Exosome-like nanovesicles derived from Phellinus linteus inhibit Mical2 expression through cross-kingdom regulation and inhibit ultraviolet-induced skin aging.

Autor: Han, Jingxia, Wu, Ting, Jin, Jing, Li, Zhiyang, Cheng, Wenjun, Dai, Xintong, Yang, Kai, Zhang, Heng, Zhang, Zhiyuan, Zhang, Haohao, Fan, Rong, Zheng, Shaoting, Liu, Haoyang, Li, Yinan, Zhao, Huan, Yao, Cheng, Lin, Tingting, Zhu, Caibin, Liu, Huijuan
Předmět:
Zdroj: Journal of Nanobiotechnology; 10/21/2022, Vol. 20 Issue 1, p1-16, 16p
Abstrakt: Background: Phellinus linteus (PL), which is a typical medicinal fungus, has been shown to have antitumor and anti-inflammatory activities. However, studies on the effect of anti-photoaging are limited. Studies have shown that exosome-like nanovesicles are functional components of many medicinal plants, and miRNAs in exosome-like nanovesicles play a cross-kingdom regulatory role. At present, research on fungi exosome-like nanovesicles (FELNVs) is few. Results: We systematically evaluated the anti-aging effects of PL. FELNVs of PL were isolated, and the functional molecular mechanisms were evaluated. The results of volunteer testing showed that PL had anti-aging activity. The results of component analysis showed that FELNVs were the important components of PL function. FELNVs are nanoparticles (100–260 nm) with a double shell structure. Molecular mechanism research results showed that miR-CM1 in FELNVs could inhibit Mical2 expression in HaCaT cells through cross-kingdom regulation, thereby promoting COL1A2 expression; inhibiting MMP1 expression in skin cells; decreasing the levels of ROS, MDA, and SA-β-Gal; and increasing SOD activity induced by ultraviolet (UV) rays. The above results indicated that miR-CM1 derived from PL inhibited the expression of Mical2 through cross-kingdom regulation and inhibited UV-induced skin aging. Conclusion: miR-CM1 plays an anti-aging role by inhibiting the expression of Mical2 in human skin cells through cross-species regulation. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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