Kashani Iraj Ragerdi, Hedayatpour Azim, Pasbakhsh Parichehr, Kafami Laya, Khallaghi Behzad, Malek Fatemeh
Department of Anatomical Sciences, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Department of Pathobiology, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran ; Shefa Neurosciences Research Center, Tehran, Iran.
Iran J Med Sci. 2015 Nov;40(6):507-14.
Progesterone as a sex steroid hormone is thought to affect and prevent demyelination, but its role in promoting myelin repair is far less investigated. In this study, remyelinating potential of progesterone in corpus callosum was evaluated on an experimental model of MS.
In this experimental study, adult male C57BL/6 mice were fed with 0.2% (w/w) cuprizone in ground breeder chow ad libitum for 6 weeks. At day zero, after cuprizone removal, mice were divided randomly into two groups: (a) placebo group, which received saline pellet implant, (b) progesterone group, which received progesterone pellet implant. Some mice of the same age were fed with their normal diet to serve as the healthy control group. Two weeks after progesterone administration, Myelin content was assessed by Luxol-fast blue staining. The myelin basic protein (MBP) and proteolipid protein (PLP) expression were assessed using Western blot analysis and the changes in the number of oligodendrocytes and oligodendroglial progenitor cells were assessed by immunohistochemistry (IHC) and flow cytometry.
Luxol-fast blue staining revealed enhanced remyelination in the progesterone group when compared with the placebo group. Densitometry measurements of immunoblots demonstrated that MBP and PLP proteins contents were significantly increased in the progesterone group compared with the placebo group. Flow cytometry and IHC analysis showed increases in Olig2 and O4 cells in the progesterone group compared with the placebo group.
Overall, our results indicate that progesterone treatment can stimulate myelin production and that it may provide a feasible and practical way for remyelination in diseases such as multiple sclerosis.
孕酮作为一种性甾体激素，被认为会影响并预防脱髓鞘，但对其促进髓鞘修复的作用研究较少。在本研究中，我们在多发性硬化症（MS）实验模型上评估了孕酮在胼胝体中的髓鞘再生潜力。
在本实验研究中，成年雄性C57BL/6小鼠自由摄食含0.2%（w/w）环磷酰胺的基础繁殖饲料6周。在第0天，去除环磷酰胺后，将小鼠随机分为两组：（a）安慰剂组，接受生理盐水丸植入；（b）孕酮组，接受孕酮丸植入。将一些同龄小鼠喂食正常饮食作为健康对照组。给予孕酮两周后，通过Luxol固蓝染色评估髓鞘含量。使用蛋白质免疫印迹分析评估髓鞘碱性蛋白（MBP）和蛋白脂蛋白（PLP）的表达，并通过免疫组织化学（IHC）和流式细胞术评估少突胶质细胞和少突胶质前体细胞数量的变化。
与安慰剂组相比，Luxol固蓝染色显示孕酮组的髓鞘再生增强。免疫印迹的光密度测量表明，与安慰剂组相比，孕酮组的MBP和PLP蛋白含量显著增加。流式细胞术和IHC分析显示，与安慰剂组相比，孕酮组的Olig2和O4细胞增加。
总体而言，我们的结果表明，孕酮治疗可以刺激髓鞘生成，并且它可能为多发性硬化症等疾病的髓鞘再生提供一种可行且实用的方法。
