蛇床子素抗变态反应的研究

蛇床子素能较强地抑制小鼠被动皮肤过敏(PCA)反应,对整体豚鼠组胺性喘息具有保护作用,对慢反应物质(SRS-A)引起的豚鼠离体回肠收缩以及豚鼠离体回肠的Schultz-Dzle反应呈明显的拮抗和阻断作用,并能抑制大鼠腹腔肥大细胞脱颗粒。上述作用均呈一定的剂量依赖关系。     

辛夷挥发油的抗过敏实验研究

目的：研究辛夷挥发油的抗过敏作用。方法：采用磷酸组织胺（HA）、氯化乙醇胆碱（Ach）所致豚鼠离体回肠收缩实验，卵白蛋白（OA）引起的致敏豚鼠离体回肠实验及大鼠肥大细胞脱颗粒实验法。结果：辛夷挥发油能显著抑制HA、Ach引起的豚鼠离体回肠收缩，对致敏豚鼠离体回肠的过敏性收缩有较强的抑制作用，并能明显阻止大鼠肥大细胞脱颗粒。结论：辛夷挥发油具有较强的抗过敏作用。     

葛根汤抗过敏药理作用的实验研究

本文运用抗过敏药理实验方法研究证明葛根汤能显著抑制小鼠耳异种ＰＣＡ及小鼠同种ＰＣＡ，阻止大鼠腹腔肥大细胞及颅骨骨膜肥大细胞脱颗粒，并能拮抗组胺对豚鼠离体回肠的收缩反应．     

大豆提取物对肥大细胞触发的抑制作用

本实验用卵清蛋白免疫大鼠,分离致敏大鼠肥大细胞,以豚鼠离体回肠收缩试验及肥大细胞脱颗粒试验研究了大豆(Glycine max)提取物对肥大细胞触发的抑制作用。实验结果表明,大豆提取物组分Ⅰ对肥大细胞脱颗粒有明显抑制作用,在其蛋白质浓度达10~4ng/ml 时,抑制率达90.2%;组分Ⅰ和组分Ⅱ对肥大细胞释放组胺有明显抑制作用。     

蛇床子超临界萃取物的止痒作用及拮抗组胺释放作用的实验研究

目的　研究蛇床子超临界萃取物的止痒作用及拮抗组胺释放的作用。方法　用 4 氨基吡啶 (4 AP)诱发小鼠舔体反应与肥大细胞释放组胺 ,记录小鼠的舔体反应 ,并测定小鼠注射 4 AP局部皮肤与血中组胺含量。结果　蛇床子超临界萃取物组 ,与模型组相比能明显抑制舔体反应数 ,差异有显著性 (P <0 0 5)。蛇床子超临界萃取物组 (除第 4组 ,即浓度为 7 5 %组外 )用药局部皮肤组胺含量明显高于模型组 ,血液中组胺含量明显低于模型组。结论　蛇床子超临界萃取物有明显的止痒作用和拮抗组胺释放的作用。     

蛇床子止痒有效成分的筛选

目的　筛选蛇床子止痒有效成分。方法　将蛇床子用系统溶媒 (石油醚、乙醚、乙酸乙酯、甲醇、蒸馏水 )顺次分别对其进行提取 ,对各提取物测定蛇床子素含量 ,并以豚鼠皮肤磷酸组胺致痒实验对蛇床子系统溶媒提取物、蛇床子挥发油及蛇床子水提物进行止痒药效学筛选。结果　蛇床子所含的各成分中 ,极性较小的挥发油和石油醚提取物为蛇床子止痒主要有效成分 ,其中蛇床子挥发油的止痒效果又显著优于石油醚提取物 ,而水提物无显著的止痒作用。结论　蛇床子的非极性的或极性小的成分是其主要的止痒成分     

白芷挥发油抗过敏的实验研究

目的研究白芷挥发油(EOAD)抗过敏作用。方法采用大鼠同种被动皮肤过敏反应(PCA),大鼠颅骨骨膜肥大细胞脱颗粒,组胺致小鼠毛细血管通透性增高的实验。结果与对照组比较,EOAD低剂量组对PCA、大鼠颅骨骨膜肥大细胞脱颗粒、组胺致小鼠毛细血管通透性增高有显著差异,EOAD高剂量组对PCA、大鼠颅骨骨膜肥大细胞脱颗粒、组胺致小鼠毛细血管通透性增高有非常显著差异。结论EOAD具有抗过敏作用,可用于过敏性疾病的治疗。     

