## 4 Discussion
Furthermore, another study based on liver cancer reported that ADE-treated group showed increase in the activity of antioxidant enzymes as compared to the DEN-treated group [44]. B(a)P treatment administered to the animals causes lung injury and other types of changes, confirmed by pathological changes: intra-alveolar hemorrhage, collagen fiber deposition, inflammatory cell infiltration, and edema, which were measured to show an important role in the lung injury [10; 45; 46]. In the current study, it was observed that B(a)P treatment causes lung injury, and various other pathological alterations, although co-administered ADE and B(a)P treatment showed a role in the maintenance of lung architecture. This result was in agreement with previous reports, as B(a)P caused lung injury, necrosis, alteration in epithelium lung architecture [47], and lung epithelium thickening as well as a mass infiltration of inflammatory cells [48]. The current finding is consistent with the earlier findings that reported that ADE showed a role in the histoarchitecture maintenance [49] and ADE treatment reduced edema, necrosis, and inflammatory cells infiltration and reestablished the cardiomyocytes architecture [50]. The tumor suppressor protein p53 causes cell cycle arrest and induces apoptosis in lung injury. Though p53 modulates apoptosis through complex and partly understood mechanisms, one recognized pathway includes activating the mitochondria-regulated death pathway via increasing gene expression of proapoptotic stimuli while decreasing the expression of antiapoptosis [51; 52; 53; 54; 55]. Immunohistochemistry findings established that Bax and VEGF levels and TUNEL staining were upregulated in the B(a)P-caused toxicity in rats, which decreased after treatment with ADE. An earlier study reported that the level of activated p53 was significantly influenced by B(a)P treatment, while this effect was noticeably decreased after curcumin and VE co-treatment. Moreover, the ratio of Bax/Bcl-2 was also considerably increased in cells exposed to B(a)P and this increase was reversed by VE co-treatment [56]. Activated Bax was significantly expressed in the lung tissues in the bleomycin-treated group and was attenuated by BIP-V5 treatment [57]. Moreover, TEM results also showed various changes as numerous swollen mitochondria, alveolar space, alveolar constriction, granular cytoplasm, and degenerative necrotic nucleated cells in the B(a)P-induced lung-injury group, which was improved in the ADE treatment group. There are several anti-inflammatory allopathic drugs that are being currently used to treat lung pathogenesis. These drugs are effective but also cause negative side effects on health. A safe and affordable alternative to allopathic medications has been found to be the use of medicinal plants to treat and manage diseases in various traditional medical systems. Ajwa dates play a vital role in health management by boosting the functions of the immune system, scavenging of reactive oxygen species, and anti-microbial activity. The overall outcome of this study demonstrated the role of Ajwa dates in the management of lung pathogenesis through antioxidant and anti-inflammatory activity. It also maintains lung tissue architecture as is evident by the decrease in the inflammatory cells, hemorrhages, congestion, and fibrosis. In addition, Ajwa date treatment significantly ameliorates collagen fiber deposition and expression pattern of VEGF and Bax proteins. In addition, it also modulates various biological activities including lipid peroxidation, angiogenesis, and apoptotic pathways. Our study, for the first time, investigated the health benefit effects of Ajwa date against lung pathogenesis and associated complications under in vivo conditions. Therefore, current investigations on Ajwa date might act as a path towards developing a potent alternative therapy against respiratory diseases, especially chronic lung diseases, in the future.