| Summary: | Chronic respiratory diseases are a leading cause of lung-related death worldwide. The vital factors causing lung pathogenesis include consistent exposure to tobacco smoke, air pollution, and occupational risks. Regarding the significant morbidity and mortality linked to lung pathogenesis, there are neither conclusive treatments nor wholly preventive strategies. In the present study, the protective mechanism of Ajwa date extract (ADE), on Benzopyrene [B(a)P]-induced lung injury in animal models was investigated using antioxidant, lipid peroxidation, anti-inflammatory activities, angiogenesis, histopathological studies, and apoptosis assays. B(a)P treatment significantly decreased the level of antioxidant enzymes such as catalase (Cat) (13.4 vs. 24.7 U/mg protein), Superoxide dismutase (SOD) (38.5 vs. 65.7 U/mg protein), Glutathione peroxidase (<i>GPx</i>) (42.4 vs. 57.3 U/mg protein) and total antioxidant capacity (TAC) (49.8 vs. 98.7 nM) as compared to the treatment group (<i>p</i> < 0.05). B(a)P treatment led to increased expression of pro-inflammatory markers such as TNF-α (88.5 vs. 72.6 pg/mL), IFN-γ (4.86 vs. 3.56 pg/mL), interleukin-6 (IL-6) (109.6 vs. 85.4 pg/mL) and CRP (1.84 vs. 0.94 ng/mL) as compared to the treatment group (<i>p</i> < 0.05). The data shows a significant increase in lipid peroxidation and angiogenesis factors such as vascular endothelial growth factor (VEGF) by B(a)P treatment (<i>p</i> < 0.05). However, ADE treatment showed an improvement of these factors. In addition, ADE treatment significantly ameliorated histopathological changes, collagen fiber deposition, and expression pattern of VEGF and Bax proteins. Furthermore, the flow cytometry data demonstrated that B(a)P intoxication enhanced the apoptosis ratio, which was significantly improved with ADE treatment. Finally, we may infer that Phyto-constituents of ADE have the potential to protect against B(a)P-induced lung pathogenesis. Therefore, Ajwa dates might be used to develop a possible potent alternative therapy for lung pathogenesis.
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