Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fatal disease with limited treatments. Jinbei Oral Liquid (JB.L), an approved TCM formulation, offers multi-target, low-toxicity benefits and preliminary anti-inflammatory effects for IPF. The "gut-lung axis" (immune-microbial-metabolic crosstalk) is critical to IPF, with gut microbiota dysbiosis and reduced short-chain fatty acids (SCFAs) driving disease. However, JB.L’s regulation of lung-intestinal microecology and the "gut microbiota-metabolite-lung immunity" axis remains unclear—this study addresses this gap. To assess the therapeutic efficacy of JB.L in rats with pulmonary fibrosis (PF) and to investigate its impact on the microbiota of PF rats, with the goal of identifying potential novel mechanisms for the treatment of IPF. A PF rat model was established by intratracheal instillation of Bleomycin (BLM) (3 mg/kg). JB.L and pirfenidone were administrated via gavage for 28 days. PF severity was assessed using lung index and Masson trichrome staining. Lung and intestinal inflammation were evaluated by HE staining, and cytokine levels were measured using ELISA. Microbiota composition in the lungs and intestines was analyzed by 16S rRNA sequencing. Short-chain fatty acids (SCFAs) in feces were quantified using GC-MS. The results showed that JB.L reduced the expression of BLM-induced lung inflammatory cytokines (TGF-β1, TNF-α, IL-1β, and IL-6) and enhanced the IFN-γ/IL-4 ratio. JB.L also alleviated intestinal inflammation in PF rats, decreasing TNF-α, IL-1β, and IL-6 levels in the intestine. Additionally, JB.L restored the balance of intestinal and lung microbiota and increased the concentrations of acetic acid, propionic acid, isobutyric acid, and isovaleric acid in the intestines of PF rats. Spearman correlation analysis further revealed that JB.L reversed the abnormal positive correlation between pro-inflammatory lung microbiota and fibrotic factors, as well as the negative correlation with the IFN-γ/IL-4 ratio. JB.L effectively alleviated PF symptoms in rats. One of its potential mechanisms may involve modulating the imbalance of lung and intestinal microbiota and increasing the concentrations of microbiota-derived metabolites—SCFAs—in the intestines of PF rats, though it should be noted that mechanistic investigations were conducted using only a single batch of JB.L.
Kong et al. (2026) studied this question.