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姜黄素脂质体通过激活线粒体自噬减轻骨髓间充质干细胞的衰老。

Curcumin liposomes alleviate senescence of bone marrow mesenchymal stem cells by activating mitophagy.

作者信息

Li Weiyao, Huang Yixin, Fan Lei, Yangzom Dekyi, Zhang Kun, Shen Liuhong, Cao Suizhong, Gu Congwei, Yu Shumin

机构信息

Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, 611130, China.

Laboratory Animal Centre, Southwest Medical University, Luzhou, 646000, China.

出版信息

Sci Rep. 2024 Dec 28;14(1):31291. doi: 10.1038/s41598-024-82614-1.

Abstract

The senescence of mesenchymal stem cells (MSCs) is closely related to aging and degenerative diseases. Curcumin exhibits antioxidant and anti-inflammatory effects and has been extensively used in anti-cancer and anti-aging applications. Studies have shown that curcumin can promote osteogenic differentiation, autophagy and proliferation of MSCs. Liposome, as a nano-carrier, provides a feasible strategy for improving the bioavailability and controlled-release profile of curcumin.This study aimed to evaluate the effects of curcumin liposomes (Cur-Lip) on the senescence of rat bone marrow mesenchymal stem cells (rBMSCs). Based on network pharmacology, we predicted the targets and mechanisms of curcumin on senescence of MSC. 23 key targets of Cur were associated with MSC senescence were screened out and mitophagy signaling was significantly enriched. Cur-Lip treatment alleviated senescence of D-galactose (D-gal)-induced rBMSCs, protected mitochondrial function, and activated mitophagy, which may be related to mitochondrial fission. Inhibition of mitophagy attenuated the protective effects of Cur-lip on mitochondrial function and senescence of rBMSCs. Our findings suggested that Cur-Lip could alleviate senescence of rBMSC and improve mitochondrial function by activating mitophagy.

摘要

间充质干细胞(MSCs)的衰老与衰老和退行性疾病密切相关。姜黄素具有抗氧化和抗炎作用,已广泛应用于抗癌和抗衰老领域。研究表明,姜黄素可以促进MSCs的成骨分化、自噬和增殖。脂质体作为一种纳米载体,为提高姜黄素的生物利用度和控释特性提供了一种可行的策略。本研究旨在评估姜黄素脂质体(Cur-Lip)对大鼠骨髓间充质干细胞(rBMSCs)衰老的影响。基于网络药理学,我们预测了姜黄素对MSCs衰老的靶点和机制。筛选出23个与MSCs衰老相关的Cur关键靶点,线粒体自噬信号通路显著富集。Cur-Lip处理可减轻D-半乳糖(D-gal)诱导的rBMSCs衰老,保护线粒体功能,并激活线粒体自噬,这可能与线粒体分裂有关。抑制线粒体自噬减弱了Cur-lip对rBMSCs线粒体功能和衰老的保护作用。我们的研究结果表明,Cur-Lip可以通过激活线粒体自噬来减轻rBMSC的衰老并改善线粒体功能。

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