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虾青素通过抑制氧化应激预防棕榈酸致骨质疏松大鼠的骨丢失。

Astaxanthin prevents bone loss in osteoporotic rats with palmitic acid through suppressing oxidative stress.

机构信息

Department of Orthopedics, The First Affiliated Hospital of Wannan Medical College, Yijishan Hospital, No. 2, Zhe Shan Xi Road, Wuhu, Anhui, People's Republic of China.

Anhui Province Key Laboratory of Noncoding RNA Basic and Clinical Transformation, No. 2, Zhe Shan Xi Road, Wuhu, Anhui, People's Republic of China.

出版信息

Redox Rep. 2024 Dec;29(1):2333096. doi: 10.1080/13510002.2024.2333096. Epub 2024 Apr 16.

DOI:10.1080/13510002.2024.2333096
PMID:38623993
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11025413/
Abstract

OBJECTIVES

The study aimed to assess the role of Astaxanthin (ATX) in palmitic acid(PA) -induced bone loss in Ovariectomized(OVX) rats.

METHODS

In the OVX rat model, we observed that PA affects bone metabolism and accelerates bone loss. Additionally, treatment with ATX was able to suppress the deleterious effects of PA and a simultaneous decrease in serum MDA levels and an increase in SOD was observed.

RESULTS

In addition, rats treated with ATX were observed to have significantly increased bone mass and elevated activity of SIRT1 and SOD2 in bone tissue. When MC3T3-E1 and RAW264.7 cells induced osteoblast and osteoclast differentiation, the ATX intervention was able to significantly restore the restriction of osteogenic differentiation and the up-regulation of osteoclast differentiation with PA therapy. Furthermore, we confirm that PA damage to cells is caused by increased oxidative stress, and that ATX can target and modulate the activity of SIRT1 to regulate the levels of oxidative stress in cells.

CONCLUSION

Summarizing, ATX may inhibit PA-induced bone loss through its antioxidant properties via the SIRT1 signaling pathway.

摘要

目的

本研究旨在评估虾青素(ATX)在棕榈酸(PA)诱导去卵巢(OVX)大鼠骨丢失中的作用。

方法

在 OVX 大鼠模型中,我们观察到 PA 影响骨代谢并加速骨丢失。此外,ATX 的治疗能够抑制 PA 的有害影响,同时观察到血清 MDA 水平降低和 SOD 水平升高。

结果

此外,用 ATX 治疗的大鼠观察到骨量显著增加,骨组织中 SIRT1 和 SOD2 的活性升高。当 MC3T3-E1 和 RAW264.7 细胞诱导成骨细胞和破骨细胞分化时,ATX 干预能够显著恢复 PA 治疗对成骨分化的限制和破骨细胞分化的上调。此外,我们证实 PA 对细胞的损伤是由氧化应激增加引起的,ATX 可以通过靶向和调节 SIRT1 的活性来调节细胞内的氧化应激水平。

结论

总之,ATX 可能通过 SIRT1 信号通路通过其抗氧化特性抑制 PA 诱导的骨丢失。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/cded72094339/YRER_A_2333096_F0012_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/5dc23d6a47ea/YRER_A_2333096_UF0001_OC.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/38f30a7dad4e/YRER_A_2333096_F0006_OC.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/b80b46637790/YRER_A_2333096_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/5dbcf5627297/YRER_A_2333096_F0009_OC.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/cab39deb9b21/YRER_A_2333096_F0011_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/cded72094339/YRER_A_2333096_F0012_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/5dc23d6a47ea/YRER_A_2333096_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/73383387394c/YRER_A_2333096_F0001_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/c2dfe77cd6e3/YRER_A_2333096_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/fd4b4817e7e4/YRER_A_2333096_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/217f87ba5299/YRER_A_2333096_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/71b38d738b5a/YRER_A_2333096_F0005_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/38f30a7dad4e/YRER_A_2333096_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/3c4ed1e7f0de/YRER_A_2333096_F0007_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/b80b46637790/YRER_A_2333096_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/5dbcf5627297/YRER_A_2333096_F0009_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/5a5277ba0cad/YRER_A_2333096_F0010_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/cab39deb9b21/YRER_A_2333096_F0011_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1222/11025413/cded72094339/YRER_A_2333096_F0012_OC.jpg

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