The Protective Effect Of Catalpol On Respiratory Syncytial Virus Infection

Respiratory syncytial virus (RSV) infection can cause severe bronchiolitis, pneumonia or even death in infants, or induce childhood asthma. Currently no specific drug is available for RSV infection. With multiple pathology roles, catalpol has significant roles in anti-oxidation and anti-infection, but has not been studied in RSV infection. This study aimed to investigate the effects and mechanism of catalpol on RSV infection via establishing a mouse RSV infection model, further illustrating the effect of catalpol on RSV infection and providing evidences for clinical treatment. BALB/c mice were used to generate a RSV infection model using intranasal drops of viral solutions, and mice were then treated with 5 mM or 10 mM catalpol. Real-time fluorescent quantitative PCR was used to measure RSV load in mouse pulmonary tissues, while ELISA was used to quantify expression of inflammatory factors including TNF-alpha and IL-1 beta. Real-time PCR and Western blot were used to test cellular expression of NF-kappa B (p65) mRNA and protein expression. ROS and SOD activity in all cells were analyzed. Compared to the control group, RSV infected mice had higher RSV load in pulmonary tissues, elevated serum TNF-alpha and IL-1 beta levels, expression of NF-kappa B mRNA and protein, higher ROS contents and lower SOD activity (p < 0.05). Catalpol can decrease RSV load and ROS contents, elevate SOD activity, decrease NF-kappa B mRNA and protein expressions, and suppress TNF-alpha and IL-1 beta levels (p < 0.05 compared to model group) in a dose-dependent manner. Catalpol can exert anti-RSV infection roles via modulating oxidation/anti-oxidation balance and inhibiting inflammation progression.