Abstract
The current study deals with the effect of a dietary flavanoid quercetin on fibrotic lung tissue in rats. Bleomycin was administered by single intratracheal instillation to Wistar rats to induce lung fibrosis. The pathologies associated with this included significantly reduced antioxidant capacity, ultimately leading to protracted inflammation of the lung tissue. The hallmark of this induced fibrosis condition was an excessive collagen deposition in peribronchial and perialveolar regions of the lung. Oral quercetin treatment over a period of twenty days resulted in significant reversal of the pathologies. The antioxidant defense in lung tissue was revived. Moreover, activity of the collagenase MMP-7, which was high in fibrotic tissue, was seen restored after quercetin administration. Trichome staining of lung tissue sections showed high collagen deposition in fibrotic rats, which may be a direct result of increased mobilization of collagen by MMP-7. This was appreciably reduced in quercetin treated animals. These results point towards an important protective role of quercetin against idiopathic lung fibrosis, which remains a widely prevalent yet incurable condition in the present times.
Highlights
Bleomycin is a commonly used chemotherapeutic agent which, induces dose-dependent pulmonary fibrosis upon long-term administration [1]
Bleomycin-induced pulmonary injury and lung fibrosis have been documented in studies using several animal models [4, 5]
The result of this study showed an increase in the level of lipid peroxidation in bleomycinadministered group over that of control group, which could be a manifestation of bleomycin induced tissue injury and damage
Summary
Bleomycin is a commonly used chemotherapeutic agent which, induces dose-dependent pulmonary fibrosis upon long-term administration [1]. Lung inflammation is considered to be a major underlying factor for the induction of pulmonary fibrosis [2]. Reactive oxygen species such as superoxide anion, hydrogen peroxide, and hydroxyl radical are reported as major mediators of lung inflammatory processes [3]. Bleomycin-induced pulmonary injury and lung fibrosis have been documented in studies using several animal models [4, 5]. The bleomycin induces the genesis of reactive oxygen species upon binding to DNA and iron, which in turn causes DNA damage [8]. Strategies aimed at reducing oxidative stress have been found to be successful in decreasing bleomycin-induced lung injury and fibrosis [10,11,12]
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