Punicalagin inhibits pro-inflammatory cytokines induced by influenza A virus

Abstract

IntroductionInfluenza A virus causes severe pneumonia in humans, leading to high morbidity and mortality. Studies have shown that an excessive immune response in overproduction of pro-inflammatory cytokines can exacerbate complications of influenza virus infection. Thus immune-targeted therapies are an appropriate strategy to control the disease. This study was conducted to investigate the effect of punicalagin on expression and concentration levels of tumor necrosis factor alpha (TNFα), interleukin 6 (IL-6) and interleukin1-β in Madin-Darby Canine Kidney (MDCK) cells. MethodsIn this experimental study, confluent MDCK cells were infected with influenza A virus (H1N1; PR8) and treated with punicalagin at different concentrations. After incubation, mRNA expression and concentration levels of TNFa, IL-6 and IL1-β were investigated using real-time polymerase chain reaction (PCR) and enzyme-linked immunesorbent assay (ELISA), respectively. ResultsThe results of quantitative Real-time PCR showed a significant increase in TNFa, IL-6 and IL1-β mRNA expression in control virus compared to cell control, and a significant, dose-dependent decrease in these expression levels in punicalagin-treated virus infected cells compared to control virus (P < 0.05). The ELISA results also confirmed the dose-dependent decrease in TNFa, IL-6 and IL1-β concentrations in protein levels in punicalagin treated, virus infected cells compared to control virus (P < 0.05). ConclusionsOur results demonstrated the anti-inflammatory effects of punicalagin, and therefore suggests that the compound can be used as an appropriate treatment of choice to control cytokines-induced inflammation in influenza A virus infection.