Mawalle Kankanamge Hasitha Madhawa Dias1, Dissanayaka Mudiyanselage Dinesh Madusanka2, Eui Jeong Han3, Hyun-Soo Kim4, You-Jin Jeon5, Youngheun Jee6, Kil-Nam Kim7, Kyounghoon Lee8, Ilekuttige Priyan Shanura Fernando9, Ginnae Ahn10. 1. Department of Food Technology and Nutrition, Chonnam National University, Yeosu, 59626, Republic of Korea. Electronic address: hasithadiasm17636@gmail.com. 2. Department of Food Technology and Nutrition, Chonnam National University, Yeosu, 59626, Republic of Korea. Electronic address: dmdmadusanka88@gmail.com. 3. Department of Food Technology and Nutrition, Chonnam National University, Yeosu, 59626, Republic of Korea. Electronic address: iosu5772@naver.com. 4. National Marine Biodiversity Institute of Korea, 75, Jangsan-ro 101 gil, Janghang-eup, Seocheon, 33662, Republic of Korea. Electronic address: gustn783@mabik.re.kr. 5. Department of Marine Life Science, School of Marine Biomedical Sciences, Jeju National University, Jeju, 63243, Republic of Korea; Marine Science Institute, Jeju National University, Jeju Self-Governing Province, 63333, Republic of Korea. Electronic address: youjinj@jejunu.ac.kr. 6. Department of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University, Jeju, 63243, Republic of Korea; Interdisciplinary Graduate Program in Advanced Convergence Technology & Science, Jeju National University, Jeju, 63243, Republic of Korea. Electronic address: yhjee@jejunu.ac.kr. 7. Chuncheon Center, Korea Basic Science Institute (KBSI), Chuncheon, 24341, Republic of Korea. Electronic address: knkim@kbsi.re.kr. 8. Division of Fisheries Science, Chonnam National University, Yeosu, 59626, Republic of Korea. Electronic address: khlee71@jnu.ac.kr. 9. Department of Marine Bio-Food Sciences, Chonnam National University, Yeosu, 59626, Republic of Korea. Electronic address: shanurabru@gmail.com. 10. Department of Food Technology and Nutrition, Chonnam National University, Yeosu, 59626, Republic of Korea; Department of Marine Bio-Food Sciences, Chonnam National University, Yeosu, 59626, Republic of Korea. Electronic address: gnahn@jnu.ac.kr.
Abstract
ETHNOPHARMACOLOGICAL RELEVANCE: Sargassum horneri (Turner) C. Agardh is well known in East Asia as an edible brown alga rich in bioactive compounds. It has an ethnopharmacological significance in traditional Chinese medicine to treat inflammatory disorders varying from edema, furuncles, dysuria to cardiovascular diseases. AIM OF THE STUDY: Surge of fine dust (FD), in densely populated areas, have been reported to cause adverse health conditions ranging from respiratory diseases to inflammatory skin disorders. The current study investigates the protective effects of an ethanol extract from S. horneri (SHE) on FD-induced inflammatory responses and impaired skin hydration in HaCaT keratinocytes. MATERIALS AND METHODS: Intracellular reactive oxygen species (ROS) generation was evaluated with the 2',7'-Dichlorofluorescin diacetate (DCFH-DA) stain. Anti-inflammatory properties of SHE in FD-stimulated HaCaT keratinocytes were investigated for the suppression of nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK) pathways and downregulation of pro-inflammatory cytokines. As a means of studying FD-induced skin barrier disruption and the effects of SHE on stratum corneum hydration-controlling factors, tight junction regulatory mediators, and hyaluronic acid (HA) production were evaluated using keratinocytes. RESULTS: SHE suppressed the intracellular ROS production, simultaneously improving cell viability in FD-stimulated keratinocytes. Also, SHE upregulated anti-inflammatory cytokine interleukin (IL)-4 while downregulating inflammatory cytokines IL-1β, IL-6, IL-8, tumor necrosis factor (TNF)-α; epidermal and epithelial cytokines IL-25, IL-33, and thymic stromal lymphopoietin (TSLP); thymus and activation-regulated chemokine (TARC), macrophage-derived chemokine (MDC) and regulated upon