Department of Food and Nutrition, Eulji University, Seongnam 13135, Republic of Korea.
College of Pharmacy, Mokpo National University, Mokpo 58554, Republic of Korea.
Int J Mol Sci. 2024 Jul 18;25(14):7850. doi: 10.3390/ijms25147850.
larvae (ADL) is an insect type that is used ethnopharmacologically to treat various diseases; however, its use as an antiaging treatment has not been widely studied. Previously, we found that an ethyl acetate (EA) fraction derived from an ADL extract (ADLE) has a high polyphenol content and antioxidant properties. In this study, we identified the underlying molecular mechanism for the protective effect of the EA fraction against UVB-induced photodamage in vitro and ex vivo. UVB treatment increased intracellular reactive oxygen species levels and DNA damage; the latter of which was significantly decreased following cotreatment with the EA fraction. Biological markers of aging, such as p16, p21, and senescence-associated β-gal levels, were induced by UVB treatment but significantly suppressed following EA-fraction treatment. UVB-induced upregulation of matrix metalloproteinase (MMP)-1 and downregulation of COL1A1 were also reversed by EA-fraction treatment in both cells and a 3D skin model, which resulted in increased keratin and collagen deposition. Moreover, EA-fraction treatment inhibited the phosphorylation of MAPKs (p38, ERK, and JNK) and nuclear factor (NF-)-kB and decreased the levels of inflammatory cytokines in UVB-treated cells. The results indicate that an EA fraction from ADLE ameliorates UVB-induced degradation of COL1A1 by inhibiting MMP expression and inactivating the MAPK/NF-κB p65/AP-1 signaling pathway involved in this process.
幼虫(ADL)是一种昆虫类型,被民族药理学用于治疗各种疾病;然而,其作为抗衰老治疗的用途尚未得到广泛研究。此前,我们发现 ADL 提取物(ADLE)的乙酸乙酯(EA)部分具有高多酚含量和抗氧化特性。在这项研究中,我们确定了 EA 部分对体外和离体 UVB 诱导光损伤的保护作用的潜在分子机制。UVB 处理会增加细胞内活性氧水平和 DNA 损伤;而在用 EA 部分共同处理后,后者显著减少。衰老的生物标志物,如 p16、p21 和衰老相关的 β-半乳糖苷酶水平,经 UVB 处理后诱导,但在用 EA 部分处理后显著抑制。EA 部分处理还可逆转 UVB 诱导的基质金属蛋白酶(MMP)-1 上调和 COL1A1 下调,在细胞和 3D 皮肤模型中均增加了角蛋白和胶原蛋白的沉积。此外,EA 部分处理抑制了 MAPKs(p38、ERK 和 JNK)和核因子(NF-)-kB 的磷酸化,并降低了 UVB 处理细胞中炎症细胞因子的水平。结果表明,ADLE 的 EA 部分通过抑制 MMP 表达和使参与该过程的 MAPK/NF-κB p65/AP-1 信号通路失活,改善了 COL1A1 的 UVB 诱导降解。