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车叶草苷通过促进自噬和调节Nrf2激活来减轻骨质疏松症。

Asperuloside alleviates osteoporosis by promoting autophagy and regulating Nrf2 activation.

作者信息

Huang Fenglan, Wang Yiteng, Liu Jinzhu, Cheng Ye, Zhang Xiaonan, Jiang Haoli

机构信息

Department of Outpatient, Shenzhen University General Hospital, Shenzhen, 518055, China.

Department of Sports Medicine, Central Hospital of Dalian University of Technology, Dalian, 116021, China.

出版信息

J Orthop Surg Res. 2024 Dec 19;19(1):855. doi: 10.1186/s13018-024-05320-8.

DOI:10.1186/s13018-024-05320-8
PMID:39702357
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11658297/
Abstract

BACKGROUND

Osteoporosis is a metabolic bone disease that has a common occurrence in postmenopausal women. Asperuloside (ASP) has been reported to exert anti-inflammatory and anti-oxidative effects in numerous diseases, such as rheumatoid arthritis and acute lung injury. However, whether ASP plays a role in osteoporosis has not been addressed.

METHODS

In vivo, ovariectomy (OVX) was used to induce mouse osteoporosis. Then, the mice were treated with 20 and 40 mg/kg ASP. In vitro, MC3T3-E1 cells were treated with 0, 1, 10, 20, 40 and 80 µM ASP. We chose 20 and 40 µM for further experiments due to no significant effects on cell viability.

RESULTS

The data indicated that ASP reduced osteoporosis in OVX mice and promoted osteogenic differentiation and mineralization in MC3T3-E1 cells. In addition, we explored that ASP protected against osteoporosis via inducing autophagy and activating Nrf2.

CONCLUSION

ASP alleviates OVX-induced osteoporosis by promoting autophagy and regulating Nrf2 activation.

摘要

背景

骨质疏松症是一种代谢性骨病,在绝经后女性中普遍存在。据报道,车叶草苷(ASP)在许多疾病中发挥抗炎和抗氧化作用,如类风湿性关节炎和急性肺损伤。然而,ASP是否在骨质疏松症中起作用尚未得到探讨。

方法

在体内,采用卵巢切除术(OVX)诱导小鼠骨质疏松症。然后,给小鼠分别用20和40mg/kg的ASP进行治疗。在体外,用0、1、10、20、40和80μM的ASP处理MC3T3-E1细胞。由于对细胞活力无显著影响,我们选择20和40μM进行进一步实验。

结果

数据表明,ASP减轻了OVX小鼠的骨质疏松症,并促进了MC3T3-E1细胞的成骨分化和矿化。此外,我们探究了ASP通过诱导自噬和激活Nrf2来预防骨质疏松症。

结论

ASP通过促进自噬和调节Nrf2激活来减轻OVX诱导的骨质疏松症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848c/11658297/16c4bf7d433e/13018_2024_5320_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848c/11658297/4b138c4ca228/13018_2024_5320_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848c/11658297/57d93a63617b/13018_2024_5320_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848c/11658297/a2363303fbef/13018_2024_5320_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848c/11658297/0cf0d450350d/13018_2024_5320_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848c/11658297/9576a9278544/13018_2024_5320_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848c/11658297/16c4bf7d433e/13018_2024_5320_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848c/11658297/4b138c4ca228/13018_2024_5320_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848c/11658297/57d93a63617b/13018_2024_5320_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848c/11658297/a2363303fbef/13018_2024_5320_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848c/11658297/0cf0d450350d/13018_2024_5320_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848c/11658297/9576a9278544/13018_2024_5320_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848c/11658297/16c4bf7d433e/13018_2024_5320_Fig6_HTML.jpg

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