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 inApplied sciences Vol. 13; no. 21; p. 11681
Main Authors Kim, Ji-Seon, Lee, Hyun-Jeong, Yoon, Eun-Jeong, Lee, Hyunsang, Ji, Youngeun, Kim, Youngseok, Park, Si-Jun, Kim, Junoh, Bae, Seunghee
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 01.11.2023
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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.
ISSN:2076-3417
2076-3417
DOI:10.3390/app132111681