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由幼虫乙酸乙酯馏分预防 UVB 诱导的光老化及其对人真皮成纤维细胞的潜在机制。

Prevention of UVB-Induced Photoaging by an Ethyl Acetate Fraction from Larvae and Its Potential Mechanisms in Human Dermal Fibroblasts.

机构信息

Department of Food and Nutrition, Eulji University, Seongnam 13135, Republic of Korea.

College of Pharmacy, Mokpo National University, Mokpo 58554, Republic of Korea.

出版信息

Int J Mol Sci. 2024 Jul 18;25(14):7850. doi: 10.3390/ijms25147850.

Abstract

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.

摘要

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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f7/11277254/e2ecab2a2282/ijms-25-07850-g001.jpg

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