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。     

蛇床子挥发油止痒作用相关机制研究

目的　研究蛇床子挥发油止痒作用的机制。方法　用形态法观察了蛇床子挥发油对组胺兴奋豚鼠离体回肠和致敏大鼠腹腔肥大细胞 (PMC)脱颗粒的影响。结果　蛇床子挥发油对组胺引起的离体回肠平滑肌收缩和PMC脱颗粒有明显的抑制作用。结论　蛇床子挥发油止痒作用与拮抗组胺和抑制肥大细胞脱颗粒作用有关     

粉尘螨口服滴剂抗过敏作用的实验研究

目的探讨粉尘螨口服滴剂的抗过敏作用特点。方法采用豚鼠回肠平滑肌过敏收缩实验和肺支气管灌注法观察粉尘螨口服滴剂对平滑肌的抑制作用 ;大鼠被动皮肤过敏反应观察其对血管通透性改变的影响和颅骨骨膜法观察其对肥大细胞脱颗粒的抑制作用。结果粉尘螨口服滴剂能够明显抑制回肠平滑肌和拮抗抗原对支气管平滑肌的收缩作用 ,对肥大细胞脱颗粒具有显著的抑制作用。结论粉尘螨口服滴剂具有显著的抗过敏作用     

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。     

粉尘螨口服滴剂抗过敏作用的实验研究

目的：探讨粉尘螨口服滴剂的抗过敏作用特点。方法：采用豚鼠回肠平滑肌过敏收缩实验和肺支气管灌注法观察粉尘螨口服滴剂对平滑肌的抑制作用；大鼠被动皮肤过敏反应观察其对血管通透性改变的影响和颅骨骨膜法观察其对肥大细胞脱颗粒的抑制作用。结果：粉尘螨口服滴剂能够明显抑制回肠平滑肌和拮抗抗原对支气管平滑肌的收缩作用，对肥大细胞脱颗粒具有显的抑制作用。结论：粉尘螨口服滴剂具有显的抗过敏作用。     

曲安奈德混悬剂注射液(痛息痛)

曲安奈德(曾称曲安缩松、去炎舒松)是一种合成的肾上腺皮质激素,属于糖皮质激素。1 药理 治疗量的本品主要起抗炎和抗过敏作用,其机理是:抑制巨噬细胞对抗原的吞噬和处理;抑制B细胞转化成浆细胞,干扰体液免疫;稳定溶酶体膜,减少溶酶体内水解酶的释放;抑制白细胞和巨噬细胞移行至血管外,减少炎症反应;增加肥大细胞颗粒的稳定性,减少组织胺释放,从而减轻血管舒张及降低毛细血管通透性;加强血管收缩,减少局部充血及体液外渗;对纤维母细胞DNA有直接抑制作用,抑制肉芽组织形成,从而抑制非感染性炎症和过敏症状。     

曲安奈德混悬剂注射液（痛息痛）

曲安奈德 (曾称曲安缩松、去炎舒松 )是一种合成的肾上腺皮质激素 ,属于糖皮质激素。1　药理治疗量的本品主要起抗炎和抗过敏作用 ,其机理是 :抑制巨噬细胞对抗原的吞噬和处理 ;抑制Ｂ细胞转化成浆细胞 ,干扰体液免疫 ;稳定溶酶体膜 ,减少溶酶体内水解酶的释放 ;抑制白细胞和巨噬细胞移行至血管外 ,减少炎症反应 ;增加肥大细胞颗粒的稳定性 ,减少组织胺释放 ,从而减轻血管舒张及降低毛细血管通透性 ;加强血管收缩 ,减少局部充血及体液外渗 ;对纤维母细胞ＤＮＡ有直接抑制作用 ,抑制肉芽组织形成 ,从而抑制非感染性炎症和过敏症状。本品的抗…     

齐墩果醇酸对过敏性休克的对抗作用

研究齐墩果醇酸(oleanolic acid,OA)对6-氨基青霉烷酸APA-蛋白致敏豚鼠过敏休克的对抗作用.方法:采用腹腔注射抗原建立豚鼠过敏休克模型,同种被动皮肤过敏反应(PCA)测定致敏豚鼠血清抗体滴度,荧光测定致敏豚鼠肺组胺含量,大鼠颅骨骨膜法测定肥大细胞脱粒率.结果:OA可明显降低APA-蛋白致敏豚鼠过敏休克的发生率和死亡率.抑制致敏豚鼠血清抗APA-抗体生成;降低肺组胺含量;抑制豚鼠PCA反应及大鼠颅骨骨膜肥大细胞脱颗粒.结论:OA对抗过敏休克作用机制与其抑制血清抗APA抗体生成,并降低组胺含量有关.     

从香兰醛合成平喘药——利喘贝

以色甘酸钠为代表的过敏介质阻释剂的发现,是平喘药物的一大进展,它的作用机理是保护肥大细胞在过敏原以及各种刺激下不易释放过敏反应介质,产生抗过敏作用,对过敏性哮     

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.     

