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Copyright (c) 2025 Shu-Ling Peng, Chiung-Man Tsai, CHIA JUI WENG, Shun-Fa Yang
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Phalaenopsis orchid flower extract attenuates high glucose-induced senescence via Nrf2/HO-1 activation and promotes wound healing in human dermal fibroblasts
Corresponding Author(s) : Chia-Jui Weng
Cellular and Molecular Biology,
Vol. 71 No. 6: Issue 6
Abstract
Skin aging in diabetic patients is closely associated with delayed wound healing and oxidative stress-mediated fibroblast dysfunction. This study investigated the protective and regenerative effects of a water extract of Phalaenopsis orchid flower (WEPF), an ornamental plant endemic to Taiwan, on high glucose (HG)-induced cellular senescence in human dermal fibroblasts (CCD-966SK), with a focus on the Nrf2/HO-1 antioxidant pathway. Cytotoxicity, cellular senescence, and ROS production were respectively assessed using MTT assay, senescence-associated β-galactosidase (SA-β-gal) staining, and DCFDA-cellular reactive oxygen species assay. Western blotting and ELISA were used to analyze the cellular senescence-related proteins. Fibroblasts treated with WEPF under HG conditions exhibited reduced senescence-associated β-galactosidase (SA-β-gal) activity, lower ROS levels, and attenuated cell cycle arrest. Protein expression profiling revealed suppression of the p53/p21Waf1, and p16INK4a/Rb pathways and decreased matrix metalloproteinase-1 (MMP-1) expression. Mechanistically, WEPF exerted its effects by activating the Nrf2/HO-1 axis and restoring the expression of senescence marker protein-30 (SMP30), thereby promoting fibroblast repair and reducing pro-inflammatory signaling. These findings support the potential of WEPF as a botanical therapeutic agent for diabetic wound healing and age-related skin deterioration.
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