Aqueous extract of Phragmites commun is rhizomes attenuates phototoxicity in skin cells
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ORIGINAL ARTICLE
Aqueous extract of Phragmites communis rhizomes attenuates phototoxicity in skin cells Sung Hyeok Kim1 · Chang Woo Ha1 · Hyosun Lim2,4 · Sohee Jang1 · Seung Namkoong1 · Sungsil Hong1 · Youn Kyu Kim2 · Jae‑Young Kim4 · Sung Ryul Lee3 · Eun‑Hwa Sohn1 Accepted: 10 October 2020 © The Korean Society of Toxicogenomics and Toxicoproteomics 2020 2020
Abstract Background Excessive sunlight exposure leads to photodamaged skin, resulting in wrinkles, roughness, relaxation, and pigmentation. We examined photoprotective effects of aqueous extracts of dried Phragmites communis rhizome (PCWE) on ultraviolet B radiation (UVB)-mediated photodamage in skin cells. Methods Human dermal fibroblasts (HDFs), melanocytes (B16F10 cells), and keratinocytes (HaCaT cells) were treated with PCWE (25–200 μg/mL), with or without UVB (30 mJ/cm2). Cell viability, cell senescence, and mRNA levels of genes involved in skin homeostasis were assessed. Anti-melanogenic effects of PCWE on B16F10 cells were evaluated. Cyclooxygenase-2 (COX-2) mRNA levels and β-hexosaminidase release were evaluated in macrophage RAW264.7 and basophilic leukemia RBL-2H3 cells, respectively. Results No significant cytotoxicity was observed in tested cells up to 200 μg/mL PCWE. In HDFs and HaCaT cells, PCWE pretreatment afforded significant, concentration-dependent photoprotection. PCWE downregulated baseline matrix metalloprotease-1 expression and elastase activity in HDFs; in HaCaT cells, telomerase reverse transcriptase and hyaluronan synthase-2 expressions were upregulated. PCWE suppressed α-melanocyte-stimulating hormone-mediated increase in melanin production and tyrosinase activity. PCWE suppressed COX-2 induction (in RAW264.7) and β-hexosaminidase release (in RBL-2H3). Conclusion PCWE exhibits good potential to attenuate photodamage in skin cells. Keywords Extracellular matrix · Photoprotection · Phragmites communis · Photoaging · Skin · Ultraviolet B irradiation
Sung Hyeok Kim, Chang Woo Ha and Hyosun Lim contributed equally to this work. * Sung Ryul Lee [email protected]
Youn Kyu Kim [email protected]
* Eun‑Hwa Sohn [email protected]
Jae‑Young Kim [email protected]
Sung Hyeok Kim [email protected]
1
Chang Woo Ha [email protected]
College of Health Sciences, Kangwon National University, Samcheok 25949, Republic of Korea
2
Hyosun Lim [email protected]
Korea Research Institute BioScience Co., Ltd, Yeoju‑si 12668, Republic of Korea
3
Department of Convergence Biomedical Science, Cardiovascular and Metabolic Disease Center, College of Medicine, Inje University, Busan 47392, Republic of Korea
4
Graduate School of Analytical Science and Technology (GRAST), Chungnam National University, Daejeon 34134, Republic of Korea
Sohee Jang [email protected] Seung Namkoong [email protected] Sungsil Hong [email protected]
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Introduction Although sunlight improves our health by enhancing vitamin D production and a sense of well-being (Mead 2008), excessive exposure can cause skin
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