Toonaciliatin K attenuates the lung injury induced by lung infection of H1N1 influenza virus by regulating the NF-κB/MyD88/TLR-7 pathway in mice.

Abstract

IntroductionH1N1 infection has a high mortality rate due to lung injury and respiratory distress. The present study determines the protective effect of toonaciliatin K against the lung injury induced by the lung infection of H1N1 influenza mice and also postulates the molecular mechanism.Material and methodsInfection was induced by exposing the anesthetized mice to H1N1 virus (10 LD50 in a volume of 30 ml) intranasally at day zero and mice were treated with toonaciliatin K 16.5 and 33 mg/kg intragastrically for 2 weeks. The effect of toonaciliatin K was assessed by estimating survival rate and lung edema by the lung index. Histopathological changes were determined by H + E staining and western blot and an RT-PCR study was also performed on the lung tissue homogenate.ResultsData of the study suggest that toonaciliatin K treatment enhances the survival rate and reduces the lung index compared to infected mice. There was a decrease in the level of chemokines and cytokines in the lung tissue of the toonaciliatin K treated group compared to infected mice. Moreover, expression of TLR-7, NF-κB p65 and MyD88 protein was found to be reduced in the lung tissue of the toonaciliatin K treated group compared to infected mice.ConclusionsData of the study suggested that toonaciliatin K protects against lung injury in lung H1N1 lung infection by regulating the TLR-7/Myd88/NF-κB p65 pathway.