Manni Luigi, Lundeberg Thomas, Holmäng Agneta, Aloe Luigi, Stener-Victorin Elisabet
Cardiovascular Institute and Wallenberg Laboratory, Sahlgrenska Academy, Göteborg University, SE-413 45 Göteborg, Sweden.
Reprod Biol Endocrinol. 2005 Jun 7;3:21. doi: 10.1186/1477-7827-3-21.
Estradiol valerate (EV)-induced polycystic ovaries (PCO) in rats is associated with an increase in ovarian sympathetic outflow. Low-frequency (2 Hz) electro-acupuncture (EA) has been shown to modulate sympathetic markers as well as ovarian blood flow as a reflex response via the ovarian sympathetic nerves, in rats with EV-induced PCO.
In the present study, we further tested the hypothesis that repeated 2 Hz EA treatments modulate ovarian sympathetic outflow in rats with PCO, induced by a single i.m. injection of EV, by investigating the mRNA expression, the amount and distribution of proteins of alpha1a-, alpha1b-, alpha1d-, and beta2-adrenoceptors (ARs), as well as the low-affinity neurotrophin receptor (p75NTR).
It was found that EV injection results in significantly higher mRNA expression of ovarian alpha1b- and alpha1d-AR in PCO rats compared to control rats. The p75NTR and beta2-ARs mRNA expression were unchanged in the PCO ovary. Low-frequency EA resulted in a significantly lower expression of beta2-ARs mRNA expression in PCO rats. The p75NTR mRNA was unaffected in both PCO and control rats. PCO ovaries displayed significantly higher amount of protein of alpha1a-, alpha1b- and alpha1d-ARs, and of p75NTR, compared to control rats, that were all counteracted by repeated low-frequency EA treatments, except for alpha1b-AR.
The present study shows that EA normalizes most of the EV-induced changes in ovarian ARs. Furthermore, EA was able to prevent the EV-induced up regulation of p75NTR, probably by normalizing the sympathetic ovarian response to NGF action. Our data indicate a possible role of EA in the regulation of ovarian responsiveness to sympathetic inputs and depict a possible complementary therapeutic approach to overcoming sympathetic-related anovulation in women with PCOS.
戊酸雌二醇(EV)诱导的大鼠多囊卵巢(PCO)与卵巢交感神经输出增加有关。在EV诱导的PCO大鼠中,低频(2Hz)电针(EA)已被证明可通过卵巢交感神经调节交感神经标志物以及卵巢血流,作为一种反射反应。
在本研究中,我们进一步检验了以下假设:通过研究α1a-、α1b-、α1d-和β2-肾上腺素能受体(ARs)以及低亲和力神经营养因子受体(p75NTR)的mRNA表达、蛋白质数量和分布,重复进行2Hz EA治疗可调节单次肌内注射EV诱导的PCO大鼠的卵巢交感神经输出。
发现与对照大鼠相比,EV注射导致PCO大鼠卵巢α1b-和α1d-AR的mRNA表达显著更高。PCO卵巢中p75NTR和β2-ARs的mRNA表达未发生变化。低频EA导致PCO大鼠中β2-ARs mRNA表达显著降低。PCO和对照大鼠中p75NTR mRNA均未受影响。与对照大鼠相比,PCO卵巢中α1a-、α1b-和α1d-ARs以及p75NTR的蛋白质数量显著更高,除α1b-AR外所有这些均被重复的低频EA治疗所抵消。
本研究表明EA可使大多数EV诱导的卵巢AR变化恢复正常。此外,EA能够预防EV诱导的p75NTR上调,可能是通过使卵巢对神经生长因子(NGF)作用的交感反应恢复正常。我们的数据表明EA在调节卵巢对交感神经输入的反应性中可能发挥作用,并描述了一种可能的补充治疗方法,以克服多囊卵巢综合征(PCOS)女性中与交感神经相关的无排卵。