Division of Nephrology, Zhongshan Hospital Fudan University, Shanghai 200032, China; Shanghai Key Laboratory of Kidney and Dialysis, Shanghai 200032, China; Department of Radiology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China.
Department of Radiology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China.
Environ Toxicol Pharmacol. 2017 Sep;54:162-168. doi: 10.1016/j.etap.2017.07.007. Epub 2017 Jul 18.
Environmental level of cadmium (Cd) exposure can induce bone loss. Emodin, a naturally compound found in Asian herbal medicines, could influence osteoblast/osteoclast differentiation. However, the effects of emodin on Cd-induced bone damage are not clarified. The aim of this study was to investigate the role of emodin on Cd-induced osteoporosis. Sprague-Dawley male rats were divided into three groups which were given 0mg/L, 50mg Cd/L and 50mg Cd/L plus emodin (50mg/kg body weight). Bone histological investigation, microCT analysis, metabolic biomarker determination and immunohistochemical staining were performed at the 12th week. The bone mass and bone microstructure index of rats treated with Cd were obviously lower than in control. Cd markedly enhanced the osteoclast formation compared with control. Emodin significantly abolished the Cd-induced bone microstructure damage (p<0.05), osteoclast formation and increase of tartrate-resistant acid phosphatase 5b level (p<0.05). Our data further showed that emodin attenuated the Cd-induced inhibition of osteoprotegerin expression and stimulation of receptor activator for nuclear factor-κ B ligand expression. Our data show that emodin suppresses the Cd-induced osteoporosis by inhibiting osteoclast formation.
环境镉(Cd)暴露水平可导致骨质流失。大黄素是一种存在于亚洲草药中的天然化合物,可影响成骨细胞/破骨细胞分化。然而,大黄素对 Cd 诱导的骨损伤的影响尚不清楚。本研究旨在探讨大黄素对 Cd 诱导的骨质疏松症的作用。将雄性 Sprague-Dawley 大鼠分为三组,分别给予 0mg/L、50mg Cd/L 和 50mg Cd/L 加大黄素(50mg/kg 体重)。在第 12 周进行骨组织学研究、microCT 分析、代谢生物标志物测定和免疫组织化学染色。与对照组相比,Cd 处理组大鼠的骨量和骨微结构指数明显降低。Cd 明显增强了破骨细胞的形成。大黄素显著消除了 Cd 诱导的骨微结构损伤(p<0.05)、破骨细胞形成和抗酒石酸酸性磷酸酶 5b 水平升高(p<0.05)。我们的数据进一步表明,大黄素减弱了 Cd 诱导的护骨素表达抑制和核因子-κ B 配体受体激活剂表达刺激。我们的数据表明,大黄素通过抑制破骨细胞形成抑制 Cd 诱导的骨质疏松症。