Jinxin oral liquid reduced lung inflammation in influenza A virus infected mice through inhibiting NOD-like receptor protein 3 pathway.

Objective: To investigate the therapeutic effects of Jinxin oral liquid (, JX) on influenza A virus（H1N1）influenza virus infected mice.

Methods: We established a model of by intranasally infecting the mice with H1N1 virus. The mice were then orally administered JX or ribavirin to evaluate their therapeutic effects in vivo. We conducted histologic and immunohistochemical analyses, enzyme linked immunosorbent assay or quantitative real-time polymerase chain reaction to assess lung damage and the expression of inflammatory cytokines. Western blot (WB) experiments was conducted to measure the activation of NOD-like receptor protein 3 (NLRP3) pathway. Flow cytometry was employed to quantify the populations of alveolar macrophages (AMs). To block the NLRP3 pathway, mice were treated with MCC950. For AMs depletion, mice were intranasally administered a single dose of clodronate liposome.

Results: Administration of JX demonstrated a protective effect against H1N1-induced lung pathology by reducing lung injury, suppressing lung inflammation, and decreasing viral titer. JX significantly inhibited the production of pro-inflammatory cytokines, such as interleukin (IL)-1β and tumor necrosis factor-ɑ, in H1N1-infected mice. JX inhibits the activation of NOD-like receptor protein 3 (NLRP3)/apoptosis-associated speck-like protein containing a caspase recruitment domain/ caspase 1 pathway in the lungs and AMs of H1N1-infected mice. The inhibitory effect of JX on IL-1β secretion was mediated by blocking the NLRP3 pathway activation in AMs.

Conclusions: These findings suggest that JX holds promise as a potential therapeutic agent for suppressing the aggressive pro-inflammatory response induced by H1N1 infection. Further research and development are warranted to explore the full potential of JX in the prevention and treatment of H1N1 infection.