2. Academic Validation
  3. Sesamin attenuates UVA-induced keratinocyte injury via inhibiting ASK-1-JNK/p38 MAPK pathways

Sesamin attenuates UVA-induced keratinocyte injury via inhibiting ASK-1-JNK/p38 MAPK pathways

  • J Cosmet Dermatol. 2023 Aug 6. doi: 10.1111/jocd.15951.
Hailong Li 1,  Lijian Zhu 1,  Zhiwei Weng 1,  Hangjie Fu 1,  Jinyuan Liu 1,  Qingqing Mao 1,  Wenxia Li 2,  Bin Ding 1,  Yi Cao 3
Affiliations

Affiliations

  • 1 College of Life Science, Zhejiang Chinese Medical University, Hangzhou, China.
  • 2 The Fourth School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, China.
  • 3 The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.
PMID: 37545137 DOI: 10.1111/jocd.15951
Abstract

Background: Ultraviolet (UV) exposure-stimulated Reactive Oxygen Species (ROS) formation in keratinocytes is a crucial factor in skin aging. Phytochemicals have become widely popular for protecting the skin from UV-induced cell injury. Sesamin (SSM) has been shown to play a role in extensive pharmacological activity and exhibit photoprotective effects.

Aim: To assess the protective effect of SSM on UVA-irradiated keratinocytes and determine its potential antiphotoaging effect.

Methods: HaCaT keratinocytes pretreated with SSM were exposed to UVA radiation at 8 J/cm2 for 10 min. Cell viability and oxidative stress indicators were evaluated using a cell counting kit-8 and Lactate Dehydrogenase (LDH), malondialdehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD) assay kits. Apoptosis and intracellular ROS levels were analyzed using annexin V-fluorescein isothiocyanate/propyridine iodide and dichlorodihydrofluorescein diacetate staining, respectively. Protein levels of matrix metalloprotein-1 (MMP-1), MMP-9, Bax/Bcl-2, and mitogen-activated protein kinase (MAPK) pathway proteins, phospho-apoptosis signal-regulating kinase-1 (p-ASK-1)/ASK-1, phospho-c-Jun N-terminal protein kinase (p-JNK)/JNK, and p-p38/p38 were determined using western blotting.

Results: Sesamin showed no cytotoxicity until 160 μmol/L on human keratinocytes. Sesamin pretreatment (20 and 40 μM) reversed the suppressed cell viability, increased LDH release and MDA content, decreased cellular antioxidants GSH and SOD, and elevated intracellular ROS levels, which were induced by UVA irradiation. Additionally, SSM inhibited the expression of Bax, MMP-1, and MMP-9 and stimulated Bcl-2 expression. In terms of the regulatory mechanisms, we demonstrated that SSM inhibits the phosphorylation of ASK-1, JNK, and p38.

Conclusion: The results suggest that SSM attenuates UVA-induced keratinocyte injury by inhibiting the ASK-1-JNK/p38 MAPK pathways.

Keywords

ASK-1-JNK/p38 MAPK pathway; keratinocyte; oxidative stress; sesamin; ultraviolet exposure.

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