Jianpi Yifei Tongluo recipe attenuates inflammation by promoting the expression of interferon regulatory factor 4 in the rat model of chronic obstructive pulmonary disease.

Objective: To examine the effects of the Jianpi Yifei Tongluo recipe (, JYTR) on chronic obstructive pulmonary disease (COPD) within an animal model and to elucidate its anti-inflammatory mechanisms.

Methods: In this study, we utilized cigarette smoke (CS) exposure and lipopolysaccharide (LPS)-induced models of COPD in rats to evaluate the effects of the JYTR on airway inflammation. Sprague-Dawley rats were randomly assigned to various groups: control, model, budesonide, synbiotics, and low, medium, and high JYTR. Pulmonary function was gauged using an animal volumetric tracer. Pathological alterations in lung tissue were examined under a light microscope. To ascertain cytokine production, we conducted enzyme-linked immunosorbent assay tests, and we employed Western blotting to measure the expression levels of interferon regulatory factor 4 (IRF4), arginase 1(Arg1), inducible nitric oxide synthase (iNOS), nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IKB-α), and P65.

Results: Compared to the control group, rats in the COPD model group exhibited significantly compromised pulmonary function and severe inflammatory pathology in the lungs. Treatment with budesonide, synbiotics, and the JYTR markedly improved pulmonary function and diminished the production of inflammatory cytokines transforming growth factor-beta (TGF-β), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6). These improvements were particularly notable in the budesonide group and the high-dose JYTR group. Additionally, the JYTR increased the expression of IRF4 and upregulated the protein expression of Arg1, while concurrently downregulating the protein expression of iNOS, phosphorylated IKB-α, and phosphorylated P65.

Conclusion: Our current study reveals that JYTR can mitigate inflammatory lung injury, enhance lung function, and lower levels of inflammatory cytokines induced by CS or LPS exposure in COPD model rats. The mechanism behind its anti-inflammatory effect likely involves the regulation of IRF4 expression and M2 polarization through the nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway.