## 4 Discussion  
ALI is a well-known clinical disease, mainly described by pulmonary inflammation, loss of alveolar-capillary-membrane integrity, oedema, and impairment of arterial oxygenation, followed by apoptosis [29]. The mortality rate of this disease is high at approximately 30-50% [30]. Different types of prostaglandam (PGs) intricately modulate ALI as the pathophysiological function of each PG differs in its specific receptor subtypes, context of activation, and target cells [19]. Different types of PGs have been reported to perform paradoxical roles, both as proinflammatory and anti-inflammatory agents in the case of injured lungs [30]. Major PGs, such as PGE\({}_{2}\) and thromboxane A2 (TXA2), function as proinflammatory agents in ALI [31,32]. However, the anti-inflammatory functions of lipoxin A4 and 15d-PG\({}_{2}\) have also been reported in ALI in experimental mice [33,34]. Some previous reports have proposed a proinflammatory role for PGD\({}_{2}\) in some respiratory disorders, arbitrated through specific signalling cascades, while others state that PGD\({}_{2}\) have a dual role as tissue-protective in the context of airway inflammation, depending upon the specific receptors involved and the severity of the disease. It is also well-reported that the breakdown product of  
Figure 9: Flow cytometry data of PGD\({}_{2}\)’s effect on apoptosis: (**a**) control group shows 97.4% viable cells; (**b**) in the LPS-treatment group (5 mg/kg b.w. ), total viable cells decreased to 87.5%; (**c**) LPS + PGD\({}_{2}\) group had a reduced apoptosis ratio of 96.9%; (**d**) PGD\({}_{2}\) (100 ug/kg b.w. )-treated animals displayed no noteworthy comparison in relation to the control animals. PGD\({}_{2}\) as 15d-PGJ\({}_{2}\) possesses anti-inflammatory functions through either PPAR-\(\gamma\)-based or PPAR-\(\gamma\)-independent reactions [19]. In the present study, the mouse model for ALI was successfully established by using 5 mg/kg b.w. LPS through i.p. injection [18]. The administration of LPS significantly enhanced the lung W/D weight ratio. The lung W/D weight ratio indicates oedema accumulation and is a function of the rate of fluid filtration across the lung capillaries. However, pretreatment with PGD\({}_{2}\) demonstrated a significantly lower W/D ratio as compared to the disease control animals. In one study, similar observations were observed in LPS-treated mice and disease control mice treated with continental acid [18]. PGD\({}_{2}\) treatment attenuates the progression of pulmonary oedema, as presented by the reduction in the lung W/D weight ratio. The activity of MPO, as chiefly found in cytoplasmic granules of neutrophil, reflects the infiltration of these cells within the lung tissues [35]. A complex setup of inflammatory cytokines, such as IL-18, IL-6, and TNF-\(\alpha\), plays a significant role in LPS-induced ALI and enhances the severity of lung damage [36]. Furthermore, various chemokines are also recruited, and they stimulate the enormous recruitment of neutrophils that ultimately leads to a steep rise in MPO activity. Treatment with PGD\({}_{2}\) significantly diminishes the rise in IL-18, IL-6, and TNF-\(\alpha\) after LPS exposure, an outcome consistent with that of the MPO level. Furthermore, the production of other inflammatory markers, such as iNOS, was also diminished by PGD\({}_{2}\) treatment. A number of molecular mechanisms have been proposed for the mediation of the pathogenic events of LPS-induced lung injury, among which oxidative stress plays a major role in mediating the disease [37]. The inflammatory responses lead to respiratory burst and superoxide production. ROS overproduction results in severe pathophysiological events. Excessive LPS-induced ROS production promotes lipid peroxidation [38]. Moreover, LPS-induced oxidative stress is associated with reduced antioxidant enzyme activity. Among the different antioxidant enzymes, catalase, SOD, and GSH are significantly depressed by LPS treatment [39].