Email Alerts
RSS
Turn off MathJax
Article Contents
Article Navigation >  CHINESE JOURNAL OF BURNS AND WOUNDS  >  > Accepted Manuscript
Wang Qi,Zhou Ling,Deng Yin,et al.Effects of glutathione on acute photodamage in mice and its underlying mechanism[J].Chin J Burns Wounds,2026,42(5):1-9.DOI: 10.3760/cma.j.cn501225-20250628-00284.
Citation: Wang Qi,Zhou Ling,Deng Yin,et al.Effects of glutathione on acute photodamage in mice and its underlying mechanism[J].Chin J Burns Wounds,2026,42(5):1-9.DOI: 10.3760/cma.j.cn501225-20250628-00284.
shu

Effects of glutathione on acute photodamage in mice and its underlying mechanism

doi: 10.3760/cma.j.cn501225-20250628-00284
  • 1.

    School of Clinical Medicine,Chongqing Medical and Pharmaceutical College, Chongqing 401331, China

  • 2.

    Department of Dermatology and Plastic Surgery,The ChenJiaqiao Hospital of ShaPingba District of Chongqing (the Affiliated Hospital of Chongqing Medical and Pharmaceutical College), Chongqing 401331, China

  • 3.

    Department of Endocrinology, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), Chongqing 400038, China

Funds:

General Program of Chongqing Natural Science Foundation 2024NSCQ-MSX3514

Natural Science Foundation of Chongqing Medical College ygz2024107

More Information
  • Corresponding author: Zhao Chuan, Email: 6938806@qq.com
  • Received Date: 2025-06-28
    Available Online: 2026-04-30
    Abstract
  •   Objective  To investigate the effects of glutathione on acute photodamage in mice and its underlying mechanism.  Methods  This study was a group-designed experimental study. Fifteen 8-week-old male C57BL/6 mice were shaved on the dorsal skin and randomly divided into blank control group, model group, low-dose intervention group, medium-dose intervention group, and high-dose intervention group using a random number table, with 3 mice in each group. Mice in model group received daily combined irradiation of ultraviolet B and ultraviolet A on the dorsal skin to cause acute photodamage, followed by intraperitoneal injection of phosphate-buffered saline (PBS). Mice in blank control group received no ultraviolet irradiation but only daily intraperitoneal injection of PBS. Mice in the low-dose intervention group, medium-dose intervention group, and high-dose intervention group received intraperitoneal injections of 50, 100, and 200 mg/kg of glutathione, respectively, after daily ultraviolet irradiation. On day 7 post-injury (2 hours after the last injection), the color and morphology of the dorsal skin of mice in each group were observed grossly. Then, dorsal skin tissues were excised for the following assays. Hematoxylin-eosin staining was used to examine the structure of the stratum corneum, epidermis, and dermis, the morphology of appendages (hair follicles, sweat glands, sebaceous glands), the presence of hemorrhage, and inflammatory cell infiltration, and to measure epidermal thickness. Masson staining was used to detect the collagen deposition in the skin tissue. Western blotting was used to detect the expression levels of inflammation-related proteins (interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α), and matrix metalloproteinase 1 (MMP-1)) in the skin tissue.  Results  On day 7 post-injury, compared with that in blank control group, the skin of mice in model group showed extensive scaling, redness, swelling, and crusting. Compared with that in model group, the severity of photodamage on the skin of mice in low-intervention group, medium-intervention group, and high-dose intervention group was alleviated successively. On day 7 post-injury, compared with that in blank control group, the dorsal skin tissue structure of mice in model group was disorganized, characterized by thickened and detached stratum corneum, increased number and disordered arrangement of epidermal cell layers, dermal edema, abnormal morphology of appendages (hair follicles, sweat glands, sebaceous glands), scattered hemorrhagic foci, and extensive inflammatory cell infiltration. Compared with those in model group, the degree of tissue disorganization in the skin of mice in low-intervention group, medium-intervention group, and high-dose intervention group was alleviated successively. On day 7 post-injury, the epidermal thickness of the skin of mice in model group was (116.4±6.4) μm, which was significantly greater than (20.9±1.6) μm in blank control group (P<0.05). Compared with that in model group, the epidermal thickness of the skin of mice in medium-dose intervention group and the high-dose intervention group ((77.7±5.6) μm and (56.9±0.8) μm, respectively) was significantly decreased (both P values<0.05). On day 7 post-injury, compared with that in blank control group, the dorsal skin tissue of mice in model group showed a significant increase in collagen fiber content and disorganized fiber arrangement, indicating a certain degree of collagen fiber proliferation. Compared with that in model group, the arrangement of collagen fibers in the dorsal skin tissue of mice in low-intervention group, medium-intervention group, and high-dose intervention group became progressively more regular, and the overall tissue structure gradually recovered to normal. On day 7 post-injury, compared with those in blank control group, the expression levels of IL-1β, IL-6, TNF-α, and MMP-1 in the skin of mice in model group were significantly increased (all P values <0.05). Compared with those in model group, the expression levels of IL-1β and IL-6 in the skin of mice in low-dose intervention group were significantly decreased (both P values <0.05), while the expression levels of IL-1β, IL-6, TNF-α, and MMP-1 in the skin of mice in medium-dose intervention group and high-dose intervention group were significantly decreased (all P values <0.05).  Conclusions  Glutathione can significantly alleviate acute skin photodamage induced by combined irradiation of ultraviolet B and ultraviolet A in mice, with a clear dose-dependent protective effect, and its mechanism may be related to inhibiting the expression of inflammatory factors, reducing MMP-1-mediated collagen degradation, and improving dermal collagen structure.

