德氏乳杆菌乳亚种ABSN20244504对UVB诱导小鼠皮肤损伤的抑制作用

宋灿琳; 任彦荣; 龙兴瑶; 裴龙英; 谭芳; 赵茹兰; 赵欣

doi:10.13386/j.issn1002-0306.2026040255

德氏乳杆菌乳亚种ABSN20244504对UVB诱导小鼠皮肤损伤的抑制作用

Inhibitory Effect of Lactobacillus delbrueckii subsp. lactis ABSN20244504 on UVB Induced Skin Damage in Mice

摘要

摘要: 为系统评估德氏乳杆菌乳亚种ABSN20244504对皮肤光损伤的防护效果及作用机制，本文探讨了德氏乳杆菌乳亚种ABSN20244504（LDSL-ABSN20244504）对紫外线B（ultraviolet B，UVB）诱导光损伤的抑制作用。本文采用UVB诱导的小鼠光损伤模型，通过评估皮肤组织切片、血清和皮肤氧化应激水平、炎症标志物、皮肤的核因子κB p65亚基（nuclear factor kappa-light-chain-enhancer of activated B cells p65 subunit，NF-κB p65）、κB抑制蛋白α（nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha，IκB-α）、肿瘤坏死因子-α（tumor necrosis factor-alpha，TNF-α）、白细胞介素-6（interleukin-6，IL-6）、IL-10、超氧化物歧化酶1（superoxide dismutase 1，SOD1）、SOD2、过氧化氢酶（catalase，CAT）、谷胱甘肽1（glutathione，GSH1）、腺苷酸活化蛋白激酶（AMP-activated protein kinase，AMPK）、肝激酶B1（liver Kinase B1，LKB1）、沉默信息调节因子2相关酶1（sirtuin 1，SIRT1）、哺乳动物雷帕霉素靶蛋白（mammalian target of rapamycin，mTOR）、过氧化物酶体增殖物激活受体γ共激活因子1α（peroxisome proliferator-activated receptor gamma coactivator 1-alpha，PGC-1α）、衔接蛋白1（adaptor protein, phosphotyrosine interacting with PH domain and leucine zipper 1，APPL1）、叉头框蛋白O（forkhead box O，FOXO）mRNA和NAD(P)H:醌氧化还原酶1（NAD(P)H:quinone oxidoreductase 1，NQO1）抗体、谷氨酸-半胱氨酸连接酶催化亚基（glutamate-cysteine ligase catalytic subunit，GCLC）抗体、核因子E2相关因子2（nuclear factor erythroid 2–related factor 2，Nrf2）蛋白表达，来评估LDSL-ABSN20244504对皮肤光损伤的保护效应。LDSL-ABSN20244504处理缓解了UVB诱导的小鼠光损伤，缓解了表皮增生和真皮丢失，减少了肥大细胞的产生，缓解了表皮结构损伤。相比于模型组，LDSL-ABSN20244504能够提高皮肤损伤小鼠血清和皮肤组织的总超氧化物歧化酶（total superoxide dismutase，T-SOD）、CAT、IL-4、IL-10水平和降低过氧化氢（H₂O₂）、晚期糖基化终末产物（advanced glycation end products，AGEs）、IL-6、IL-1β、TNF-α水平。同时LDSL-ABSN20244504还能够提高皮肤损伤小鼠皮肤组织的钠钾三磷酸腺苷酶（Na⁺/K⁺-ATPase）、烟酰胺腺嘌呤二核苷酸激酶（nicotinamide adenine dinucleotide kinase，NADK）水平。RT-qPCR结果表明LDSL-ABSN20244504能够上调皮肤损伤小鼠皮肤组织中SOD1、SOD2、CAT、GSH1、IκB-α、IL-10、AMPK、LKB1、SIRT1、PGC-1α、APPL1、FOXO mRNA表达和下调NF-κB p65、TNF-α、IL-6、mTOR mRNA表达。同时，LDSL-ABSN20244504也能够上调皮肤损伤小鼠皮肤组织中NQO1、GCLC和Nrf2蛋白表达。由此可以看出LDSL-ABSN20244504具有抑制UVB导致的皮肤损伤，效果优于抗氧化剂维生素C，且LDSL-ABSN20244504活菌口服的效果也高于灭活LDSL-ABSN20244504涂抹皮肤。

Abstract: To systematically evaluate the protective effect and mechanism of Lactobacillus delbrueckii subsp. lactis ABSN20244504 against skin photodamage, this study investigated the inhibitory effect of Lactobacillus delbrueckii subsp. lactis ABSN20244504 (LDSL-ABSN20244504) on ultraviolet B (UVB)-induced photodamage. In this study, a UVB-induced mouse photodamage model was used to evaluate the protective effects of LDSL-ABSN20244504 against skin photodamage by assessing skin tissue sections, levels of oxidative stress in serum and skin, inflammatory markers, the mRNA expression of nuclear factor kappa-light-chain-enhancer of activated B cells p65 subunit (NF-κB p65), inhibitor of nuclear factor kappa B alpha (IκB-α), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), IL-10, superoxide dismutase 1 (SOD1), SOD2, catalase (CAT), AMP-activated protein kinase (AMPK), liver kinase B1 (LKB1), sirtuin 1 (SIRT1), mammalian target of rapamycin (mTOR), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), adaptor protein phosphotyrosine interacting with PH domain and leucine zipper 1 (APPL1), and forkhead box O (FOXO), the levels of glutathione 1 (GSH1), as well as the protein expression of NAD(P)H:quinone oxidoreductase 1 (NQO1), glutamate-cysteine ligase catalytic subunit (GCLC), and nuclear factor erythroid 2–related factor 2 (Nrf2). Treatment with LDSL-ABSN20244504 alleviated UVB-induced photodamage in mice, as evidenced by reduced epidermal hyperplasia and dermal loss, decreased mast cell production, and mitigation of epidermal structural damage. Compared with the model group, LDSL-ABSN20244504 increased the levels of total superoxide dismutase (T-SOD), catalase (CAT), IL-4, and IL-10 in the serum and skin tissue of skin-injured mice, while decreasing the levels of hydrogen peroxide (H₂O₂), advanced glycation end products (AGEs), IL-6, IL-1β, and TNF-α. Additionally, LDSL-ABSN20244504 elevated the levels of Na⁺/K⁺-ATPase and nicotinamide adenine dinucleotide kinase (NADK) in the skin tissue of skin-injured mice. RT-qPCR results showed that LDSL-ABSN20244504 upregulated the mRNA expression of SOD1, SOD2, CAT, GSH1, IκB-α, IL-10, AMPK, LKB1, SIRT1, PGC-1α, APPL1, and FOXO, and downregulated the mRNA expression of NF-κB p65, TNF-α, IL-6, and mTOR in the skin tissue of skin-injured mice. Moreover, LDSL-ABSN20244504 also upregulated the protein expression of NQO1, GCLC and Nrf2 in the skin tissue of skin-injured mice. These findings indicate that LDSL-ABSN20244504 inhibits UVB-induced skin damage, with an effect superior to that of the antioxidant vitamin C, and that oral administration of live LDSL-ABSN20244504 is more effective than topical application of inactivated LDSL-ABSN20244504 to the skin.