α抑制素片段和单胺能神经递质对大鼠黄体功能的影响

EFFECT OF HUMAN INHIBIN α-FRAGMENTS AND MONOAMINERGIC NEUROTRANSMITTERS ON PROGESTERONE(P_4) PRODUCTION BY CORPUS LUTEUM(CL) OF RAT IN VITRO

本工作采用细胞离休孵育方法观察了抑制素α亚基Ｎ末端片段Ｐ^（３２）（１－３２）、Ｐ^（３２－Ｔｙｒ）（１－３２－Ｔｙｒ）和外源性单胺能神经递质─儿茶酚胺［去甲肾上腺素（ＮＥ），肾上腺素（Ｅ），多巴胺（ＤＡ）和五羟色胺（５－ＨＴ）］对大鼠黄体孕酮分泌的影响。结果显示：（１）Ｐ^（３２）和Ｐ^（３２－Ｔｙｒ）１００ｎｇ显著抑制黄体细胞的孕酮（Ｐ_４）分泌。（２）儿茶酚胺－肾上腺素和去甲肾上腺素（０．１ｍｍｏｌ／Ｌ），以及ＤＡ（１０μｍｏｌ／Ｌ）均使黄体基础与ｈＣＧ致Ｐ_４分泌明显增加（Ｐ＜０．００１）。对基础Ｐ_４分泌，它们的强度是ＮＥ＞Ｅ＞ＤＡ，而对ｈＣＧ致Ｐ_４分泌则相反，ＤＡ＞Ｅ＞ＮＥ。Ｐ^（３２），Ｐ^（３２－Ｔｙｒ）对ＮＥ刺激的基础和ｈＣＧ致Ｐ４分泌有所加强，而对Ｅ刺激的Ｐ_４分泌则显著抑制。（３）酚妥拉明（α）与心得安（β）阻断剂本身可显著降低基础与ｈＣＧ致Ｐ_４分泌，心得安对ｈＣＧ作用的抑制明显大于酚妥拉明；两者均加强Ｐ^（３２），Ｐ^（３２－Ｔｙｒ）对Ｐ_４分泌的抑制。（４）５－ＨＴ０．５μｍｏｌ／Ｌ则显著抑制黄体Ｐ_４分泌，并使Ｐ^（３２），Ｐ^（３２－Ｔｙｒ）的抑制作用大为减弱。以上结果提示：（１）黄体细胞上?

The effects of exogenenous monoaminergic neurotransmitters (norepinephrine, NE; epinephrine, E; dopamine, DA and 5-HT) and inhibin α N-terminal fragments P32 (1-32), p32-Tyr on P4 production by incubated rat CL cells were studied. The results demonstrated that: (1) α fragments caused significant inhibition on P4 production. (2) 0. 1 mmol/L NE (or E) and 10 μmol/L DA produced a marked increase in both hasal and hCG induced P4 production by CL cells (P<0. 001). The rank orders of potency of the catecholamines in stimulating P4 production were different, for hasal P4 production, NE>E>DA; but for hCG induced P4 production, DA>E>NE, i. e. the order just reversed. Addition of P32-Tyr significantly neutrolized the stimulatory action of E, but only slightly increaed the action of NE. (3) α receptor blocker phentolamine and α receptor blocker propranolol were effective in decreasing hasal and hCG-induced P4 production,the latter being more effective than the former. It was further shown that both blockers augmented the inhibitory effect of α-fragments on P4 production. (4) UnlikeNE, E, and DA, 5-HT at 0. 5 μmol/L exerted inhibitory effect on the hasal and hCG-induced P4 production, but profoundly supressed the inhibitory effect of α-fragmentson P4 production. The above results suggested: (1) Adrenergic, DA and 5-HT receptors are present in rat CL, where catecholamine might exert a stimulating effect on hasal and hCG-inducedP4 production via different pathways. (2) The inhibitory effect of P32, p32-Tyr on P4 production might be related to their inhibition by partial blocking α/β receptors, which were antagnized by 5-HT. (3) The action of P32, P32-TYr on P4 production is brought on the participation of neurotransmitters NE, E, DA and 5-HT.