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虾青素介导的 Nrf2 激活可改善糖皮质激素诱导的氧化应激和线粒体功能障碍，并改善大鼠糖皮质激素诱导的股骨头坏死的骨形成受损。

Astaxanthin-mediated Nrf2 activation ameliorates glucocorticoid-induced oxidative stress and mitochondrial dysfunction and impaired bone formation of glucocorticoid-induced osteonecrosis of the femoral head in rats.

机构信息

The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang Province, China.

Key Laboratory of Orthopedics of Zhejiang Province, Wenzhou, 325000, Zhejiang Province, China.

出版信息

J Orthop Surg Res. 2024 May 14;19(1):294. doi: 10.1186/s13018-024-04775-z.

DOI:10.1186/s13018-024-04775-z
PMID:38745231
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11092235/
Abstract

BACKGROUND

Osteonecrosis of the femoral head caused by glucocorticoids (GIONFH) is a significant issue resulting from prolonged or excessive clinical glucocorticoid use. Astaxanthin, an orange-red carotenoid present in marine organisms, has been the focus of this study to explore its impact and mechanism on osteoblast apoptosis induced by dexamethasone (Dex) and GIONFH.

METHODS

In this experiment, bioinformatic prediction, molecular docking and dynamics simulation, cytotoxicity assay, osteogenic differentiation, qRT-PCR analysis, terminal uridine nickend labeling (TUNEL) assay, determination of intracellular ROS, mitochondrial function assay, immunofluorescence, GIONFH rat model construction, micro-computed tomography (micro-CT) scans were performed.

RESULTS

Our research demonstrated that a low dose of astaxanthin was non-toxic to healthy osteoblasts and restored the osteogenic function of Dex-treated osteoblasts by reducing oxidative stress, mitochondrial dysfunction, and apoptosis. Furthermore, astaxanthin rescued the dysfunction in poor bone quality, bone metabolism and angiogenesis of GIONFH rats. The mechanism behind this involves astaxanthin counteracting Dex-induced osteogenic damage by activating the Nrf2 pathway.

CONCLUSION

Astaxanthin shields osteoblasts from glucocorticoid-induced oxidative stress and mitochondrial dysfunction via Nrf2 pathway activation, making it a potential therapeutic agent for GIONFH treatment.

摘要

背景

糖皮质激素（GIONFH）引起的股骨头坏死是由于长期或过量临床使用糖皮质激素导致的一个重大问题。虾青素是一种存在于海洋生物中的橙红色类胡萝卜素，本研究聚焦于探讨其对地塞米松（Dex）诱导的成骨细胞凋亡和 GIONFH 的影响及其机制。

方法

本实验进行了生物信息学预测、分子对接和动力学模拟、细胞毒性测定、成骨分化、qRT-PCR 分析、末端尿嘧啶核苷酸末端标记（TUNEL）检测、细胞内 ROS 测定、线粒体功能测定、免疫荧光、GIONFH 大鼠模型构建、微计算机断层扫描（micro-CT）扫描。

结果

我们的研究表明，低剂量虾青素对健康成骨细胞无毒，通过降低氧化应激、线粒体功能障碍和细胞凋亡，恢复了 Dex 处理的成骨细胞的成骨功能。此外，虾青素挽救了 GIONFH 大鼠的骨质量差、骨代谢和血管生成功能障碍。其作用机制涉及虾青素通过激活 Nrf2 通路来拮抗 Dex 诱导的成骨损伤。

结论

虾青素通过激活 Nrf2 通路来保护成骨细胞免受糖皮质激素诱导的氧化应激和线粒体功能障碍，使其成为治疗 GIONFH 的潜在治疗剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45ff/11092235/a74cf547176e/13018_2024_4775_Fig11_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45ff/11092235/020ec16cec27/13018_2024_4775_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45ff/11092235/f24d4a88111b/13018_2024_4775_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45ff/11092235/2ce8aabf91ad/13018_2024_4775_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45ff/11092235/10f61280e291/13018_2024_4775_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45ff/11092235/d7b96530080e/13018_2024_4775_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45ff/11092235/cfd6b14359b2/13018_2024_4775_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45ff/11092235/622a22d838b1/13018_2024_4775_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45ff/11092235/a74cf547176e/13018_2024_4775_Fig11_HTML.jpg

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