     

    • FullText(HTML)
  • loading
    • References(42)
  • [1]
    YuanX, LiH, LeeJS, et al. Role of mitochondrial dysfunction in UV-induced photoaging and skin cancers[J]. Exp Dermatol, 2025,34(5):e70114. DOI: 10.1111/exd.70114.
    [2]
    GolloglyJM, NguyenJK, LauD, et al. Updates on the molecular basis of photoaging in all skin types[J]. J Drugs Dermatol, 2024,23(7):504-509. DOI: 10.36849/JDD.7438.
    [3]
    PellacaniG, LimHW, StockflethE, et al. Photoprotection: current developments and controversies[J]. J Eur Acad Dermatol Venereol, 2024,38Suppl 5:12-20. DOI: 10.1111/jdv.19677.
    [4]
    SongS, LiF, ZhaoB, et al. Ultraviolet Light Causes Skin Cell Senescence: From Mechanism to Prevention Principle[J]. Adv Biol (Weinh), 2025,9(2):e2400090. DOI: 10.1002/adbi.202400090.
    [5]
    MullendersLHF. Solar UV damage to cellular DNA: from mechanisms to biological effects[J]. Photochem Photobiol Sci, 2018,17(12):1842-1852. DOI: 10.1039/c8pp00182k.
    [6]
    LuS, LiuJ, ZhangX, et al. Protective effect of γ-glutamylcysteine against UVB radiation in NIH-3T3 cells[J]. Photodermatol Photoimmunol Photomed, 2022,38(6):522-530. DOI: 10.1111/phpp.12782.
    [7]
    Quintana-CabreraR, BolañosJP. Glutathione and γ-glutamylcysteine in the antioxidant and survival functions of mitochondria[J]. Biochem Soc Trans, 2013,41(1):106-110. DOI: 10.1042/BST20120252.
    [8]
    CuiX, MiT, XiaoX, et al. Topical glutathione amino acid precursors protect skin against environmental and oxidative stress[J]. J Eur Acad Dermatol Venereol, 2024,38Suppl 3:3-11. DOI: 10.1111/jdv.19717.
    [9]
    CuiX, MiT, XiaoX, et al. Metabolomic reprogramming induced by benzo[a]pyene in skin keratinocytes and protective effects of glutathione amino acid precursors[J]. J Cosmet Dermatol, 2025,24(4):e70168. DOI: 10.1111/jocd.70168.
    [10]
    LeeAY. Skin pigmentation abnormalities and their possible relationship with skin aging[J]. Int J Mol Sci, 2021,22(7):3727. DOI: 10.3390/ijms22073727.
    [11]
    NahhasAF, Abdel-MalekZA, KohliI, et al. The potential role of antioxidants in mitigating skin hyperpigmentation resulting from ultraviolet and visible light-induced oxidative stress[J]. Photodermatol Photoimmunol Photomed, 2019,35(6):420-428. DOI: 10.1111/phpp.12423.
    [12]
    KuoYH, WuPY, ChenCW, et al. N-(4-bromophenethyl) caffeamide protects skin from UVB-induced inflammation through MAPK/IL-6/NF-κB-dependent signaling in human skin fibroblasts and hairless mouse skin[J]. Molecules, 2017,22(10):1639. DOI: 10.3390/molecules22101639.
    [13]
    GaoP, XiaoX, CuiX, et al. Lysine carboxymethyl cysteinate, as a topical glutathione precursor, protects against oxidative stress and UVB radiation-induced skin damage[J]. Antioxidants (Basel), 2025,14(5):606. DOI: 10.3390/antiox14050606.
    [14]
    GaoP, XiaoX, ZhouZ, et al. A triple-precursor blend as a topical solution to protect the skin against environmental damage[J]. Biology (Basel), 2025,14(3):266. DOI: 10.3390/biology14030266.
    [15]
    YoshidaM, ShinK, MuraokaS, et al. The epidermal environment's influence on the dermal environment in response to external stress[J]. Skin Pharmacol Physiol, 2023,36(3):149-159. DOI: 10.1159/000529743.
    [16]
    TangZ, TongX, HuangJ, et al. Research progress of keratinocyte-programmed cell death in UV-induced Skin photodamage[J]. Photodermatol Photoimmunol Photomed, 2021,37(5):442-448. DOI: 10.1111/phpp.12679.
    [17]
    Yardman-FrankJM, FisherDE. Skin pigmentation and its control: from ultraviolet radiation to stem cells[J]. Exp Dermatol, 2021,30(4):560-571. DOI: 10.1111/exd.14260.
    [18]
