a comparison of the effects of quercetin hydrate with those of vitamin e on the levels of il-13, pdgf, tnf-α, and inf-γ in bleomycin-induced pulmonary fibrosis in rats

results the administration of quercetin hydrate significantly reduced the concentration of il-13, pdgf-β, and tnf-α and increased the concentrations of inf-γ in balf. conclusions according to the experimental results, quercetin hydrate reduced the concentration of inflammatory fibrotic factors, such as il-13, pdgf-β, and tnf-α, and increased the level of the antifibrotic factor inf-γ, and the effects of quercetin hydrate appeared stronger than those of vit e. in cases of exposure to fibrogenic factors, quercetin hydrate can be prescribed as a prophylactic agent for pulmonary fibrosis. objectives this study investigated and compared the inhibitory effects of quercetin hydrate with those of vitamin e (vit e), a well-known antioxidant, on bleomycin (blm)-induced pulmonary fibrosis in rats. materials and methods this study used sprague-dawley male rats, with a weight range of 200 - 250 g. the positive control group received a single-dose of blm (7.5 iu/kg) through an intratracheal injection (positive control group). the negative control group received normal saline. the other groups were treated with different doses of quercetin hydrate (25, 50, and 75 mg/kg) or daily intraperitoneal injections of vit e (10 mg/kg) for 1 week before and 3 weeks after a single dose of blm via intratracheal administration. four weeks later, bronchoalveolar lavage fluid (balf) was collected for measurement of cytokines. background pulmonary fibrosis is a deadly and destructive disease. various chemicals, drugs, and environmental factors are responsible for pulmonary fibrosis. the disease can also be idiopathic. a number of inflammatory mediators and cytokines, such as interleukin-13 (il-13), platelet‐derived growth factor (pdgf), and tumor necrosis factor α (tnf-α), play an important role in pulmonary fibrosis. profibrotic cytokines accelerate the maturation and proliferation of fibroblasts, which ultimately increases the amount of collagen deposits in the alveolar cell wall. in contrast, the interferon-γ (inf-γ) cytokine has antifibrotic properties.