白芷挥发油抗过敏的实验研究

目的 研究白芷挥发油(EOAD)抗过敏作用.方法 采用大鼠同种被动皮肤过敏反应(PCA),大鼠颅骨骨膜肥大细胞脱颗粒,组胺致小鼠毛细血管通透性增高的实验.结果 与对照组比较,EOAD低剂量组对PCA、大鼠颅骨骨膜肥大细胞脱颗粒、组胺致小鼠毛细血管通透性增高有显著差异,EOAD高剂量组对PCA、大鼠颅骨骨膜肥大细胞脱颗粒、组胺致小鼠毛细血管通透性增高有非常显著差异.结论 EOAD具有抗过敏作用,可用于过敏性疾病的治疗.     

N-(3’,4’,5’-三甲氧基肉桂酰)邻氨基苯甲酸对抗原诱发的离体豚鼠回肠收缩、大鼠肥大细胞脱颗粒及组胺释放的影响

实验证明 N-(3′,4′,5′-三甲氧基肉桂酰)邻氨基苯甲酸(TOA)管内浓度80μg/ml 能明显抑制抗原诱发的主动致敏豚鼠离体回肠收缩。TOA 管内浓度25和50μg/ml 能显著抑制亲同种细胞抗体介导的大鼠肠系膜肥大细胞脱颗粒和腹腔肥大细胞组胺释放。     

N—（3′，4′，5′—三甲氧基肉桂酰）邻氨基苯甲酸对抗原诱发的离体豚鼠回肠收缩、大鼠肥大细胞脱颗粒及组胺释放的影响

实验证明N－（3′，4′，5′－三甲氧基肉桂酰）邻氨基苯甲酸（TOA）管内浓度80μg/ml能明显抑制抗原诱发的主动致敏豚鼠离体回肠收缩。TOA管内浓度25和50μg/ml能显著抑制亲同种细胞抗体介导的大鼠肠系膜肥大细胞脱颗粒和腹腔肥大细胞组胺释放。     

辛夷酯素抗过敏作用机理探讨

目的探讨辛夷酯素抗过敏作用机理,为指导抗过敏药物的研发及指导I临床用药提供参考及思路。方法分别用形态法和荧光法观察辛夷酯素药物血清冻干粉对致敏大鼠腹腔肥大细胞（PMC）脱颗粒和组织胺释放的影响,研究辛夷酯素的抗过敏作用,探讨抗过敏机制。结果给药15rain、60rain后,制备的药物血清冻干粉对PMC脱颗粒和组织胺释放有明显的抑制作用,且存在一定的时效关系。其抗过敏的机理可能与其稳定肥大细胞细胞膜,抑制其脱颗粒和释放过敏介质有关。结论辛夷酯素对过敏症状有明显的抑制作用,其抗过敏机制与抑制PMC释放过敏性介质组织胺有关。     

Piceatannol,a Syk-selective tyrosine kinase inhibitor,attenuated antigen challenge of guinea pig airways in vitro

Activation of nontransmembrane protein tyrosine kinases, such as Lyn and Syk, has been shown to be the earliest detectable signaling response to Fc receptor (Fc epsilon RI) cross-linking on mast cells leading to mast cell degranulation. The present study examined the effects of piceatannol (3,4,3',5'-tetrahydroxy-trans-stilbene, 10-100 microM), a Syk-selective tyrosine kinase inhibitor, on ovalbumin-induced anaphylactic contraction of isolated guinea pig bronchi and release of histamine and peptidoleukotrienes from chopped lung preparations. Pretreatment with piceatannol slightly suppressed ovalbumin-induced peak anaphylactic bronchial contraction but markedly (P<0.05) facilitated relaxation of the anaphylactically contracted bronchi. Piceatannol did not inhibit direct histamine-, leukotriene D(4)- or KCl-induced bronchial contraction, nor revert an existing anaphylactic bronchial contraction. Piceatannol, at 30 microM and above, significantly (P<0.05) prevented ovalbumin-induced release of both histamine and peptidoleukotrienes from lung fragments. Piceatannol did not inhibit exogenous arachidonic acid-induced release of peptidoleukotrienes from lung fragments. Our data show for the first time that inhibition of Syk tyrosine kinase can attenuate anaphylactic bronchial contraction in vitro, probably via inhibition of mast cell degranulation.     

