Lee Ming-Che, Yang Ying-Chin, Chen Yen-Cheng, Chang Bee-Song, Li Yi-Chen, Huang Shih-Che
Department of Surgery, Buddhist Tzu Chi General Hospital, Hualien, Taiwan.
Department of Surgery, School of Medicine, Tzu Chi University, Hualien, Taiwan.
Tzu Chi Med J. 2016 Apr-Jun;28(2):54-58. doi: 10.1016/j.tcmj.2016.03.004. Epub 2016 May 31.
Estrogen interacts with a membrane receptor, G protein-coupled estrogen receptor (GPER). It was reported that 17β-estradiol was able to inhibit contraction of the human colon and cause relaxation of the guinea pig gallbladder, however, the involvement of GPER was not clarified. The aim of the present study was to investigate the effect of estrogen on human gallbladder motility and the possible role of GPER.
Relaxation of human gallbladder strips were measured using isometric transducers. Expression of GPER was evaluated by reverse transcription polymerase chain reaction (PCR), realtime PCR, and immunohistochemistry.
In human gallbladder strips, 17β-estradiol and G-1 elicited marked and rapid relaxation, whereas tamoxifen produced mild concentration-dependent relaxation. The relative efficacies to cause relaxation were as follows: 17β-estradiol = G-1 > tamoxifen. The relaxant response of 17β-estradiol was not attenuated by tetrodotoxin or conotoxin GVIA. This implies that nerve stimulation was not involved in the 17β-estradiol-induced gallbladder relaxation. Analysis by reverse transcription PCR and real-time PCR showed that GPER was expressed in the human gallbladder. Further analysis by immunohisto-chemistry revealed that GPER was expressed in the gallbladder muscle. This suggests that 17β-estradiol relaxes the human gallbladder via GPER.
These results demonstrate for the first time that 17β-estradiol and GPER agonist G-1 cause relaxation of the human gallbladder, probably through GPER. Estrogen might play an important role in the control of human gallbladder motility.
雌激素与一种膜受体——G蛋白偶联雌激素受体（GPER）相互作用。据报道，17β-雌二醇能够抑制人结肠收缩并使豚鼠胆囊松弛，然而，GPER在其中的作用尚未阐明。本研究的目的是探讨雌激素对人胆囊运动的影响以及GPER可能发挥的作用。
使用等长换能器测量人胆囊条的松弛情况。通过逆转录聚合酶链反应（PCR）、实时PCR和免疫组织化学评估GPER的表达。
在人胆囊条中，17β-雌二醇和G-1引起显著且快速的松弛，而他莫昔芬产生轻度浓度依赖性松弛。引起松弛的相对效力如下：17β-雌二醇 = G-1 > 他莫昔芬。17β-雌二醇的松弛反应未被河豚毒素或芋螺毒素GVIA减弱。这意味着神经刺激不参与17β-雌二醇诱导的胆囊松弛。逆转录PCR和实时PCR分析表明，GPER在人胆囊中表达。免疫组织化学进一步分析显示，GPER在胆囊肌肉中表达。这表明17β-雌二醇通过GPER使人类胆囊松弛。
这些结果首次证明，17β-雌二醇和GPER激动剂G-1可能通过GPER使人类胆囊松弛。雌激素可能在控制人类胆囊运动中发挥重要作用。
