Abstract
BackgroundAdrenomedullin (AM), a 52-amino acid ringed-structure peptide with C-terminal amidation, was originally isolated from human pheochromocytoma. AM are widely distributed in various tissues and acts as a local vasoactive hormone in various conditions.MethodsIn the present study, we investigated the efficacy of AM on the animal model of bleomycin (BLM)-induced lung injury. Mice were subjected to intratracheal administration of BLM and were assigned to receive AM daily by an intraperitoneal injection of 200 ngr/kg.Results and DiscussionMyeloperoxidase activity, lung histology, immunohistochemical analyses for cytokines and adhesion molecules expression, inducible nitric oxide synthase (iNOS), nitrotyrosine, and poly (ADP-ribose) polymerase (PARP) were performed one week after fibrosis induction. Lung histology and transforming growth factor beta (TGF-β) were performed 14 and 21 days after treatments. After bleomycin administration, AM-treated mice exhibited a reduced degree of lung damage and inflammation compared with BLM-treated mice, as shown by the reduction of (1) myeloperoxidase activity (MPO), (2) cytokines and adhesion molecules expression, (3) nitric oxide synthase expression, (4) the nitration of tyrosine residues, (5) poly (ADP-ribose) (PAR) formation, a product of the nuclear enzyme poly (ADP-ribose) polymerase (PARP) (6) transforming growth factor beta (TGF-β) (7)and the degree of lung injury.ConclusionsOur results indicate that AM administration is able to prevent bleomycin induced lung injury through the down regulation of proinflammatory factors.
Highlights
Adrenomedullin (AM), a 52-amino acid ringed-structure peptide with C-terminal amidation, was originally isolated from human pheochromocytoma
Our results indicate that AM administration is able to prevent bleomycin induced lung injury through the down regulation of proinflammatory factors
Effects of AM on BLM-induced lung injury, body weight, and fluid content 7 days after BLM administration the pulmonary lesions observed in mice consisted of multifocal areas of severe inflammation and intense fibrosis (Figure 1B)
Summary
Adrenomedullin (AM), a 52-amino acid ringed-structure peptide with C-terminal amidation, was originally isolated from human pheochromocytoma. Idiopathic pulmonary fibrosis (IPF) is one of the most common forms of interstitial lung disease (ILD) characterized by inexorable, progressive fibrosis involving this critical space. The role of inflammation in the pulmonary fibrosis is still debated, even if several data suggest that the Several studies suggest that fibrosis is the end result of chronic inflammatory reactions induced by a variety of stimuli including persistent infections, autoimmune reactions, allergic responses, chemical insults, radiation [3] and tissue injury [4]. Perivascular inflammatory cell infiltrates are found in lungs from patients with pulmonary hypertension (PH), compared to healthy controls. Patients with idiopathic or associated PH exhibit higher circulating levels and pulmonary expression of various inflammatory cytokines and chemokines, including interleukin-1beta (IL-1b), IL-6 and monocyte chemoattractant protein (MCP-1) [5]
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