Skin-protective and anti-inflammatory effects of Hibiscus syriacus L. (Mugunghwa): A comparative study of five parts of the plant
Eunson Hwang, Tae‐Hoo Yi, Jung-Eun Yang, SulWoong Park, HienT T. Ngo, Seul-A Seo, EunByeol Go, Jeong-Seung Hwang
Abstract
Aim: The skin barrier is vulnerable to internal and external elements. However, certain plant extracts have promise for protecting the skin. Hibiscus syriacus L. is a Korean national plant (mugunghwa) that has been traditionally used to treat some skin diseases; however, its pharmacological activities are poorly understood. The present study has evaluated the skin-protective effect of mugunghwa flowers (MF), cortexes (MC), roots (MR), leaves (ML), and seeds (MS) in external factor-stimulated human epidermal keratinocytes (HaCaTs), normal human dermal fibroblasts (NHDFs), and a widely used murine macrophage cell line (RAW 264.7 cells). Materials and Methods and Results: The active components were identified as palmitic acid and linoleic acid by high-performance liquid chromatography analysis. The parts of mugunghwa had low 2,2-diphenyl-1-picrylhydrazyl scavenging activities but moderate 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt scavenging capacity. All parts' extracts at 100 μg/mL decreased nitric oxide production in inflammation-induced RAW 264.7 cells and mRNA expression of the cytokines interleukin-6/1β and the enzymes inducible nitric oxide synthase/cyclooxygenase-2. On HaCaTs, MF, MC, and MR (10–50 μg/mL) significantly increased hyaluronan production over that of controls. Moreover, MF activated NAD (P) H:quinone oxidoreductase 1 and heme oxygenase-1 and inhibited intracellular reactive oxygen species production. Treatment with MF, MC, MR, ML, and MS (10 μg/mL) reduced the scratching wound site in NHDFs to be considered by vascular endothelial growth factor signaling activation. Conclusion: Taken together, among all the five parts of the mugunghwa plant, MF effectively inhibited lipopolysaccharide, ultraviolet B irradiation, and scratching wound-induced inflammation in skin cells.