中药桑寄生的抗Ⅰ型变态反应作用

目的:从传统中药中筛选抗Ⅰ型变态反应物质.方法:体外和体内(口服)给药,使用肥大细胞作为靶细胞,观察药物对其脱颗粒和释放组胺的影响.结果:桑寄生提取物(HT)对刀豆蛋白(Con A)诱导的肥大细胞脱颗粒呈明显的抑制作用,且呈剂量依赖关系.对卵白蛋白致敏大鼠肥大细胞的脱颗粒,桑寄生提取物同样有明显的抑制作用.口服该提取物也能抑制组胺的释放,抑制率达85%.结论:桑寄生提取物在体内外都显示出对肥大细胞的脱颗粒反应有非常显著的抑制作用.该提取物有可能开发成防治速发型变态反应的药物.     

Characterization of protease-activated receptors in rat peritoneal mast cells

Activation of protease-activated receptor (PAR)-1 or PAR-2 elicits inflammation most probably via mast cell degranulation in vivo. The present study aimed at characterizing PARs in rat peritoneal mast cells (PMC). Messenger RNA for PAR-1, but not for PAR-2, was detected in PMC. Thrombin, the PAR-1 agonist SFLLR-NH2 or the PAR-2 agonist SLIGRL-NH2 failed to induce histamine release from PMC. Surprisingly, the PAR-2-inactive control peptide LSIGRL-NH2 triggered histamine release from PMC. Thus, PAR-1, but not PAR-2, are expressed in PMC, whereas neither PAR-1 nor PAR-2 are considered to be involved in degranulation of PMC. LSIGRL-NH2 does not appear to be appropriate as a control peptide for PAR-2 in inflammation studies.     

杠柳苷元对肥大细胞脱颗粒及释放组胺影响的研究

目的:研究香加皮提取单体化合物杠柳苷元对大鼠和小鼠肥大细胞脱颗粒及组胺释放的影响。方法:大鼠腹腔注射百日咳疫苗、后腿注射卵白蛋白致敏,用于测定肥大细胞脱颗粒反应及制备抗血清;取致敏大鼠的血清稀释后对小鼠进行腹腔注射,测定肥大细胞脱颗粒反应;以荧光分光光度法测定组胺浓度。结果:杠柳苷元对体外培养肥大细胞的组胺释放有显著的抑制作用,实验剂量即可使组胺释放浓度降低(69.4±8.6)%,其抑制作用呈显著的剂量依赖关系;杠柳苷元对抗原致敏大鼠肥大细胞的组胺释放也有显著的抑制作用,在20μg·mL-1浓度时即可使组胺释放浓度减少73.55%;杠柳苷元口服给予致敏小鼠后,在50mg·kg-1剂量时即可使小鼠组胺释放浓度减少80%以上,并呈显著的剂量依赖关系。结论:杠柳苷元对体外培养的肥大细胞、致敏大鼠肥大细胞的组胺释放有显著的抑制作用;口服给予杠柳苷元可使小鼠显著减少肥大细胞的组胺释放。鉴于肥大细胞脱颗粒及组胺释放在炎症反应中的作用,可认为杠柳苷元是香加皮具有抗炎作用的有效成分之一。     

钾通道开放剂拮抗4-氨基吡啶诱发大鼠肥大细胞释放组胺

4-氨基吡啶(4-AP)能诱发大鼠腹腔肥大细胞(PMC)释放组胺,且呈浓度依赖关系。钾通道开放剂二氮嗪(Dia),米诺地尔(Min)及钙拮抗剂硝苯啶(Nif)均能明显抑制4-AP诱发大鼠PMC释放组胺。实验结果提示,大鼠肥大细胞膜上可能存在钾通道,4-AP可能通过阻滞钾通道,使钙通道开放,Ca²⁺内流增加而促进组胺释放,钾通道开放剂可能是一类新的组胺释放拮抗剂。     

