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

To systematically evaluate the protective effect and mechanism of Lactobacillus delbrueckii subsp. Lactis ABSN20244504 against skin photodamage, this study investigated he 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.