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作 者:尹娟娟[1] 邓洁英[1] 史轶蘩[1] 任祖渊[1]
机构地区:[1]北京协和医院
出 处:《中国病理生理杂志》1996年第4期364-368,共5页Chinese Journal of Pathophysiology
基 金:国家自然科学基金
摘 要:为了解生长抑素(SRIF)在人垂体生长激素(GH)分泌瘤发病中的作用,在25例肢端肥大症患者体外地养的垂体瘤细胞观察了SRIF激动剂(SMS),抑制性鸟苷酸调节蛋白(Gi)拮抗剂百日咳毒素(PT)和钙离子载体A23187对GH分泌的影响.以及SMS对细胞内cAMP水平的抑制作用。发现:SMS可以使84.0%(21/125例)的GH瘤细胞GH分泌量明显抑制,揭示SRIF受体及受体后过程的功能基本正常;在31.6%(6/19例)患者的GH瘤细胞PT不能阻断SMS对GH分泌的抑制作用,提示这些瘤细胞膜上Gi的功能异常;在35.0%(7/20例)用者的GH瘤细胞A23187未能拮抗SMS对GH分泌的抑制作用,说明SRIF对Ca ̄(2+)通道功能的调节有异常。在部分瘤细胞SMS对GH分泌和细胞内cAMP的作用不一致。上述结果表明SRIF对垂体GH瘤细胞GH分泌的抑制作用由第二信使介导,但部分瘤细胞存在着受体后Gi和/或Ca ̄(2+)通道功能的缺陷。In order to investigate the role of somatostatin(SRIF)on the pathogenesis ofhuman pituitary GH-secreting adenomas,the effects of the SRIF agonist SMS201-995(SMS),Gi protein inhibitor pertussis toxin(PT) and Ca(2+) ionophone A23187 on GH secretionin 25 cases of human pituitary GH adenomas in eell cuIture were observed.The effect ofSMS on intracellular cAMP level was also studied.Addition of 100nmol/L SMS to culturemedium of tumor cells caused a significant decrease of GH secretion in 21 out of 25 cases(84.0%) indicating that the function of SRIF reeeptor are normal.PT blocked theinhibitory effect of SMS 0n GH secretion in 13 out of 19 cases(68.4%),but not in theother 6 cases(31.6%)which may show abnormality in Gi.Ca(2+) ionophone A23187 did notabolish the SMS-indueed inhibition of GH release in 7 out of 20 cases (35%) demostratingabnomal function in Ca(2+) channel.It was observed that the actions of SMS on intracellularcAMP level and GH release were not consistent in 4 out of 10 cases of cultured GHadenoma cell tested.These results showed that cAMP and Ca(2+) are second messengersfor the action of SMS in about half pituitary GH adenomas,but the defects ofGi/Ca(2+) channel in certain cases may alleviate the inhibitory effect of SMS on GH secre-tion,it may be responsible to hypersecretion of those GH secreting adenomas.
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