Bleomycin (BLM) induced cellular damage causes inflammation in the alveolar compartment and impairment of fibrinolytic system leads to alveolar epithelial cell apoptosis. Here, we describe novel inflammatory pathway associated with p53-fibrinolytic system and apoptosis of alveolar epithelial cells and pharmacological efficiency of curcumin against this action. In the present study we used C57BL/6 mice. The specific dose and time interval of curcumin were analyzed to assess the intervention. Experiments were designed to investigate the IL-17A mediated modulation in the alveolar epithelial cell apoptosis and injury. Various techniques such as Western blot, RT-PCR, Immunohistochemistry were used for this study. We observed that the BLM-induced lung injury and its progression were successfully regulated by the effective dose and time intervention of curcumin. There was also decreased expression of chemokines, p53, and fibrinolytic components such as PAI-1 and increased uPA, uPAR expression, and decreased alveolar epithelial cell apoptosis, which indicates the IL-17A mediated novel inflammatory pathway. It is confirmed that the IL-17A involved in the modulation of p53-fibrinolytic system and epithelial cell apoptosis in BLM induced mice. The cross-talk between the inflammatory, fibrinolytic, and apoptotic pathways were resolved by curcumin intervention. This pathway and intervention could serve as a modern therapy to resolve the complications to cure the lung injury and its progression.
Keywords: IL-17A; alveolar epithelial cells; apoptosis; bleomycin; curcumin; p53.
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