摘要
为研究氨甲酰胆碱(CCh)所致CCL137细胞中毒蕈碱型乙酰胆碱受体(mAChR)失敏时磷脂酶A2(PLA2)激活的机理,应用百日咳杆菌毒素(PTX),抗-βγ血清和纯化的Giβγ,分别观察了它们对PLA2活性的影响.当在培养液中加入PTX或抗-βγ血清时,可见CCh不再能引起CCL137细胞中mAChR失敏和PLA2激活.反之,加入Giβγ或GTP-γ-S则使PLA2激活,且呈剂量依赖关系,前者尤为明显.结果表明,Giβγ在CCh所致CCL137细胞的PLA2激活中起重要作用.
That the activation of phospholipase A2 (PLA2)played an important role in carbacholinduced desensitization of mAChR has been reported previously by us. In the present study, pertussis toxin(PTX), antiβγ sera and purified Giβγ from bovine brain were used to elucidate the mechanism of PLA2 activation. The mAChR desensitization and PLA2 activation induced by carbachol were abolished when PTX or antiGiβγ serum was involved in the reaction system. On the other hand, the addition of Giβγ or GTPγS, which binds to Gα subunit with high affinity and releases free Gβγ, activated phospholipase A2 in a concentrationdependent manner. These data suggest that the Giβγ subunit is involved in the carbacholinduced activation of PLA2 in CCL137 cells.
出处
《中国药理学与毒理学杂志》
CAS
CSCD
北大核心
1998年第1期47-51,共5页
Chinese Journal of Pharmacology and Toxicology
基金
国家自然科学基金
关键词
Gi蛋白
βγ亚基
氨甲酰胆碱
磷脂酰A2
受体
receptor
muscarinic
carbachol
phospholipases A
pertussis toxins
guanine nucleotidebinding protein
α and βγ subunit