor antagonists on, and the relative potency of selected agonists in modulating, the field stimulation-evoked (3 Hz, 2 min) [³H]-noradrenaline overflow. In addition, the apparent affinity constants of 8-phenyltheophylline (8-PT) and 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) in antagonizing the prejunctional effects of purinoceptor agonists were estimated.The relatively A₁-selective DPCPX 10 and 100 nmol/l increased the evoked [³H]-noradrenaline overflow by about 25%–35%a indicating a minor inhibition of evoked release by endogenous purinoceptor agonists probably via an A₁ adenosine receptor. Whereas the A₁/A₂-antagonist 8-PT failed to increase the evoked [³H]-noradrenaline overflow in the absence of exogenous agonists (without or with dipyridamole 1 pmol/l present), the relatively A₂-selective antagonist CP-66,713 (4-amino-8-chloro -1-phenyl(1,2,4)triazolo(4,3-a)quinoxaline) 100 nmol/l decreased it by 20%–30% in the absence and continuous presence of DPCPX. This may be compatible with a minor A₂-mediated facilitation by an endogenous purinoceptor agonist.All exogenous agonists tested (except UTP 100 mol/l) inhibited the evoked [³H]-noradrenaline overflow. The relative order of agonist potency (IC4o, concentration in mol/l for inhibition of evoked release by 40%) was CPA (N⁶-(cyclopentyl)adenosine, 0.004) > R-PIA (R(–)N6-(2phenylisopropyl)adenosine, 0.066) = CHA (N⁶-(cyclohexyl)adenosine, 0.082) > NECA (N⁵-(ethyl-carboxamido)adenosine 0.44) > ADO (adenosine, 4.1). ATP was n early equipotent with ADO. Maximum inhibition was 70%–80% and similar for all agonists. Adenosine deaminase 1 u/ml failed to affect the ATP-induced, but abolished the adenosine-induced prejunctional inhibition. The adenosine uptake inhibitor S-p-nitrobenzyl-6-thioguanosine (NBTG) failed to enhance the potency of ADO and ATP. The A₁-selective antagonist DPCPX 10 nmol/l did not reduce the ATP potency indicating an effect of ATP per se not mediated via an A₁ purinoceptor.Prejunctional affinity constants of 8-PT were 6.07 when tested against adenosine (in the presence of dipyridamole), and 6.60 against CHA. The apparent -log K_B of DPCPX tested against CPA was 9.71. The high DPCPX affinity is compatible with an A₁ adenosine receptor mediating inhibition of sympathetic neurotransmission in rat iris. This receptor may not be the only prejunctional purinoceptor on rat iris sympathetic nerves. The receptor by which ATP acts prejunctionally in this tissue remains to be determined.This study was supported by the Deutsche Forschungsgemeinschaft (Fu 163/2 and 163/3) Send offprint requests to H. Fuder at the above address