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Regulatory Mechanism of Eosinophil Peroxidase Release From Guinea Pig Eosinophils

机译:豚鼠嗜酸性粒细胞释放嗜酸性粒细胞过氧化物酶的调控机制

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References(24) Cited-By(3) The regulatory mechanism of degranulation of guinea pig peritoneal eosinophils was studied by determination of eosinophil peroxidase(EPO)release.β−Agonists, such as isoproterenol, salbutamol and fenoterol, effectively inhibited A23187−induced EPO release from guinea pig eosinophils.The inhibitory effects of β−agonists were attenuated by pretreatment with either propranolol, a non−selective β−antagonist, or ICI 118, 551, a selective β2−antagonist.Both theophylline and dibutyryl−cAMP(db−cAMP)also significantly inhibited A23187−induced EPO release.The inhibition of EPO release induced by db−cAMP was attenuated by pretreatment with KT5720, a protein kinase A inhibitor.In addition, calphostin C as well as cytochalasin D effectively inhibited A23187−induced EPO release.From the results of the present study, it was concluded that an increase in intracellular Ca2+ concentration may lead to exocytosis of eosinophil granules through activation of protein kinase C and microfilaments.β−Agonists and theophylline were effective in inhibiting degranulation of eosinophils by increasing intracellular cAMP level coupled with the activation of protein kinase A.
机译:参考文献(24)(3)通过测定嗜酸性粒细胞过氧化物酶(EPO)的释放来研究豚鼠腹膜嗜酸性粒细胞脱粒的调节机制.β-激动剂(如异丙肾上腺素,沙丁胺醇和非诺特罗)有效抑制A23187诱导的EPO。豚鼠嗜酸性粒细胞释放β-激动剂的抑制作用可通过使用非选择性β-拮抗剂普萘洛尔或选择性β2-拮抗剂ICI 118、551进行预处理来减弱,茶碱和二丁酰cAMP(db- cAMP)还显着抑制A23187诱导的EPO释放.db-cAMP诱导的EPO释放的抑制通过蛋白激酶A抑制剂KT5720的预处理得以减弱;此外,钙磷蛋白C和细胞松弛素D有效抑制了A23187诱导的EPO。从本研究的结果可以得出结论,细胞内Ca2 +浓度的增加可能通过激活蛋白激酶C和m导致嗜酸性粒细胞的胞吐作用。 β-激动剂和茶碱可通过增加细胞内cAMP水平并激活蛋白激酶A来有效抑制嗜酸性粒细胞脱颗粒。

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