Magnoliae flos inhibits mast cell-dependent immediate-type allergic reactions.

The mast cell plays a pivotal role in initiating allergic response by secreting intracytoplasmic granular mediators such as histamine. Magnoliae flos has been used for the treatment of allergic disease in Korea. However, its effect in experimental models remains unknown. The present report describes an inhibitory effect of Magnoliae flos on mast cell-mediated immediate-type allergic reactions. Topical application of compound 48/80 can induce an ear swelling response in normal (WBB6F1-+/+) mice but not in the congenic mast cell-deficient WBB6F1-W/Wv mice. Magnoliae flos inhibited concentration-dependently mast cell-dependent ear swelling response induced by compound 48/80 by topical application. Magnoliae flos inhibited concentration-dependently passive cutaneous anaphylaxis induced by anti-dinitrophenyl (DNP) IgE in rats by topical application. Magnoliae flos also inhibited concentration-dependently the histamine release from the rat peritoneal mast cells by compound 48/80 or anti-DNP IgE. Moreover, Magnoliae flos had a significant inhibitory effect on compound 48/80-induced systemic anaphylactic reaction. These results indicate that Magnoliae flos inhibits immediate-type allergic reactions by inhibition of mast cell degranulation in vivo and in vitro.     

Action of Dracocephalum argunense on mast cell-mediated allergy model

The discovery of drugs for the treatment of allergic disease is an important subject in human health. Stimulation of mast cells starts the process of degranulation resulting in releasing of mediators, such as histamine. In this report, we investigated the effect of aqueous extract of Dracocephalum argunense Fisch. (Labiatae) (DAAE) on the mast cell-mediated allergic response and studied its possible mechanisms of action, focusing on the histamine release and pro-inflammatory cytokine secretion in mast cells. DAAE inhibited compound 48/80-induced systemic reactions and serum histamine release in mice. In addition, DAAE attenuated IgE-mediated skin allergic reaction. DAAE dose-dependently reduced IgE-induced histamine release from mast cells. The level of cAMP was transiently increased by treatment of DAAE. DAAE specifically blocked the phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore A23187-induced p38 mitogen-activated protein kinase (MAPK) activation. DAAE decreased the secretion of pro-inflammatory cytokines, such as tumor necrosis factor-alpha and interleukin-6 in mast cells. Our findings provide evidence that DAAE inhibits mast cell derived allergic reactions, and involvement of cAMP for histamine release and p38 MAPK for pro-inflammatory cytokine secretion in these effects.     

Anti-allergic effects of Teucrium japonicum on mast cell-mediated allergy model

The mast cell-mediated immediate-type allergic reaction is involved in many allergic diseases such as asthma, allergic rhinitis, and sinusitis. Stimulation of mast cells starts the process of degranulation resulting in release of mediators such as histamine and an array of inflammatory cytokines. In this report, we investigated the effect of aqueous extract of Teucrium japonicum Houttuyn (Labiatae) (AXTJ) on the mast cell-mediated allergy model and studied its possible mechanisms of action. AXTJ inhibited compound 48/80-induced systemic reactions and serum histamine release in mice. AXTJ decreased immunoglobulin E-mediated passive cutaneous anaphylaxis reaction. AXTJ reduced histamine release and intracellular calcium from rat peritoneal mast cells activated by compound 48/80. In addition, AXTJ attenuated activation of nuclear factor (NF)-κB, and downstream tumor necrosis factor (TNF)-α expression in phorbol 12-myristate 13-acetate and calcium ionophore A23187-stimulated human mast cells. Our findings provide evidence that AXTJ inhibits mast cell-derived allergic reactions and involvement of intracellular calcium, TNF-α, and NF-κB in these effects.     

Suppression of mast cell-mediated allergic reaction by Amomum xanthiodes.

The mast cell-mediated immediate-type allergic reaction is involved in many allergic diseases such as asthma, allergic rhinitis and sinusitis. Stimulation of mast cells starts the process of degranulation resulting in release of mediators such as histamine and an array of inflammatory cytokines. In this report, we investigated the effect of aqueous extract of Amomum xanthiodes (Zingiberaceae) (AXE) on the mast cell-mediated allergy model and studied its possible mechanisms of action. AXE inhibited compound 48/80-induced systemic reactions and serum histamine release in mice. AXE decreased immunoglobulin E (IgE)-mediated passive cutaneous anaphylaxis reaction. AXE reduced histamine release and intracellular calcium from rat peritoneal mast cells activated by compound 48/80. Furthermore, AXE decreased the activation of p38 mitogen-activated protein kinase (MAPK) but not extracellular signal-regulated kinase and c-jun N-terminal kinase, and downstream tumor necrosis factor (TNF)-alpha production in phorbol 12-myristate 13-acetate and calcium ionophore A23187-stimulated human mast cells. Our findings provide evidence that AXE inhibits mast cell-derived allergic reactions, and that intracellular calcium, TNF-alpha, and p38 MAPK are involved in these effects.     

