金松双黄酮通过抑制 NF-κB/IκBα 信号通路减轻去卵巢小鼠的骨丢失。
Ginkgetin attenuates bone loss in OVX mice by inhibiting the NF-κB/IκBα signaling pathway.
机构信息
Department of Orthopaedics, 923rd Hospital of PLA, Nanning, China.
Graduate School, Guilin Medical College, Guilin, China.
出版信息
PeerJ. 2024 Jul 10;12:e17722. doi: 10.7717/peerj.17722. eCollection 2024.
BACKGROUND
Osteoporosis is a disease associated with bone resorption, characterized primarily by the excessive activation of osteoclasts. Ginkgetin is a compound purified from natural ginkgo leaves which has various biological properties, including anti-inflammation, antioxidant, and anti-tumor effects. This study investigated the bone-protective effects of ginkgetin in ovariectomized (OVX) mice and explored their potential signaling pathway in inhibiting osteoclastogenesis in a mouse model of osteoporosis.
METHODS
Biochemical assays were performed to assess the levels of Ca, ALP, and P in the blood. Micro CT scanning was used to evaluate the impact of ginkgetin on bone loss in mice. RT-PCR was employed to detect the expression of osteoclast-related genes (ctsk, c-fos, trap) in their femoral tissue. Hematoxylin and eosin (H&E) staining was utilized to assess the histopathological changes in femoral tissue due to ginkgetin. The TRAP staining was used to evaluate the impact of ginkgetin osteoclast generation . Western blot analysis was conducted to investigate the effect of ginkgetin on the expression of p-NF-κB p65 and IκBα proteins in mice.
RESULTS
Our findings indicate that ginkgetin may increase the serum levels of ALP and P, while decreasing the serum level of Ca in OVX mice. H&E staining and micro CT scanning results suggest that ginkgetin can inhibit bone loss in OVX mice. The TRAP staining results showed ginkgetin suppresses the generation of osteoclasts in OVX mice. RT-PCR results demonstrate that ginkgetin downregulate the expression of osteoclast-related genes (ctsk, c-fos, trap) in the femoral tissue of mice, and this effect is dose-dependent. Western blot analysis results reveal that ginkgetin can inhibit the expression of p-NF-κB p65 and IκBα proteins in mice.
CONCLUSION
Ginkgetin can impact osteoclast formation and activation in OVX mice by inhibiting the NF-κB/IκBα signaling pathway, thereby attenuating bone loss in mice.
背景
骨质疏松症是一种与骨吸收有关的疾病，其主要特征是破骨细胞过度激活。银杏素是从天然银杏叶中纯化的一种化合物，具有多种生物学特性，包括抗炎、抗氧化和抗肿瘤作用。本研究探讨了银杏素对去卵巢（OVX）小鼠的骨保护作用，并在骨质疏松症小鼠模型中探讨了其抑制破骨细胞形成的潜在信号通路。
方法
通过生化分析检测血液中 Ca、ALP 和 P 的水平。采用 micro CT 扫描评估银杏素对小鼠骨丢失的影响。采用 RT-PCR 检测股骨组织中破骨细胞相关基因（ctsk、c-fos、trap）的表达。采用苏木精和伊红（H&E）染色评估银杏素对股骨组织的组织病理学变化。采用 TRAP 染色评估银杏素对破骨细胞生成的影响。采用 Western blot 分析检测银杏素对 NF-κB p65 和 IκBα 蛋白表达的影响。
结果
我们的研究结果表明，银杏素可能增加 OVX 小鼠血清中 ALP 和 P 的水平，同时降低血清中 Ca 的水平。H&E 染色和 micro CT 扫描结果表明，银杏素可抑制 OVX 小鼠的骨丢失。TRAP 染色结果表明，银杏素可抑制 OVX 小鼠破骨细胞的生成。RT-PCR 结果表明，银杏素可下调小鼠股骨组织中破骨细胞相关基因（ctsk、c-fos、trap）的表达，且呈剂量依赖性。Western blot 分析结果表明，银杏素可抑制 NF-κB p65 和 IκBα 蛋白的表达。
结论
银杏素通过抑制 NF-κB/IκBα 信号通路，影响 OVX 小鼠破骨细胞的形成和激活，从而减轻小鼠的骨丢失。
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