Basic reseach for a remedy to allergic tissue inflammation

过敏性组织炎症治疗的基础研究

• 批准号: 05671833
• 负责人: NAGAI Hiroichi
• 金额: $ 1.34万
• 依托单位: Gifu Pharmaceutical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1993
• 资助国家: 日本
• 起止时间: 1993 至 1994
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-05671833/
• 关键词: Allergic tissue inflammation; Allergic airway inflammation; Arthritis; Nephritis; MRL; lpr Yaa; Cyclophosphamide; type II collagen関節炎; 自己免疫疾患モデル; lpr Yaa; 腎炎; メゾポルフィリン; アレルギー; サイトカイン; 自己免疫疾患; インターロイキン

The present study was carried out to investigate the remedy for allergic tissue inflammation including ariway inflammation, dermatitis and nephritis. Regarding a mimic model for above diseases, there is scarecely oppotunity to obtain an appropriate model for pharmacological study. In the first part of the present study, we have tried to develop a new pharmacological model to an allergic tissue inflammatory disease. The first experiment was focused on the airway inflammation resultd in the airway hyperreactivity. We have obtained two appropriate models for airway hyperreactivity in guinea pigs and mice. These models show similar clinical symptoms to human disease. Thromboxane A2 and interleukin 5 play an important role for the onset and development of airway obstraction. Secondary, we have developed new pharmacological models for atopic dermatitis in mice. We used monoclonal IgE antibody for passively sensitization. Topical application of antigen leads atopic dermatitis in the skin lesion. We find the role of tumour necrosis factor for onset of the dermatitis. The last study was conducted to investigate autoimmune tissue inflammation, arthritis and nephritis. We are now evaluating the pharmacologica value of our new models, MRL/lpr Yaa mice and SEB-induced arthritis. The results are not good enough to report. We will complete the study in the near feature.

本研究进行了研究，以调查包括Ariway炎症，皮炎和肾炎在内的过敏组织炎症的疗法。关于上述疾病的模拟模型，获得适当的药理学研究模型没有很大的对立性。在本研究的第一部分中，我们试图将新的药理学模型开发为过敏组织炎症性疾病。第一个实验的重点是气道炎症导致气道高反应性。我们已经获得了两个适当的模型，用于豚鼠和小鼠的气道高反应性。这些模型显示出与人类疾病相似的临床症状。血栓烷A2和白介素5对于气道观测的发作和发展起着重要作用。次要，我们开发了用于小鼠特应特应性皮炎的新药理模型。我们使用单克隆IgE抗体进行了被动敏化。抗原的局部应用导致皮肤皮炎在皮肤病变中。我们发现肿瘤坏死因子在皮炎发作中的作用。进行了最后一项研究，以研究自身免疫组织炎症，关节炎和肾炎。现在，我们正在评估新模型的药物学价值，MRL/LPR YAA小鼠和SEB诱导的关节炎。结果不足以报告。我们将在近乎特征中完成研究。

项目成果

T.Iwama: "Effect of NZ-107 on airway inflammation and cell activation in guinea pigs" J.Pharm.Pharmacol.45. 286-291 (1993)

T.Iwama：“NZ-107 对豚鼠气道炎症和细胞活化的影响”J.Pharm.Pharmacol.45。

T.Iwama: "Effect of murine recombinant interleukin-5 on bronchial reactivity in guinea pigs" Clin.Exp.Allergy. 23. 32-38 (1993)

T.Iwama：“鼠重组白细胞介素 5 对豚鼠支气管反应性的影响”Clin.Exp.Allergy。

A.Arimura, F.Asanuma, Y.Matumoto, A.Kurosawa, H.Jyoyama and H.Nagai: "Effect of the selective thromboxane A2 receptor antagonist, S-1452, on antigen-induced sustained bronchial hyperresponsiveness" Eur.J.Pharmacol.260. 201-209 (1994)

A.Arimura、F.Asanuma、Y.Matumoto、A.Kurosawa、H.Jyoyama 和 H.Nagai：“选择性血栓素 A2 受体拮抗剂 S-1452 对抗原诱导的持续支气管高反应性的影响”Eur.J。

H.Nagai, Y.Takaoka, H.Kamada and H.Mori: "The model of arthritis induced by superantigen in mice" Life Science. 55, PL. 233-237 (1994)

H.Nagai、Y.Takaoka、H.Kamada 和 H.Mori：“小鼠超抗原诱导的关节炎模型”生命科学。

T.Abe, T.Omata, K.Yosida, Y.Segawa, K.Matsuda and H.Nagai: "Antiallergic effect of ZCR-2060 : Effect on allergic cutaneous reactions and rhinitis models in mice and rats" Japan J.Pharmacol.66. 95-103 (1994)

T.Abe、T.Omata、K.Yosida、Y.Sekawa、K.Matsuda 和 H.Nagai：“ZCR-2060 的抗过敏作用：对小鼠和大鼠过敏性皮肤反应和鼻炎模型的影响”Japan J.Pharmacol。