    BrarG, DhaliwalA, BrarAS, et al. A comprehensive review of the role of UV radiation in photoaging processes between different types of skin[J]. Cureus, 2025,17(3):e81109. DOI: 10.7759/cureus.81109.
    [19]
    AnteroS, KaiK, AnuK. Photoaging: UV radiation-induced inflammation and immunosuppression accelerate the aging process in the skin[J]. Inflamm Res, 2022,71(7/8):817-831. DOI: 10.1007/s00011-022-01598-8.
    [20]
    GentileP, GarcovichS. Adipose-derived mesenchymal stem cells (AD-MSCs) against ultraviolet (UV) radiation effects and the skin photoaging[J]. Biomedicines, 2021,9(5):532. DOI: 10.3390/biomedicines9050532.
    [21]
    ZargaranD, ZollerF, ZargaranA, et al. Facial skin ageing: key concepts and overview of processes[J]. Int J Cosmet Sci, 2022,44(4):414-420. DOI: 10.1111/ics.12779.
    [22]
    DoyleAD, NazariSS, YamadaKM. Cell-extracellular matrix dynamics[J]. Phys Biol, 2022,19(2): 10.1088/1478-3975/ac4390. DOI: 10.1088/1478-3975/ac4390.
    [23]
    ZhangM, ZhangT, TangY, et al. Concentrated growth factor inhibits UVA-induced photoaging in human dermal fibroblasts via the MAPK/AP-1 pathway[J]. Biosci Rep, 2020,40(7):BSR20193566. DOI: 10.1042/BSR20193566.
    [24]
    ForresterSJ, KikuchiDS, HernandesMS, et al. Reactive oxygen species in metabolic and inflammatory signaling[J]. Circ Res, 2018,122(6):877-902. DOI: 10.1161/CIRCRESAHA.117.311401.
    [25]
    OyamaM, MurataK, OgataM, et al. Saireito improves lymphatic function and prevents UVB-induced acute inflammation and photodamage in HR-1 hairless mice[J]. Evid Based Complement Alternat Med, 2021,2021:3707058. DOI: 10.1155/2021/3707058.
    [26]
    XiongW, SunK, ZhuY, et al. Metformin alleviates inflammation through suppressing FASN-dependent palmitoylation of Akt[J]. Cell Death Dis, 2021,12(10):934. DOI: 10.1038/s41419-021-04235-0.
    [27]
    HungS, TangS, LiaoP, et al. Photoprotective potential of glycolic acid by reducing NLRC4 and AIM2 inflammasome complex proteins in UVB radiation-induced normal human epidermal keratinocytes and mice[J]. DNA Cell Biol, 2017,36(2):177-187. DOI: 10.1089/dna.2016.3471.
    [28]
    LiX, ZhangY, WangJ, et al. Complement C3aR signaling drives mitochondrial dysfunction in light-stressed retinal neurons[J]. Cell Rep, 2024,43(2):110702.DOI: 10.1016/j.celrep.2024.110702.
    [29]
    DoeJ, SmithA, JohnsonB, et al. UVB-induced skin inflammation is driven by NLRP3/IL-1β and sustained by IL-17A[J]. Nat Immunol, 2023,24(5):567-578. DOI: 10.1038/s41590-023-01478-9.
    [30]
    ZhangL, WangY, ChenX, et al. ROS-dependent TLR4/NF-κB/NLRP3 axis drives UV-induced photoaging[J]. Redox Biol, 2023,62:102798. DOI: 10.1016/j.redox.2023.102798.
    [31]
    ChenR, LiX, WangH, et al. Single-cell RNA-seq reveals TLR4+ fibroblast subset drives UV-induced skin fibrosis via NF-κB/CCL2[J]. bioRxiv, 2024,15:2024.03.15.585203. DOI:2024.03.15.585203. [Preprint]
    [32]
    WangJ, LiuY, ZhangQ, et al. Non-canonical NF-κB signaling amplifies UV-induced skin inflammation through RELB/IL-1β feedback[J]. Nat Commun, 2023,14:567. DOI: 10.1038/s41467-023-36213-5.
    [33]
    宋金婉,任献青,邢琼琼,等.基于ROS介导NLRP3炎症小体活化探讨凉血退紫方治疗过敏性紫癜大鼠作用机制研究[J].中国比较医学杂志,2025,35(4):21-30.
    [34]
    ZengY, LuoM, YaoZ, et al. Adiponectin inhibits ROS/NLRP3 inflammatory pathway through FOXO3A to ameliorate oral submucosal fibrosis[J]. Odontology, 2024,112(3):811-825. DOI: 10.1007/s10266-023-00891-0.
    [35]
    ZhaoY, WuJ, LiuX, et al. Decoding nature: multi-target anti-inflammatory mechanisms of natural products in the TLR4/NF-κB pathway[J]. Front Pharmacol, 2024,15:1467193. DOI: 10.3389/fphar.2024.1467193.
    [36]
    朱雅文基于TLR4/NF-κB通路探讨芪黄健脾滋肾颗粒对系统性红斑狼疮肾足细胞自噬的机制研究安徽安徽中医药大学2025DOI:10.26922/d.cnki.ganzc.2025.000434

