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氧化应激激活移植的脂肪来源干细胞,在脱发治疗中发挥抗氧化作用。

Oxidative stress activates the transplanted adipose-derived stem cells to exert antioxidant effects in alopecia treatment.

作者信息

Sun Xuer, Chen Minliang

机构信息

Senior Department of Burns and Plastic Surgery, The Fourth Medical Center of PLA General Hospital, Beijing, People's Republic of China.

出版信息

Redox Rep. 2025 Dec;30(1):2503128. doi: 10.1080/13510002.2025.2503128. Epub 2025 Jun 6.

DOI:10.1080/13510002.2025.2503128
PMID:40479645
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12147514/
Abstract

BACKGROUND

Alopecia is a global dermatological challenge. Adipose-derived stem cells (ADSC) show therapeutic potential, but their mechanisms in promoting hair regrowth, particularly under oxidative stress conditions, remain unclear..

OBJECTIVE

To investigate ADSC's role in promoting hair regrowth by mitigating oxidative stress.

METHODS

Using H₂O₂-stressed HaCaT cells, ADSC's protective effects were evaluated via conditioned medium (CM) and co-culture. Assessments included cell viability, colony formation, ROS, MDA, antioxidant enzymes, and 8-OHdG. Nrf2 activation was analyzed by immunofluorescence and Western blot. A mouse radiation injury model validated findings.

RESULTS

Non-pretreated ADSC offered limited oxidative protection to HaCaT cells. Conversely, H₂O₂-pretreated ADSC significantly enhanced HaCaT viability and proliferation in both CM and co-culture systems. This involved paracrine activation of the Nrf2 pathway in HaCaT cells, boosting antioxidant enzymes, accelerating ROS clearance, and reducing lipid peroxidation. These effects were reversible with Nrf2 inhibition. In vivo, CM from H₂O₂-stimulated ADSC promoted hair regrowth in irradiated mice, outperforming CM from non-pretreated ADSC by activating Nrf2 and reducing tissue oxidative damage.

CONCLUSIONS

Oxidative stress potentiates the protective capacity of ADSC against oxidative via Nrf2-dependent paracrine mechanisms, offering a promising strategy for alopecia treatment.

摘要

背景

脱发是一项全球性的皮肤病学挑战。脂肪来源干细胞(ADSC)显示出治疗潜力,但其促进头发生长的机制,尤其是在氧化应激条件下的机制仍不清楚。

目的

研究ADSC通过减轻氧化应激在促进头发生长中的作用。

方法

使用过氧化氢应激的HaCaT细胞,通过条件培养基(CM)和共培养评估ADSC的保护作用。评估包括细胞活力、集落形成、活性氧(ROS)、丙二醛(MDA)、抗氧化酶和8-羟基脱氧鸟苷(8-OHdG)。通过免疫荧光和蛋白质印迹分析Nrf2的激活情况。用小鼠辐射损伤模型验证研究结果。

结果

未经预处理的ADSC对HaCaT细胞的氧化保护作用有限。相反,过氧化氢预处理的ADSC在CM和共培养系统中均显著提高了HaCaT细胞的活力和增殖能力。这涉及HaCaT细胞中Nrf2途径的旁分泌激活,增强抗氧化酶,加速ROS清除,并减少脂质过氧化。这些作用可通过抑制Nrf2而逆转。在体内,过氧化氢刺激的ADSC的CM促进了受辐射小鼠的头发生长,通过激活Nrf2和减少组织氧化损伤,其效果优于未经预处理的ADSC的CM。

结论

氧化应激通过Nrf2依赖的旁分泌机制增强了ADSC的抗氧化保护能力,为脱发治疗提供了一种有前景的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72c/12147514/61298d6f7cda/YRER_A_2503128_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72c/12147514/c8c334179263/YRER_A_2503128_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72c/12147514/6795b8e16148/YRER_A_2503128_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72c/12147514/210bef9b9021/YRER_A_2503128_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72c/12147514/aa5f292d9206/YRER_A_2503128_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72c/12147514/465da255963a/YRER_A_2503128_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72c/12147514/61298d6f7cda/YRER_A_2503128_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72c/12147514/c8c334179263/YRER_A_2503128_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72c/12147514/6795b8e16148/YRER_A_2503128_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72c/12147514/210bef9b9021/YRER_A_2503128_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72c/12147514/aa5f292d9206/YRER_A_2503128_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72c/12147514/465da255963a/YRER_A_2503128_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72c/12147514/61298d6f7cda/YRER_A_2503128_F0006_OC.jpg

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本文引用的文献

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Oxidative Stress Response in Adipose Tissue-Derived Mesenchymal Stem/Stromal Cells.脂肪组织来源的间充质干细胞/基质细胞中的氧化应激反应。
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Intrinsic ROS Drive Hair Follicle Cycle Progression by Modulating DNA Damage and Repair and Subsequently Hair Follicle Apoptosis and Macrophage Polarization.
内源性 ROS 通过调节 DNA 损伤和修复,进而调节毛囊细胞凋亡和巨噬细胞极化,驱动毛囊周期进展。
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Mesenchymal stem cells-derived small extracellular vesicles alleviate diabetic retinopathy by delivering NEDD4.间充质干细胞衍生的小细胞外囊泡通过递送 NEDD4 缓解糖尿病视网膜病变。
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