## 4 Discussion
Whereas, the treatment with diosmin restored the antioxidant status significantly [49]. In the current study, compared with the control group, B(a)P treatment showed that VEGF levels were significantly higher (\(p<0.05\)). Compared with the B(a)P group, the Qureated group showed significantly lower (\(p<0.05\)) VEGF levels. A previous study reported that a significant increase in the VEGF level in B(a)P group compared with control group,while the C. ignea treatment group showed lower levels [50]. Another study reported that the VEGF level was high in the B(a)P-treated group [29]. VEGF-induced tube formation of RF/6A cells and its migration importantly inhibited by quercetin in a dose-dependent manner [51]. The lung sections of control animals showed a normal architecture of cells with small uniform nuclei. Benzopyrene-treated animal lung tissue shows loss of architecture with infiltration of inflammatory cells, hemorrhages and congestion. However, these changes were observed to be significantly fewer as mild inflammatory cell intrude in the Qu pretreatment group, and this demonstrates that Qu protects the lung against B(a)P damage. The previous results demonstrate that B(a)P administration caused severe destruction of the alveolar architecture and necrosis of the alveolar epithelium [13]. Similarly, other findings reported that histological sections of the control group showed normal lung tissue architecture. The B(a)P-treated group shows destruction of the alveolar architecture, and diosmin protects the lung against B(a)P damage [49]. The B(a)P administration in rats cause various types of changes in the tissue as thickening of the lung epithelium, alveolar architecture damage and increased infiltration of inflammatory cells. Moreover, the other changes such as congestion, fibrosis and hemorrhage have also been noticed in B(a)P-treated groups [52]. The ultrastructural changes observed that the B(a)P-treated group exhibited various types of alterations. The B(a)P-intoxicated rats treated with Qu displayed less changes or normal organelles structures. It was noticed that B(a)P induced severe collagen deposition in lung tissues, thus indicating an interstitial fibrosis as compared with the control. Whereas the control group and Qu-treated rats showed normal collagen distribution. However, this finding advocates that Qu plays an important role in the inhibition of fibrosis. A previous study described that lung cancer bearing animals induced by B(a)P showed increased collagen deposition. Pretreatment with Capsaicin markedly reduced collagen accumulation, thereby preserving the near-normal architecture [53]. In the B(a)P-treated group, various types of alterations were seen such as the formation of a damaged discontinuous layer of squamous alveolar cells cytoplasm. The fused basal laminae are interrupted and the cytoplasm of the capillary endothelium is swollen, ruptured, multinucleated and the lung shows compression of the interalveolar spaces which appears as clerts. B(a)P-intoxicated rats treated with Qu displayed less or normal organelles structures. The B(a)P-treated group showed high cytoplasmic expression of COX-2 protein, whereas Qu treatment significantly decrease the COX-2 protein expression. Previous study based on benzopyrene reported that B(a)P-treated lung cell stained positive by antibodies against COX-2. Moreover, Rutin pretreatment significantly reduced expression in a dose-dependent manner [54]. Another study has demonstrated that significantly increased expression of proinflammatory markers (NF-\(\kappa\)B, IL-6 and COX-2) in B(a)P-treated mice as compared to vehicle-treated mice [49]. In addition, some other studies reported that COX-2 protein distribution was upregulated LPS administration; this was mainly in neutrophils, alveolar macrophages and alveolar epithelial type II cells. However, pretreatment with quercetin efficiently prevented the increase of COX-2 [55]. B(a)P significantly enhances the expressional pattern of NF-kB, COX-2 and IL-6.