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| 八子补肾胶囊对衰老小鼠骨质量的保护作用及其对SIRT6/NF-κB/ cathepsin K通路的影响 |
| Bazi Bushen capsules improves bone quality and regulates SIRT6/NF-κB/cathepsin K pathway in aged mice |
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| DOI：10.3969/j.issn.1006-7108.2021.03.001 |
| 中文关键词: 八子补肾胶囊 衰老 老年性骨质疏松 SIRT6/NF-κB/cathepsin K信号通路 |
| 英文关键词:Bazi Bushen (BZBS) capsules aging senile osteoporosis SIRT6/NF-κB/cathepsin K signaling pathway |
| 基金项目:国家自然科学基金项目（NSFC81874373，82074235） |
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| 中文摘要: |
| 目的 探讨八子补肾胶囊（BZBS）对D-半乳糖（D-gal）和亚硝酸钠（NaNO2）诱导的衰老小鼠的骨保护作用及可能的作用机制。方法 ICR雄性小鼠连续腹腔注射D-gal和NaNO2三个月造成衰老小鼠模型，并于造模第25天开始用BZBS干预，连续干预65 d。然后收集股骨，分别用HE染色评价骨微结构的变化，三点弯曲实验评估骨生物力学性能，Micro-CT扫描观察骨组织形态计量学参数，红外光谱法分析骨材料特性，免疫组织化学染色法测定骨组织中的SIRT6、NF-κB和cathepsin K蛋白表达水平。结果 BZBS能明显抑制D-gal和NaNO2诱导的衰老小鼠的骨形态破坏，提高骨组织矿物质含量。此外，BZBS能上调衰老小鼠血清中的 T-AOC、SOD、GSH、GSH/GSSG水平，降低MDA水平，提高骨组织中SIRT6的表达，抑制NF-κB乙酰化，降低cathepsin K的表达。结论 BZBS能提高衰老小鼠的骨质量，这种作用可能与调节氧化还原平衡进而调控SIRT6/NF-κB/cathepsin K信号通路有关。 |
| 英文摘要: |
| Objective To explore the protective effect of Bazi Bushen (BZBS) capsules on the bone quality of aged mice induced by D-galactose (D-gal) and sodium nitrite (NaNO2) and the potential underlying mechanism involved in this process. Methods Male ICR mice were intraperitoneally injected with D-gal and NaNO2 continuously for 3 months to induce aged mice model and treated with BZBS from the 25th day for 65 days. Then the femurs were collected, and the changes of bone microstructure were observed with HE staining. The biomechanical properties of the bone were evaluated with three-point bending experiment. Bone material properties were analyzed by FTIR. The morphometric parameters of the bone tissue were observed with micro-CT. SIRT6, NF-κB, and cathepsin K protein expressions in the bone tissue were determined with immunohistochemical staining. Results BZBS significantly protected the bone morphology from destruction in aged mice induced by D-gal and NaNO2, and increased the mineral content of the bone tissue. In addition, BZBS increased the levels of T-AOC, SOD, GSH, and GSH/GSSG in aged mice and decreased MDA. The expression of SIRT6 in the bone increased, the acetylation of NF-κB decreased, and the expression of cathepsin K decreased. Conclusion BZBS may regulate the SIRT6/NF-κB/cathepsin K signaling pathway by restoring the redox balance, thereby improving the bone quality of aged mice. |
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