The ethyl acetate fraction ofSargassum muticumattenuates ultraviolet B radiation-induced apoptotic cell death via regulation of MAPK- and caspase-dependent signaling pathways in human HaCaT keratinocytes
| Autor: | Hee Kyoung Kang, Young Sang Koh, Mi Hee Ko, Eun Sook Yoo, Sun Jin Boo, Weon Jong Yoon, Jin Won Hyun, Ji Won Cha, Nam Ho Lee, Jian Zheng, Cheng Wen Yao, Ki Cheon Kim, Mei Jing Piao |
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| Rok vydání: | 2014 |
| Předmět: |
Keratinocytes
MAPK/ERK pathway Cell Survival MAP Kinase Signaling System Ultraviolet Rays Cell Pharmaceutical Science Apoptosis DNA Fragmentation Acetates Biology Cell Line Drug Discovery medicine Humans Viability assay Phosphorylation Fragmentation (cell biology) Pharmacology Microscopy Confocal integumentary system Caspase 3 Plant Extracts Sargassum General Medicine Flow Cytometry Apoptotic body Caspase 9 Cell biology HaCaT medicine.anatomical_structure Complementary and alternative medicine Molecular Medicine DNA fragmentation Signal Transduction |
| Zdroj: | Pharmaceutical Biology. 52:1110-1118 |
| ISSN: | 1744-5116 1388-0209 |
| Popis: | Our previous work demonstrated that an ethyl acetate extract derived from Sargassum muticum (Yendo) Fenshol (SME) protected human HaCaT keratinocytes against ultraviolet B (UVB)-induced oxidative stress by increasing antioxidant activity in the cells, thereby inhibiting apoptosis.The aim of the current study was to further elucidate the anti-apoptotic mechanism of SME against UVB-induced cell damage.The expression levels of several apoptotic-associated and mitogen-activated kinase (MAPK) signaling proteins were determined by western blot analysis of UVB-irradiated HaCaT cells with or without prior SME treatment. In addition, the loss of mitochondrial membrane potential (Δψm) was detected using flow cytometry or confocal microscopy and the mitochondria membrane-permeate dye, JC-1. Apoptosis was assessed by quantifying DNA fragmentation and apoptotic body formation. Furthermore, cell viability was evaluated using the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay.SME absorbed electromagnetic radiation in the UVB range (280-320 nm) of the UV/visible light spectrum. SME also increased Bcl-2 and Mcl-1 expression in UVB-irradiated cells and decreased the Bax expression. Moreover, SME inhibited the UVB-induced disruption of mitochondrial membrane potential and prevented UVB-mediated increases in activated caspase-9 and caspase-3 (an apoptotic initiator and executor, respectively) levels. Notably, treatment with a pan-caspase inhibitor enhanced the anti-apoptotic effects of SME in UVB-irradiated cells. Finally, SME reduced the UVB-mediated phosphorylation of p38 MAPK and JNK, and prevented the UVB-mediated dephosphorylation of Erk1/2 and Akt.The present results indicate that SME safeguards HaCaT keratinocytes from UVB-mediated apoptosis by inhibiting a caspase-dependent signaling pathway. |
| Databáze: | OpenAIRE |
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