Prostate Research Cooperative, Medicinal Chemistry and Drug Action, Monash Institute of Pharmaceutical Sciences, Monash University, 381 Royal Parade, Parkville, VIC 3052, Australia.
Naunyn Schmiedebergs Arch Pharmacol. 2010 Apr;381(4):321-8. doi: 10.1007/s00210-010-0492-y. Epub 2010 Feb 24.
This study characterised the inhibitory actions of prostaglandins on smooth muscle contractility in the rat prostate gland. Immunohistochemical studies were carried out to identify and localise the two isoforms of cyclooxygenase (COX) enzyme and the subtypes of prostanoid receptors present in the rat prostate. Isolated organ bath studies were carried out to pharmacologically characterise the subtype of prostanoid receptor mediating the inhibitory effects of prostanoids on the rat prostate. Immunohistochemical studies confirmed the presence of mainly COX-2 within the prostatic stroma. Isolated organ bath studies showed that prostaglandin E(2) (PGE(2); 10 nM-10 microM) but not prostaglandin D(2) (10 nM-10 microM), PGF2alpha (10 nM-10 microM), prostacyclin (10 nM-10 microM) or U46619 (10 nM-10 microM) inhibited nerve-mediated contractile responses to electrical field stimulation. Similarly, sulprostone (10 nM-10 microM) had no affect on the magnitude of the electrically evoked contractions. PGE(2) (0.1-10 microM) did not affect contractions elicited by noradrenaline or adenosine 5'-triphosphate. PGE(2)-mediated inhibition of electrical field stimulation induced contractions was attenuated by AH 6809 (10 microM) but not SC 19220 (10 microM) or AH 23848 (10 microM). It is concluded that prostaglandins can inhibit contractions of the rat prostate gland through a prostanoid receptor of the EP(2) subtype.
这项研究描述了前列腺素对大鼠前列腺平滑肌收缩性的抑制作用。通过免疫组织化学研究，确定并定位了大鼠前列腺中存在的两种环氧化酶（COX）同工酶和前列腺素受体亚型。通过离体器官浴研究，对介导前列腺素抑制大鼠前列腺收缩的前列腺素受体亚型进行了药理学特征描述。免疫组织化学研究证实，前列腺基质中主要存在 COX-2。离体器官浴研究表明，前列腺素 E2（PGE2；10 nM-10 microM）但不是前列腺素 D2（10 nM-10 microM）、PGF2alpha（10 nM-10 microM）、前列环素（10 nM-10 microM）或 U46619（10 nM-10 microM）抑制了电刺激引起的神经介导的收缩反应。同样，舒前列素（sulprostone）（10 nM-10 microM）对电诱发收缩的幅度没有影响。PGE2（0.1-10 microM）对去甲肾上腺素或腺苷 5'-三磷酸引起的收缩没有影响。PGE2 介导的电刺激诱导收缩的抑制作用被 AH 6809（10 microM）减弱，但不受 SC 19220（10 microM）或 AH 23848（10 microM）的影响。结论是，前列腺素可以通过 EP（2）亚型的前列腺素受体抑制大鼠前列腺的收缩。
