Lawsone modulates oxidative stress, apoptosis, and enhances growth factor expression in human dermal fibroblasts under hyperglycemic conditions
摘要
Delayed wound healing is a serious issue in diabetes, which is driven by metabolic and non-metabolic factors. Dysfunction and decreased lifespan of fibroblast cells play a key role in this condition. Lawsone (2-hydroxy-1,4-naphthoquinone), the main active component of Lawsonia inermis, is well known for its anticancer and regenerative effects, although these effects vary depending on concentration and experimental conditions. Regarding the importance of Diabetic wound treatment, this study examines how lawsone affects fibroblast behavior under high-glucose conditions, focusing on cell viability, apoptosis, intracellular Reactive Oxygen Species (ROS) levels, migration, and the expression of repair-related genes Nerve Growth Factor (NGF) and Transforming Growth Factor-beta (TGF-β).
MethodsHuman dermal fibroblasts were cultured under high-glucose (85–140mM) conditions, in the presence or absence of lawsone (10µg/mL). The MTT assay assessed cell viability, migration by the scratch assay, apoptosis by Annexin V- Fluorescein Isothiocyanate/Propidium Iodide (FITC/PI) flow cytometry, and ROS levels by 2’,7’-dichlorodihydrofluorescein diacetate (H₂DCFDA) staining. quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) was used to quantify NGF and TGF-β mRNA expression.
ResultsHigh glucose significantly impaired fibroblast viability and migration, increased apoptosis and ROS production, and downregulated TGF-β expression. Co-treatment with lawsone markedly restored cell viability and migration, suppressed oxidative stress and apoptosis, and enhanced NGF and TGF-β transcription, indicating reactivation of reparative pathways (p ≤ 0.05).
ConclusionLawsone exhibits potent cytoprotective and pro-regenerative effects in human dermal fibroblasts under hyperglycemic stress, independent of its known anticancer activity. These findings highlight lawsone as a natural candidate for promoting diabetic wound healing and warrant further mechanistic and in vivo investigations.