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

INTRODUCTION: H1N1 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 METHODS: Infection 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. RESULTS: Data 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. CONCLUSIONS: Data 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.