## 4 Discussion
Exaggerated inflammation is generally demonstrated as triggering apoptosis, which plays a serious role in the pathological events of inflammatory diseases [40]. The infiltration of inflammatory cells and their accumulation within the alveolar cavity contribute to the apoptosis and necrosis of pulmonary cells [41; 42]. Apoptosis is regarded as a major reason for lung injury, and its inhibition demonstrates a reduction in ARDS morbidity [43]. The anti-apoptotic effects were evaluated by TUNEL assay, and the results demonstrated that PGD\({}_{2}\) treatment alleviates lung cell apoptosis in vivo. The substantial decrease in apoptosis was also supported by flow cytometry. Previous studies have reported the antifibrotic role of PGE\({}_{2}\), while PGF\({}_{2\alpha}\) acts as a pulmonary fibrosis mediator [44]. In the current study, the anti-inflammatory role of PGD\({}_{2}\) was demonstrated in mice. The disease control mice showed enhanced inflammation, denoted by the enhanced expression of inflammatory mediators, followed by neutrophil infiltration. Although the disease-stage-dependent role of PGD\({}_{2}\) needs to be examined in more depth, as PGD\({}_{2}\) has been stated to improve bleomycin-induced fibrosis, partially by suppressing early inflammatory response. In parallel, it has been demonstrated that inflammasome signals suppress lung inflammation, followed by reduced fibrosis [45]. PGD\({}_{2}\) locally produced within neutrophils and monocytes may also suppress the infiltration of immune cells [19]. PGD\({}_{2}\) from the resident lung cells is accountable for anti-inflammatory responses, including the suppression of vascular permeability in acute lung injury [19]. Besides its anti-inflammatory role, PGD\({}_{2}\) might have a direct role on fibroblasts as it attenuates collagen secretion induced by TGF-\(\beta\) in human lung fibroblasts by activating the D-proteinoid receptor [46]. The role of PGD\({}_{2}\) in the inhibition of proliferation of mouse lung fibroblasts through the D-prostaglandin receptor has also been reported [47]. It was further confirmed that PGD\({}_{2}\) has no role in apoptosis as assessed by TUNEL assay [48]. Thus, the anti-inflammatory and antifibrotic roles of PGD\({}_{2}\) signify that it is a potential therapeutic option. In this regard, the protective role of PGD\({}_{2}\) in anti-inflammatory action and bleomycin-induced pulmonary fibrosis has been previously verified [48]. In the current study, it was observed that LPS treatment of the mice induced lung injury and various other pathological alterations although the co-administered PGD\({}_{2}\) and LPS treatment showed a role in the maintenance of lung architecture. These results were in agreement with previous reports that LPS induction in mice causes various types of pathological changes in the lung tissues, such as inflammatory cell infiltration, congestion and oedema [18; 49]. The expression of iNOS is elevated during the inflammatory insults. The IHC staining for iNOS in different animal groups demonstrated that LPS-intoxication significantly enhances iNOS expression. However, PGD\({}_{2}\) pretreatment significantly reduces the expression of iNOS. These observations are in agreement with a previous study, which demonstrates that continental acid treatment to LPS-intoxicated mice shows decreased iNOS expression [18]. Furthermore, the role of PGs in disease management should be investigated in more depth. The temporal and spatial variations of each PG synthase expression that elucidate their roles is highly significant. The overall significance of this study is briefly described here, as there are very few studies demonstrating the mechanism of LPS and the protective role of PGD\({}_{2}\) in lung pathogenesis. Thus, in this study, we tried to find the possible mechanism of PGD\({}_{2}\) in lung protection through the modulation of inflammation. In parallel, the overproduction of cytokines by RAW264.7 macrophages was observed after stimulation with LPS.