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姜黄素通过 SIRT3-SOD2-ROS 信号通路调节自噬以改善膝骨关节炎大鼠模型股四头肌萎缩。

Curcumin regulates autophagy through SIRT3-SOD2-ROS signaling pathway to improve quadriceps femoris muscle atrophy in KOA rat model.

机构信息

Department of Rehabilitation Medicine, First Affiliated Hospital of Gannan Medical University, 128 Jinling Road, Zhanggong District, Ganzhou, 341000, Jiangxi, China.

Ganzhou Intelligent Rehabilitation Technology Innovation Center, Ganzhou, Jiangxi, China.

出版信息

Sci Rep. 2024 Apr 8;14(1):8176. doi: 10.1038/s41598-024-58375-2.

DOI:10.1038/s41598-024-58375-2
PMID:38589505
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11001965/
Abstract

Knee osteoarthritis (KOA) usually leads to quadriceps femoris atrophy, which in turn can further aggravate the progression of KOA. Curcumin (CUR) has anti-inflammatory and antioxidant effects and has been shown to be a protective agent for skeletal muscle. CUR has been shown to have a protective effect on skeletal muscle. However, there are no studies related to whether CUR improves KOA-induced quadriceps femoris muscle atrophy. We established a model of KOA in rats. Rats in the experimental group were fed CUR for 5 weeks. Changes in autophagy levels, reactive oxygen species (ROS) levels, and changes in the expression of the Sirutin3 (SIRT3)-superoxide dismutase 2 (SOD2) pathway were detected in the quadriceps femoris muscle of rats. KOA led to quadriceps femoris muscle atrophy, in which autophagy was induced and ROS levels were increased. CUR increased SIRT3 expression, decreased SOD2 acetylation and ROS levels, inhibited the over-activation of autophagy, thereby alleviating quadriceps femoris muscle atrophy and improving KOA. CUR has a protective effect against quadriceps femoris muscle atrophy, and KOA is alleviated after improvement of quadriceps femoris muscle atrophy, with the possible mechanism being the reduction of ROS-induced autophagy via the SIRT3-SOD2 pathway.

摘要

膝骨关节炎（KOA）通常会导致股四头肌萎缩，进而进一步加重 KOA 的进展。姜黄素（CUR）具有抗炎和抗氧化作用，已被证明是骨骼肌的保护剂。CUR 已被证明对骨骼肌具有保护作用。但是，没有关于 CUR 是否改善 KOA 引起的股四头肌萎缩的相关研究。我们在大鼠中建立了 KOA 模型。实验组大鼠喂食 CUR 5 周。检测大鼠股四头肌中自噬水平、活性氧（ROS）水平的变化以及 Sirutin3（SIRT3）-超氧化物歧化酶 2（SOD2）途径表达的变化。KOA 导致股四头肌萎缩，其中诱导自噬并增加 ROS 水平。CUR 增加了 SIRT3 的表达，降低了 SOD2 的乙酰化和 ROS 水平，抑制了自噬的过度激活，从而缓解了股四头肌萎缩并改善了 KOA。CUR 对股四头肌萎缩具有保护作用，改善股四头肌萎缩后可缓解 KOA，其可能的机制是通过 SIRT3-SOD2 途径减少 ROS 诱导的自噬。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa42/11001965/dd83aa88a44b/41598_2024_58375_Fig6_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa42/11001965/8558775dcd4b/41598_2024_58375_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa42/11001965/dd83aa88a44b/41598_2024_58375_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa42/11001965/b0c6356d6198/41598_2024_58375_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa42/11001965/e37b720cf454/41598_2024_58375_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa42/11001965/7f18ed21ff46/41598_2024_58375_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa42/11001965/bf16502c7cc1/41598_2024_58375_Fig4_HTML.jpg
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