中国骨质疏松杂志

丹酚酸B通过抗氧化作用改善高脂饮食小鼠牙槽骨骨质疏松的实验研究

Salvianolic acid B prevents mandibular osteoporosis through anti-oxidation in high fat diet exposed mice

DOI：10.3969/j.issn.1006.7108.2017.03.001

英文关键词:Salvianolic acid B Mice mandibles High fat diet Osteoporosis Animal experimentation

基金项目:国家自然科学基金（81273995，81274140);教育部和国家外专局高等学校学科创新引智计划资助项目（B07007)

作者	单位
王丽丽1 马如风1 于娜1 刘海霞1 朱如愿1 柳辰玥2 张淑静1 高誉珊1 葛东宇1 牛建昭1 高思华3 张东伟3*	1.北京中医药大学基础医学院,北京100029 2.北京中医药大学中药学院,北京100029 3.北京中医药大学糖尿病研究中心,北京100029

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中文摘要:

目的探索丹酚酸B改善髙脂饮食引起的小鼠牙槽骨骨量丢失的作用以及可能的作用机制。方法 C57BL/6J雄性小鼠30只，分为3组：正常组、高脂饮食组和丹酚酸B组，每组10只。除正常组外，其他两组给予髙脂饮食，丹酚酸B组用丹酚酸B[125 mg/(kg?d)]干预，治疗12 w后，取小鼠牙槽骨,然后分别用双能X射线测量骨密度，HE染色观察骨微结构，免疫组织化学染色分析牙槽骨核因子-κB-p65( nuclear factor-kappa B, NF-κB-p65 )、组织蛋白酶K ( Cathepsin K)、超氧化物歧化酶 (superoxide dismutase,SOD)和NADPH oxidase 4 (Nox4)的表达情况。结果丹酚酸B能明显改善高脂饮食诱发的小鼠牙槽骨骨密度下降以及骨微结构破坏。同时，丹酚酸B能上调高脂饮食小鼠牙槽骨SOD的表达，下调Nox4、NF-κB-p65和 Cathepsin K的表达。结论丹酚酸B可能通过调节Nox4/SOD/NF-κB/Cathepsin K通路改善高脂饮食引起的氧化应激，从而抑制高脂饮食诱发的小鼠牙槽骨骨量丢失。本研究将为丹参及其有效成分治疗骨质疏松提供科学的实验依据。

英文摘要:

Objective This study is aimed to assess the effect of salvianolic acid B (Sal-B) on high fat diet (HFD) -induced mandibular bone loss and to identify the potential signaling pathway involved in this process. Methods Thirty C57BL/6J male mice were randomly divided into 3 groups, normal group, HFD group and Sal-B group, with 10 mice in each group. All the mice except that in normal group were treated with high fat diet. Mice in Sal-B group received Sal-B [ 125 mg/(kg?d) ] for 12 weeks. The effects of Sal-B on bone mineral density (BMD) and micro-structures were evaluated using dual energy X-ray absorptiometry and hematoxylin and eosin staining. The expressions of nuclear factor-kappa B ( NF-κB) -p65, Cathepsin K, superoxide dismutase (SOD), and NADPH oxidase 4 (Nox4) in mandibles were determined with immunohistochemical staining. Results Sal-B treatment reversed the disorganized mandible bone micro-structures and descending BMD in HFD mice. Sal-B also up-regulated the expression of SOD and down-regulated the expression of Nox4, NF-κB-p65，and Cathepsin K in the mandibles triggered by HFD. Conclusion Sal-B treatment prevents the HFD-induced oxidative stress by regulating Nox4/SOD/NF-κB/Cathepsin K signaling pathway, and inhibits mandible osteoporosis. Our finding may offer a new source to discover the applications of salvia miltiorrhiza and its constituents for the treatment of osteoporosis.

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