Laboratory analysis shows carvacrol improves cell viability and reduces apoptosis in A549 lung epithelial cells exposed to elastase, indicating potential COPD benefits.
Chronic obstructive pulmonary disease (COPD) represents a significant global health issue characterised by mechanisms such as inflammation, apoptosis, and oxidative stress. Carvacrol, a phenolic compound known for its antioxidant and anti-inflammatory effects, may mitigate damage caused by oxidative stress and apoptosis. This research aimed to explore the protective effects of carvacrol against elastase-induced apoptosis and oxidative stress in A549 lung epithelial cells. A549 cells were cultured and treated with elastase (60 mU/ml) along with varying concentrations of carvacrol (0.1, 0.2, and 0.4 mmol/L) for 24 hours. Cytotoxicity was evaluated using the MTT assay. Malondialdehyde (MDA) levels were measured as a marker of oxidative stress, while total antioxidant capacity (TAC) and the expression of apoptotic genes BAX and BCL2 were assessed via RT-PCR. Both H₂O₂ and elastase significantly reduced cell viability, increased MDA levels and BAX expression, and decreased TAC and BCL2 expression. Treatment with carvacrol in combination with elastase led to a dose-dependent increase in cell viability, a reduction in MDA levels and BAX expression, and an enhancement in TAC and BCL2 expression, with the strongest protective effect observed at 0.4 mmol/L. Pearson's correlation analysis revealed a positive correlation between TNF-α and BAX expression (r = 0.43, P = 0.002), a negative correlation between TNF-α and BCL2 expression (r = -0.62, P = 0.0031), and a negative correlation between BAX and BCL2 expression (r = -0.56, P = 0.007). Carvacrol demonstrated significant protective effects on pulmonary epithelial cells exposed to elastase-induced oxidative stress, reducing apoptosis and enhancing antioxidant capacity. While our in vitro results suggest potential mechanisms that could be targeted in COPD, we acknowledge that these findings are preliminary. Further studies involving in vivo models and clinical trials are essential to validate the therapeutic relevance of these observations.
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Hoseininejad et al. (2025) studied this question.
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