Phalaenopsis orchid flower extract attenuates high glucose-induced senescence via Nrf2/HO-1 activation and promotes wound healing in human dermal fibroblasts.

Jul 6, 2025Cellular and molecular biology (Noisy-le-Grand, France)

Orchid flower extract reduces high sugar-induced cell aging and helps wound healing by activating protective cell pathways in human skin cells

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Abstract

Fibroblasts treated with the water extract of Phalaenopsis orchid flower (WEPF) showed reduced senescence-associated β-galactosidase activity and lower ROS levels under high glucose conditions.

WEPF treatment was associated with decreased cell cycle arrest in fibroblasts exposed to high glucose.
The extract suppressed pathways linked to cellular senescence, including p53/p21Waf1 and p16INK4a/Rb.
Lower levels of matrix metalloproteinase-1 (MMP-1) were observed in WEPF-treated fibroblasts.
Activation of the Nrf2/HO-1 antioxidant pathway was identified as a mechanism for WEPF's protective effects.
Restoration of senescence marker protein-30 (SMP30) levels was noted, suggesting a role in fibroblast repair.

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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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