The development of inflammatory models with endotoxin and its evaluation

内毒素炎症模型的建立及其评价

• 批准号: 07807209
• 负责人: UENO Akinori
• 金额: $ 1.28万
• 依托单位: Kitasato University School of Pharmaceutical Sciences
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1995
• 资助国家: 日本
• 起止时间: 1995 至 1996
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07807209/
• 关键词: endotoxin; bradykinin; des-Arg9-bradykinin; receptor; induction; inflammation; cyclooxygenase; rats; ブラジキニン(brady kinin); 血圧(blood pressure); 回腸(ileum); ラット(rat); エンドトキシン(endotoxin); 受容体(receptor); 発現(induction)

It was shown that bradykinin might involve in the permeability increase with intradermally injected endotoxin in rats. It was found that the hypotensive and contractile responses to des-Arg9-bradykinin were induced in rats previously treated with endotoxin. From the experimental results with antagonists and inhibitors of protein synthesis, it could be concluded that both responses mediated via newly induced B1 receptors. Furthermore, cyclooxygenase-2 was also induced by treatment of rat macrophages with endotoxin. And the inflammatory models was established by the intraperitoneal or intrapleural injection of endotoxin into rats.

结果表明，在大鼠内注射内注射的内毒素内注射的内毒素可能会参与渗透性的增加。发现在先前用内毒素治疗的大鼠中诱导了对DES-Arg9-胸蛋白的降压和收缩反应。从与蛋白质合成的拮抗剂和抑制剂的实验结果中可以得出的结论是，这两种反应通过新诱导的B1受体介导的。此外，还通过内毒素治疗大鼠巨噬细胞来诱导环氧合酶-2。炎症模型是通过腹膜内或胸膜内注射内毒素进入大鼠建立的。

项目成果

Matsumoto, H., Naraba, H., Murakami, M., Kudo, I., Yamaki, K., Ueno, A.and Oh-ichi, S.: "Concordant induction of prostaglandin E2 synthase with cyclooxygenase-2 leads to preferred production of prostaglandin E2 over thrombaxane and prostaglandin D2 in lip

Matsumoto, H.、Naraba, H.、Murakami, M.、Kudo, I.、Yamaki, K.、Ueno, A. 和 Oh-ichi, S.：“前列腺素 E2 合酶与环氧合酶 2 的协调诱导导致

Ueno,A.,et al: "Involvement of bradykinin in endotoxin-induced vascular permeability increase in the skin of rats." Eur,J.Pharmacol.284. 211-214 (1995)

Ueno,A.,et al：“缓激肽参与内毒素诱导的大鼠皮肤血管通透性增加。”

Ueno,A.,et al: "The mediators involved in endotoxin-induced vescular permeability increase in the rat and their interactions." Jap.J.Pharmacol. 70. 285-290 (1996)

Ueno,A.,et al：“参与内毒素诱导的大鼠血管通透性增加的介质及其相互作用。”

Ueuo, A. et al: "The mediators involved in endotoxin-induced vascular permeability increase in the rat skin and their interactions" Jap. J. Pharmacol. (in press). (1996)

Ueuo, A. 等人：“参与内毒素诱导的大鼠皮肤血管通透性增加的介质及其相互作用”

Tokumasu, T., Ueno, A.and Oh-ishi, S.: "A hypotensive response induced by des-Arg9-bradykinin in young Brown/Norway rats pretreated with endotoxin." Eur.J.Pharmacl.274. 225-228 (1995)

Tokumasu, T.、Ueno, A. 和 Oh-ishi, S.：“用内毒素预处理的年轻 Brown/Norway 大鼠中 des-Arg9-缓激肽诱导的低血压反应。”