The effect of compound 48/80, substance P and pentagastrin on the isolated guinea pig atrium

It has been shown that histamine is present in guinea pig hearts. In the present work, the effect of some substances, known to liberate mast cell histamine, on the isolated guinea pig atria was studied. Compound 48/80 (100 micrograms/ml), pentagastrin (10(-6) M) and substance P (10(-5) M) were added 2-3 times to the isolated organs and the frequency of contractions was measured. At the end of experiments, the atria were examined histologically for mast cell degranulation. Compound 48/80 and pentagastrin increased the frequency of contractions of isolated atria. Substance P provoked a dose-dependent decrease of contraction frequency; this effect was diminished by atropine (10(-5) M). All three substances provoked pronounced degranulation of mast cells present in the atrium, the effect of substance P being significantly greater than the effects of the other two substances. It can be concluded that mast cells, present in guinea pig atrium, are sensitive to the histamine liberators used; histamine is released in quantities high enough to produce an effect.     

牛膝多糖对抗原诱导的肥大细胞活化的影响

目的观察牛膝多糖(achyranthes bidentata polysaccha-rides,ABPS)对肥大细胞活化脱颗粒的影响。方法运用大鼠被动皮肤过敏反应(PCA)实验,用比色测定法检测ABPS在体内对肥大细胞(MC)影响;体外实验将ABPS分为高、中、低3个剂量组,然后分别将其加入抗原致敏的RBL-2H3细胞中(大鼠嗜碱性粒细胞白血病细胞,国际公认的MC研究模型细胞),观察ABPS对RBL-2H3细胞脱颗粒的影响。结果ABPS能明显抑制大鼠PCA、RBL-2H3细胞脱颗粒,并能抑制RBL-2H3细胞释放组胺、肿瘤坏死因子α及白细胞介素4;抑制RBL-2H3细胞中Akt和p38的磷酸化。结论ABPS的抗过敏作用与抑制肥大细胞的脱颗粒及炎性物质释放有关;ABPS抑制肥大细胞的活化与抑制Akt和p38的活性相关。     

桑黄多糖对肥大细胞脱颗粒的机制

目的:观察桑黄多糖的抗过敏作用并探讨其可能的作用机制。方法:通过IgE诱导大鼠被动皮肤过敏反应(PCA)实验,用比色法测定桑黄多糖在体内对肥大细胞影响。体外实验观察桑黄多糖对IgE诱导组胺释放、细胞内钙摄入及其他炎性介子的影响。结果:桑黄多糖明显抑制了肥大细胞脱颗粒、组胺的释放、细胞内钙摄入以及肿瘤坏死因子-α、白细胞介素6的释放(P<0.05)。结论:桑黄多糖抗过敏作用与抑制肥大细胞脱颗粒及炎性介子的释放有关。     

Study of the mechanism of inhibitory action of tranilast on chemical mediator release

We investigated the mechanism of inhibitory action of tranilast on chemical mediator release by antigen-antibody reactions. Tranilast (10(-5)-10(-3) M) inhibited antigen (DNP-Ascaris)-induced histamine release from sensitized purified rat mast cells (PMC), but did not show an obvious influence on intracellular cyclic AMP. 45Ca uptake into PMC induced by antigen (300 micrograms/ml) was obviously suppressed by tranilast (10(-6)-10(-3) M). Tranilast (10(-4) M) inhibited antigen-induced histamine release from and 45Ca uptake into PMC independently of the presence or absence of glucose in the medium. On the other hand, 2-deoxyglucose (10(-2) M) markedly inhibited both responses in the absence but not in the presence of glucose. Tranilast slightly inhibited Ca-induced contraction of guinea pig taenia coli, but had no influence on aggregation of rabbit platelets. Verapamil (10(-6)-10(-4) M) had no effect on antigen-induced histamine release, but it markedly suppressed Ca-induced contraction and platelet aggregation. From these results, we suggest that the mechanism of inhibitory action of tranilast on the release of antigen-induced chemical mediator from mast cells involves the suppression of Ca uptake, but that its mode of action is apparently different from those of 2-deoxyglucose and verapamil.