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虾青素介导修复 tBHP 诱导的软骨细胞损伤。

Astaxanthin mediated repair of tBHP-Induced cellular injury in chondrocytes.

机构信息

Department of Orthopedics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.

Department of Orthopedics, The People's Hospital of Puyang, Puyang, People's Republic of China.

出版信息

Redox Rep. 2024 Dec;29(1):2422271. doi: 10.1080/13510002.2024.2422271. Epub 2024 Nov 4.

DOI:10.1080/13510002.2024.2422271
PMID:39495906
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11536701/
Abstract

OBJECTIVE

This study investigates how astaxanthin (AST) counters tert-butyl hydroperoxide (tBHP)-induced cellular damage in C28/I2 chondrocytes, focusing on the circ-HP1BP3/miR-139-5p/SOD1 signaling pathway and its use in sustained-release microspheres for osteoarthritis treatment.

METHODS

We employed a variety of techniques including real-time quantitative PCR, Western blot, ELISA, and dual-luciferase reporter gene assays to explore AST's molecular effects. Additionally, the efficacy of AST-loaded sustained-release microspheres was evaluated in vitro and in a mouse model of osteoarthritis.

RESULTS

AST significantly enhanced SOD1 expression, reducing apoptosis and inflammation in damaged cells. The AST-loaded microspheres showed promising in vitro drug release, improved cell viability, and reduced oxidative stress. In the osteoarthritis mouse model, they effectively decreased joint inflammation and increased the expression of chondrocyte markers.

CONCLUSION

Astaxanthin effectively mitigates oxidative stress and inflammation in chondrocytes via the circ-HP1BP3/miR-139-5p/SOD1 pathway. The development of AST-loaded microspheres offers a novel and promising approach for osteoarthritis therapy, potentially extending to osteoarthritis treatment.

摘要

目的

本研究旨在探讨虾青素(AST)如何抵抗叔丁基过氧化物(tBHP)诱导的 C28/I2 软骨细胞损伤,重点关注 circ-HP1BP3/miR-139-5p/SOD1 信号通路及其在骨关节炎治疗中的缓释微球中的应用。

方法

我们采用了多种技术,包括实时定量 PCR、Western blot、ELISA 和双荧光素酶报告基因检测,以探讨 AST 的分子作用。此外,还评估了 AST 负载的缓释微球在体外和骨关节炎小鼠模型中的疗效。

结果

AST 显著增强了 SOD1 的表达,减轻了受损细胞的凋亡和炎症。AST 负载的微球显示出有前途的体外药物释放、提高细胞活力和降低氧化应激的效果。在骨关节炎小鼠模型中,它们有效地减轻了关节炎症并增加了软骨细胞标志物的表达。

结论

虾青素通过 circ-HP1BP3/miR-139-5p/SOD1 通路有效减轻软骨细胞的氧化应激和炎症。AST 负载微球的开发为骨关节炎治疗提供了一种新颖而有前途的方法,可能扩展到骨关节炎的治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d7/11536701/0f90e9cfaed5/YRER_A_2422271_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d7/11536701/08efa413c19e/YRER_A_2422271_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d7/11536701/a5b869623c92/YRER_A_2422271_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d7/11536701/25638cfd608c/YRER_A_2422271_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d7/11536701/b224237a8182/YRER_A_2422271_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d7/11536701/ed438f89c1ae/YRER_A_2422271_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d7/11536701/6a21b45f8fac/YRER_A_2422271_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d7/11536701/0f90e9cfaed5/YRER_A_2422271_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d7/11536701/08efa413c19e/YRER_A_2422271_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d7/11536701/a5b869623c92/YRER_A_2422271_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d7/11536701/25638cfd608c/YRER_A_2422271_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d7/11536701/b224237a8182/YRER_A_2422271_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d7/11536701/ed438f89c1ae/YRER_A_2422271_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d7/11536701/6a21b45f8fac/YRER_A_2422271_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d7/11536701/0f90e9cfaed5/YRER_A_2422271_F0007_OC.jpg

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