FIGURE 8.

Diagrammatic representation of the plausible mechanisms by which DRDE-30 confers protection against bleomycin-induced pulmonary injury. Bleomycin-induced lung injury is initiated with the production of reactive intermediates causing oxidative stress, and subsequent damage to the endothelial and the epithelial cells. This leads to the disruption of the barrier between the alveolar and the capillary network, causing infiltration of inflammatory cells into the lung tissue. Release of inflammatory mediators and pro-fibrogenic cytokines by the immune cells promotes proliferation of myofibroblasts, collagen deposition and ultimately organ failure, which may culminate into death of the organism. DRDE-30 provides protection against bleomycin-induced lung damage by activating anti-oxidant pathways and abrogating the inflammatory and fibrotic changes.