Wu Jie-Zhou, Liu Peng-Cheng, Liu Run, Cai Ming
Department of Orthopedics, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.
Department of Orthopedics, Affiliated Hospital of Chengdu University, Chengdu, China.
Cell Physiol Biochem. 2018;46(4):1727-1736. doi: 10.1159/000489248. Epub 2018 Apr 23.
BACKGROUND/AIMS: Chronic alcohol abuse is an important risk factor for osteopenia. However, few studies have focused on the efficacy and mechanism of action of icariin on alcohol-induced osteopenia. The aim of this study was to investigate the efficacy and underlying mechanism of action of icariin in the treatment of chronic high-dose alcohol-induced osteopenia in a rat model.
Thirty-six adult male Sprague-Dawley rats were randomly divided into four groups: sham, alcohol, and low-dose and high-dose icariin groups. Bone volume fraction (BV/TV), bone mineral density (BMD), bone biomechanical properties, and bone morphology were assessed after 16 weeks. Reverse-transcription PCR was used to detect mRNA expression levels of alkaline phosphatase (ALP), collagen type I (Col I), osteocalcin (OC), runt-related transcription factor 2 (Runx2), bone morphogenetic protein-2 (BMP-2), and osteoprotegerin (OPG).
Bone metabolic markers and biomechanical properties in the alcohol group were decreased significantly compared with the sham group. BV/TV, BMD, mineral apposition rate (MAR), percent trabecular area (%Tb.Ar), and bone biomechanical properties were elevated in the low-dose and high-dose icariin groups relative to the alcohol group. ALP, Col I, OC, Runx2, BMP-2, and OPG mRNA levels in the icariin group were significantly elevated in comparison with the alcohol group.
Icariin can prevent overall progression of chronic high-dose alcohol-induced osteopenia in a rat model, in a dose-dependent manner. Icariin promotes bone formation and inhibits bone loss, and effectively restores bone structure and strength in chronic high-dose alcohol-induced osteopenic rats. Bone metabolism reversal is evidenced by increased BV/TV, BMD, MAR, %Tb.Ar, and biomechanical properties and elevated ALP, Col I, OC, Runx2, BMP-2, and OPG mRNA levels.
背景/目的：长期酗酒是骨质减少的一个重要风险因素。然而，很少有研究关注淫羊藿苷对酒精性骨质减少的疗效及作用机制。本研究旨在探讨淫羊藿苷治疗大鼠慢性高剂量酒精性骨质减少的疗效及潜在作用机制。
将36只成年雄性Sprague-Dawley大鼠随机分为四组：假手术组、酒精组、低剂量淫羊藿苷组和高剂量淫羊藿苷组。16周后评估骨体积分数（BV/TV）、骨密度（BMD）、骨生物力学性能和骨形态。采用逆转录聚合酶链反应检测碱性磷酸酶（ALP）、I型胶原（Col I）、骨钙素（OC）、 runt相关转录因子2（Runx2）、骨形态发生蛋白-2（BMP-2）和骨保护素（OPG）的mRNA表达水平。
与假手术组相比，酒精组的骨代谢标志物和生物力学性能显著降低。低剂量和高剂量淫羊藿苷组的BV/TV、BMD、矿物质沉积率（MAR）、小梁面积百分比（%Tb.Ar）和骨生物力学性能相对于酒精组有所升高。与酒精组相比，淫羊藿苷组的ALP、Col I、OC、Runx2、BMP-2和OPG mRNA水平显著升高。
淫羊藿苷可以剂量依赖性方式预防大鼠慢性高剂量酒精性骨质减少的整体进展。淫羊藿苷促进骨形成并抑制骨丢失，有效恢复慢性高剂量酒精性骨质减少大鼠的骨结构和强度。BV/TV、BMD、MAR、%Tb.Ar、生物力学性能增加以及ALP、Col I、OC、Runx2、BMP-2和OPG mRNA水平升高证明了骨代谢的逆转。