activation, normally T-expressed, and presumably secreted expression and suppressed (RANTES) chemokine, MAPK and NF-κB mediators in a dose-dependent manner. Furthermore, SHE ameliorated filaggrin, involucrin, lymphoepithelial Kazal-type-related inhibitor (LEKTI), signifying its beneficial effects on deteriorated skin hydration caused by FD-induced inflammation. SHE further exhibited its skin protective effects regulating the tight junction proteins; Occludin, zonula occludens (ZO)-1, claudin-1, claudin-4, claudin-7, and claudin-23 while increasing the production of HA minimizing skin damage. CONCLUSIONS: Anti-inflammatory effects of, SHE against FD-induced keratinocyte inflammation is attributable to the suppression of upstream MAPK and NF-κB mediators. SHE indicated potential anti-inflammatory properties attenuating deteriorated skin barrier function in HaCaT keratinocytes. The effects are attributable to the polyphenols and other antioxidant compounds in SHE. Further studies could envisage the use of SHE for developing rejuvenating cosmetics.
ETHNOPHARMACOLOGICAL RELEVANCE: Sargassum horneri (Turner) C. Agardh is well known in East Asia as an edible brown alga rich in bioactive compounds. It has an ethnopharmacological significance in traditional Chinese medicine to treat inflammatory disorders varying from edema, furuncles, dysuria to cardiovascular diseases. AIM OF THE STUDY: Surge of fine dust (FD), in densely populated areas, have been reported to cause adverse health conditions ranging from respiratory diseases to inflammatory skin disorders. The current study investigates the protective effects of an ethanol extract from S. horneri (SHE) on FD-induced inflammatory responses and impaired skin hydration in HaCaT keratinocytes. MATERIALS AND METHODS: Intracellular reactive oxygen species (ROS) generation was evaluated with the 2',7'-Dichlorofluorescin diacetate (DCFH-DA) stain. Anti-inflammatory properties of SHE in FD-stimulated HaCaT keratinocytes were investigated for the suppression of nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK) pathways and downregulation of pro-inflammatory cytokines. As a means of studying FD-induced skin barrier disruption and the effects of SHE on stratum corneum hydration-controlling factors, tight junction regulatory mediators, and hyaluronic acid (HA) production were evaluated using keratinocytes. RESULTS:SHE suppressed the intracellular ROS production, simultaneously improving cell viability in FD-stimulated keratinocytes. Also, SHE upregulated anti-inflammatory cytokine interleukin (IL)-4 while downregulating inflammatory cytokines IL-1β, IL-6, IL-8, tumor necrosis factor (TNF)-α; epidermal and epithelial cytokines IL-25, IL-33, and thymic stromal lymphopoietin (TSLP); thymus and activation-regulated chemokine (TARC), macrophage-derived chemokine (MDC) and regulated upon activation, normally T-expressed, and presumably secreted expression and suppressed (RANTES) chemokine, MAPK and NF-κB mediators in a dose-dependent manner. Furthermore, SHE ameliorated filaggrin, involucrin, lymphoepithelial Kazal-type-related inhibitor (LEKTI), signifying its beneficial effects on deteriorated skin hydration caused by FD-induced inflammation. SHE further exhibited its skin protective effects regulating the tight junction proteins; Occludin, zonula occludens (ZO)-1, claudin-1, claudin-4, claudin-7, and claudin-23 while increasing the production of HA minimizing skin damage. CONCLUSIONS: Anti-inflammatory effects of, SHE against FD-induced keratinocyte inflammation is attributable to the suppression of upstream MAPK and NF-κB mediators. SHE indicated potential anti-inflammatory properties attenuating deteriorated skin barrier function in HaCaT keratinocytes. The effects are attributable to the polyphenols and other antioxidant compounds in SHE. Further studies could envisage the use of SHE for developing rejuvenating cosmetics.