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摘要
Although estradiol has been reported to influence pain sensitivity, the role of estriol (an estradiol metabolite and another widely used female sex hormone) remains unclear. In this study, pain behavior tests, whole-cell patch clamp recording and Western blotting were used to determine whether estriol plays a role in pain signal transduction and transmission. Either systemic or local administration of 17 beta-estradiol produced a significant rise of mechanical pain threshold, while estriol lacked this effect in normal and ovariectomized (OVX) rats following estriol replacement. Local administration of 17 beta-estradiol or estriol significantly decreased ATP-induced spontaneous hind-paw withdrawal duration (PWD), which was blocked by an estrogen receptor antagonist. ICI 182, 780. However, systemic application of estriol in normal or OVX rats lacked this similar effect. In cultured dorsal root ganglion neurons, estriol attenuated alpha,beta-methylene ATP-induced transient currents which were blocked by ICI 182, 780. In complete Freund's adjuvant treated (CFA) rats, systemic application of 17 beta-estradiol or estriol decreased the mechanical pain threshold significantly, but did not change the inflammatory process. Similar effects were observed after estriol replacement in OVX rats. The expression of c-fos in lumbosacral spinal cord dorsal horn (SCDH) was increased significantly by administration of 17 beta-estradiol but not estriol, and not by estriol replacement in OVX rats. These results suggest that 17 beta-estradiol but not estriol plays an antihyperalgesic role in physiological pain. However, both peripheral 17 beta-estradiol and estriol play antihyperalgesic roles in ATP-induced inflammatory pain. Systemic application of estriol as well as 17 beta-estradiol plays hyperalgesic roles in CFA-induced chronic pain.
- 出版日期2012-2
- 单位天津市中医药研究院附属医院; 中国人民解放军第二军医大学
