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. 1. Introduction Bleomycin is a commonly used chemotherapeutic agent which, however, induces dose-dependent pulmonary fibrosis upon long-term administration [1]. Interstitial pulmonary fibrosis is characterized by an altered cellular composition of the alveolar region with excessive deposition of collagen. However, 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]. Nevertheless, the direct linkage between reactive oxygen species formation and pulmonary fibrosis has not been established conclusively. Bleomycin-induced pulmonary injury and lung fibrosis have been documented in studies using several animal models [4, 5]. These models have been widely used for studying the mechanisms involved in the progression of human pulmonary fibrosis and the impact of various drugs on this progression [6, 7]. The bleomycin induces the genesis of reactive oxygen species upon binding to DNA and iron, which in turn causes DNA damage [8]. The interaction of bleomycin with DNA is postulated to initiate the inflammatory and fibroproliferative changes through a concerted action of various cytokines leading to collagen accumulation in the lung [5]. Further, it is reported that
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