[Effect of Viola tianshanica extract on innate immune response in mice infected with influenza A virus based on...

This study aims to investigate the effect of Viola tianshanica Maxim. extract(VTME) on the innate immune response in mice infected with influenza A virus. Mice were randomly divided into a control group, a virus-infected group, an oseltamivir group, and low-, medium-, and high-dose VTME groups, with 10 mice in each group. The model of influenza pneumonia in mice was established via nasal inhalation of influenza A virus(H1N1/PR8), and intragastric administration began on the day of infection, once a day for 4 days, with the lung tissues collected 24 h later. The pathological changes in lung tissues were evaluated by hematoxy-lin-eosin(HE) staining. The protein expression of retinoic acid-inducible gene-Ⅰ(RIG-Ⅰ) and NOD-like receptor thermal protein domain associated protein 3(NLRP3) in lung tissues was detected by immunohistochemistry. The mRNA expression of RIG-Ⅰ, interferon regulatory factor 3(IRF3), interferon-beta(IFN-β), NLRP3, cysteinyl aspartate specific proteinase-1(caspase-1), gasdermin D(GSDMD), and interleukin-1 beta(IL-1β) in lung tissues was measured by quantitative real-time polymerase chain reaction(qRT-PCR). The protein expression of RIG-Ⅰ, IRF3, phosphorylated IRF3(p-IRF3), IFN-β, NLRP3, caspase-1, apoptosis-associated speck-like protein containing a CARD(ASC) and IL-1β in lung tissues was determined by Western blot. The results showed that, when compared with the virus-infected group, VTME intervention significantly alleviated pathological injury in the lung tissue. Immunohistochemical analysis revealed that VTME markedly reduced the protein expression of RIG-Ⅰ and NLRP3 in the lung tissue. Additionally, qRT-PCR and Western blot experiments indicated that VTME intervention significantly decreased the mRNA and protein expression of RIG-Ⅰ, IRF3, and IFN-β, decreased the mRNA expression of NLRP3, caspase-1, GSDMD, and IL-1β, and simultaneously reduced the protein expression of NLRP3, caspase-1, ASC, and IL-1β. Collectively, the mechanism of VTME on influenza virus-infected mice may be related to the regulation of innate immune response through inhibiting the expression of related genes and proteins in the RIG-Ⅰ signaling pathway and NLRP3 inflammasome signaling pathway.