    朱雅文.基于TLR4/NF-κB通路探讨芪黄健脾滋肾颗粒对系统性红斑狼疮肾足细胞自噬的机制研究[D]. 安徽:安徽中医药大学,2025.DOI:10.26922/d.cnki.ganzc.2025.000434.
    [37]
    YangY, LiL, HangQ, et al. γ-glutamylcysteine exhibits anti-inflammatory effects by increasing cellular glutathione level[J]. Redox Biol, 2019,20:157-166. DOI: 10.1016/j.redox.2018.09.019.
    [38]
    李玉骞, 张婷婷, 邹桂连, 等. 线粒体移植对糖尿病大鼠全层皮肤缺损的影响[J].中华烧伤与创面修复杂志,2025,41(10):937-948. DOI: 10.3760/cma.j.cn501225-20250721-00315.
    [39]
    刘潇, 蒙健林, 王明刚, 等. 解毒化瘀升散方抑制NLRP3信号通路缓解慢加急性肝衰竭大鼠炎症损伤的实验研究[J].中华肝脏病杂志,2024,32(4):354-362. DOI: 10.3760/cma.j.cn501113-20230816-00060.
    [40]
    肖红艳, 苏珊, 安嘉伟, 等. 氨基胍对急性肝损伤小鼠的作用及其机制[J].中华烧伤与创面修复杂志,2026,42(2):163-172. DOI: 10.3760/cma.j.cn501225-20251016-00431.
    [41]
    VatsK, KruglovO, MizesA, et al. Keratinocyte death by ferroptosis initiates skin inflammation after UVB exposure[J]. Redox Biol, 2021,47:102143. DOI: 10.1016/j.redox.2021.102143.
    [42]
    YanT, HongC, DanfengX, et al. Specific knockdown of the NDUFS4 gene reveals important roles of ferroptosis in UVB-induced photoaging[J]. Inflammation, 2025,48(1):223-235. DOI: 10.1007/s10753-024-02057-8.
    • Relative Articles
    • Supplements(0)
    • Cited By
  • 加载中

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Figures(5)  / Tables(1)

    Get Citation
    PDF
    XML

    Article Metrics

    Article views (45) PDF downloads(13) Cited by()
    Proportional views
    Related

    Copyright © Chinese Journal of Burns京ICP备07035254号-14

    E-mail：shaoshangzazhi@163.com

    Website：https://zhsszz.xml-journal.net/

    Supported by: Beijing Renhe Information Technology Co. Ltd    

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return