Protective Effect of Iris germanica L. Rhizome-Derived Exosome against Oxidative-Stress-Induced Cellular Senescence in Human Epidermal Keratinocytes
Plant-derived exosomes can exert therapeutic effects against various dermatological conditions. Several studies have demonstrated that plant-derived exosomes can have positive effects on the skin, preventing aging, hyperpigmentation, and hair loss. In this study, the protective effects of Iris germa...
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Published in | Applied sciences Vol. 13; no. 21; p. 11681 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Basel
MDPI AG
01.11.2023
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Subjects | |
Online Access | Get full text |
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Summary: | Plant-derived exosomes can exert therapeutic effects against various dermatological conditions. Several studies have demonstrated that plant-derived exosomes can have positive effects on the skin, preventing aging, hyperpigmentation, and hair loss. In this study, the protective effects of Iris germanica L. rhizome-derived exosomes (Iris-exosomes) on oxidative-stress-induced cellular dysfunction were investigated in human epidermal keratinocytes (nHEKs). Iris-exosomes with a diameter range of 100–300 nm were detected. In the cytotoxicity assay, Iris-exosomes with up to 107 particles per milliliter were found to possess no cytotoxicity, and we recovered H2O2-induced cell viability loss. In nHEKs, H2O2-induced ROS levels were significantly reduced using Iris-exosomes and additionally associated with increases in antioxidant enzyme transcription. The H2O2-induced SA-β-gal-positive nHEKs were decreased using Iris-exosomes; these effects correlate with the changed levels of cell cycle arrest marker p21. Furthermore, the H2O2-induced loss of in vitro wound-healing properties and early detection of keratin 1 and 10—keratinization markers—were restored to control levels using Iris-exosomes. Altogether, these results indicate the possibility that Iris-exosomes exert antioxidant and anti-senescence effects in order to protect against oxidative-stress-induced cellular dysfunction in nHEKs. |
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ISSN: | 2076-3417 2076-3417 |
DOI: | 10.3390/app132111681 |