Excessive exposure to ultraviolet (UV) radiation results in premature aging of the skin. Lentinan polysaccharide (LNT), has been reported in the literature to exhibit a variety of biological functions, such as anti-inflammatory, antioxidant, and anticancer activities. In this research, the function and underlying mechanisms of LNT in UVB-induced photoaging were evaluated in vivo and in vitro. Initially, we developed a UVB-induced photoaging model in HDFs. The results indicated that following UVB irradiation, the positive rate of β-galactosidase, the proportion of dead cells, the generation of ROS, the expression of the senescence-associated secretory phenotype (SASP), the mRNA levels of inflammatory factors, as well as the activity of matrix metalloproteinases (MMPs) were upregulated in HDFs. In contrast, the components of the extracellular matrix (ECM), were decreased. Simultaneously, the impact of UVB exposure on the dorsal skin of mice exhibited a similar pattern. LNT was demonstrated to effectively mitigate the aforementioned changes and inhibit UVB-induced skin photoaging and damage in mice. Mechanistically, our findings revealed that LNT inhibited UVB-activated nuclear factor kappa B (NF-κB), the mitogen-activated protein kinase (MAPK) pathways and the P21/P16 axis. This property of LNT presents considerable potential for the development of therapeutic strategies aimed at delaying skin photoaging.
Keywords: Lentinan; Photoaging; UVB.
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