Differential release of serotonin without comparable histamine under diverse conditions in the rat mast cell

Pretreatment of mast cells with various psychotropic agents was shown to permit preferential release of serotonin without substantial release of histamine or massive degranulation. Differential release involved both endogenous, granule-stored serotonin, and exogenous radiolabeled serotonin that had been taken up by the cell. This phenomenon occurred in mast cells stimulated to secrete with suboptimal concentrations of the classic mast cell secretagogue compound 48/80, was associated with drugs of several different structures and known mechanisms of action, and could be inhibited by certain prostaglandins. Furthermore, differential release of serotonin occurred in mast cells of retired breeders without the use of drugs or other exogenous agents. Light microscopic studies of mast cells undergoing differential release showed minimal degranulation, indicating that most of the serotonin release did not occur via classic exocytosis. The ability of mast cell to selectively release serotonin, by a mechanism unlike that occurring in allergic anaphylactic secretion, constitutes one of the first instances of differential release from secretory cells, suggests a new mechanism of release of secretory products, and expands the potential role of mast cells in the pathophysiology of the body.     

Inhibition of anaphylaxis like reaction and mast cell activation by Sitagliptin

Mast cells stimulation activates degranulation process resulting in releasing of mediators, such as histamine. In this study, the effect of aqueous extract of sitagliptin, a selective dipeptidylpeptidase-4 inhibitor, on the mast cell-mediated allergic response was studied with the possible mechanisms of action, focusing on the histamine release and pro-inflammatory cytokine secretion in mast cells. Sitagliptin produced dose dependent inhibition in compound 48/80-induced systemic reactions. In addition, sitagliptin attenuated IgE-mediated skin allergic reaction. Sitagliptin dose-dependently reduced compound 48/80- and IgE-induced histamine release from mast cells. Sitagliptin decreased the secretion of pro-inflammatory cytokines, tumor necrosis factor-α, in mast cells. So, the finding of this study provides evidence that sitagliptin inhibits mast cell derived allergic reactions, and involvement of pro-inflammatory cytokine secretion in such effects.     

Chrysin suppresses mast cell-mediated allergic inflammation: involvement of calcium, caspase-1 and nuclear factor-κB

A great number of people are suffering from allergic inflammatory diseases such as asthma, atopic dermatitis, and sinusitis. Therefore discovery of drugs for the treatment of these diseases is an important subject in human health. Chrysin (5,7-dihydroxyflavone) is a natural flavonoid contained in propolis, blue passion flower, and fruits. Several studies reported that chrysin has beneficial effects including anti-tumor and anti-oxidant activities. The aim of the present study was to elucidate whether chrysin modulates the allergic inflammatory reaction and to study its possible mechanisms of action using mast cell-based in vitro and in vivo models. Chrysin inhibited immediate-type systemic hypersensitivity and serum histamine release. Chrysin attenuated immunoglobulin E-mediated local anaphylaxis. These inhibitory effects of chrysin on the systemic and local allergic reaction were more potent than cromolyn, a known anti-allergic drug. Chrysin reduced histamine release from mast cells. The inhibitory effect of chrysin on the histamine release was mediated by the modulation of intracellular calcium. In addition, chrysin decreased gene expression of pro-inflammatory cytokines such as, tumor necrosis factor-α, IL (interleukin)-1β, IL-4, and IL-6 in mast cells. The inhibitory effect of chrysin on the pro-inflammatory cytokine was nuclear factor-κB and caspase-1 dependent. Our findings provide evidence that chrysin inhibits mast cell-derived allergic inflammatory reactions by blocking histamine release and pro-inflammatory cytokine expression, and suggest the mechanisms of action. Furthermore, in vivo and in vitro anti-allergic inflammatory effect of chrysin suggests a possible therapeutic application of this agent in allergic inflammatory diseases.     

Inhibitory effect of putranjivain A on allergic inflammation through suppression of mast cell activation

A great number of people are suffering from allergic inflammatory disease such as asthma, atopic dermatitis, and sinusitis. Therefore discovery of drugs for the treatment of these diseases is an important subject in human health. Putranjivain A (PJA), member of ellagitannin, is known to possess beneficial effects including anti-cancer and anti-viral activities. The aim of the present study was to elucidate whether PJA modulates the allergic inflammatory reaction and to study its possible mechanisms of action using mast cell-based in vitro and in vivo models. The study was performed in anaphylaxis mouse model and cultured mast cells. PJA inhibited the expression of pro-inflammatory cytokines in immunoglobulin E-stimulated mast cells. PJA reduced this expression by inhibiting nuclear factor (NF)-κB and nuclear factor of activated T cell. The oral administration of PJA reduced systemic and cutaneous anaphylaxis, the release of serum histamine, and the expression of the histamine H₁ receptor. In addition, PJA attenuated the activation of mast cells. PJA inhibited the release of histamine from various types of mast cells by the suppression of intracellular calcium. The inhibitory activity of PJA on the allergic reaction was similar to that of disodium cromoglycate, a known anti-allergic drug. These results suggest that PJA can facilitate the prevention or treatment of allergic inflammatory diseases mediated by mast cells.