## 4 Discussion  
To better understand the link between lung injury and inflammation, the lung injury rats models were developed by using benzopyrene (B(a)P). Benzopyrene is a potent carcinogen and plays a significant role in the initiation of lung injury and the development and progression of cancer. Plant-based phenolic compounds have demonstrated a significant role in cancer management, chiefly by controlling reactive oxygen species (ROS) level [37; 38]. In the current study, it was found that a significant increase in serum lactate dehydrogenase (LDH) occurs in rats by the intoxication of B(a)P as compared to that of control rats, whereas the Qu pre-treatment significantly reduced the levels of serum lactate dehydrogenase compared with the B(a)P group. One study reported that the B(a)P-treated group showed a significant increase in serum LDH when compared to the control group. Carvacrol pretreatment significantly decreased toward the normal [39]. Another study has reported that B(a)P increases the level of LDH in lung injury animal models, whereas glycyrrhizic acid shows a protective role through the suppression of LDH level [12] and B(a)P causes liver pathogenesis [40]  
Another study based on mice models reported that B(a)P increases the level of MDA [41]. In addition, a notable increase in LDH activity and MDA level was observed after B(a)P treatment, which was reduced with naringenin treatment recommending its protective role on lung epithelium cells [42]. It was reported that inflammation, due to the expression of inflammatory cytochemokines such as interleukin (IL)-6 and tumor necrosis factor-alpha (TNF)-\(\alpha\)), shows a significant role in lung injury onset [43; 44]. Furthermore, the development of lung inflammation is matched by the activation, expression, and secretion of several pro-inflammatory mediators from the lung parenchyma and vascular cells such as cytokines, leukotriene, and adhesion molecules [45]. It was noticed that Qu meaningfully decreased the levels of inflammatory markers, which certainly improved the inflammation in lung injury caused by B(a)P and might be the reason for Qu regulating the production of IL-\(\beta\), IL-6 and TNF-\(\alpha\) and preventing the formation of lung pathogenesis. It has been reported that lipopolysaccharideaccharide increases the inflammatory markers, which are counteracted by the quercetin pretreatment [46]. TNF-\(\alpha\), IL-\(\beta\) and IL-6 levels was high in the B(a)P-only treatment group animals in comparison to the control group. Whereas the pre-treatment with quercetin importantly decreased such inflammatory markers in comparison to the disease control group. Some previous studies have also demonstrated that inflammatory marker is enhanced in the B(a)P group. Moreover, it was observed that a B(a)P plus curcumin treatment significantly lowers the inflammatory cytokines such as TNF-\(\alpha\), IL-6 and C-reactive protein (CRP) levels [47]. Another finding revealed that B(a)P administration raises the levels of lung injury markers. Naringenin treatment attenuated the levels of oxidative stress by restoring antioxidant enzymes and significantly decreases the inflammatory responses. Meanwhile, naringenin excellently decreased the expression of NF-\(\kappa\)B and COX-2 induced by B(a)P intoxication [42]. In the present study, it was observed that B(a)P treatment significantly decreased the antioxidant enzymes levels as compared to control group. Pre-treatment with Qu significantly increased the antioxidant enzyme level compared with the B(a)P treatment. Moreover, B(a)P treatment rats showed a significant increase in lung MDA levels as compared to the control group. Treatment with Qu significantly decreased MDA levels in the lung injury rats. The current finding was in accordance with previous finding that reported a decrease in the level of antioxidant enzymes after B(a)P treatment [48]. In addition, another study demonstrated that B(a)P treatment causes a decrease in antioxidant proteins.