Corilagin protects the acute lung injury by ameliorating the apoptosis pathway

This study elucidates the protective effect of corilagin in acute lung injury rat model. Lung injury induced by ischemia/reperfusion (I/R) model was established by isolating the lungs from the rats. Ischemia was produced for the duration of 1h and thereafter reperfusion was done for 90min in isolated lung in presence and absence of corilagin (20 and 40mg/ml). Effect of corilagin was evaluated by estimating the pulmonary vein oxygen partial pressure (PaO2), airway compliance and tidal volume. Moreover the level of oxidative stress parameter, pro inflammatory parameters, phosphorylation of JNK and apoptosis rate was estimated in lung tissues. There was significant increase in the PaO2, airway compliance and tidal volume in corilagin treated group than I/R group. Treatment with corilagin significantly increases the activity of superoxide dismutase (SOD) and level of adenosine triphosphate (ATP) and decreases the level of MDA in the tissue homogenate of I/R induced lung injury model. Whereas expressions of proinflammatory gene such as tumor necrosis factor α, interlukin-6, IL-1β and cycloxygenase -2 (COX-2) was found to be reduced in corilagin treated group than I/R group. Posphorylation of JNK and apoptotic rate was also found to be decreased in corilagin treated group than I/R group. Present report concludes that treatment with corilagin attenuates the lung injury in ex vivo I/R induced lung injury rat model by decreasing oxidative stress, pro-inflammatory mediators and its anti apoptotic activity.