Adelmidrol: A New Promising Antioxidant and Anti-Inflammatory Therapeutic Tool in Pulmonary Fibrosis

被引:55
作者
Fusco, Roberta [1 ]
Cordaro, Marika [2 ]
Genovese, Tiziana [1 ]
Impellizzeri, Daniela [1 ]
Siracusa, Rosalba [1 ]
Gugliandolo, Enrico [1 ]
Peritore, Alessio Filippo [1 ]
D'Amico, Ramona [1 ]
Crupi, Rosalia [3 ]
Cuzzocrea, Salvatore [1 ,4 ]
Di Paola, Rosanna [1 ]
机构
[1] Univ Messina, Dept Chem Biol Pharmaceut & Environm Sci, I-98166 Messina, Italy
[2] Univ Messina, Dept Biomed Dent & Morphol & Funct Imaging, Via Consolare Valeria, I-98125 Messina, Italy
[3] Univ Messina, Dept Vet Sci, I-98168 Messina, Italy
[4] St Louis Univ, Dept Pharmacol & Physiol Sci, Sch Med, St Louis, MO 63104 USA
关键词
oxidative stress; pulmonary fibrosis; biochemistry; NITRIC-OXIDE SYNTHASE; OXIDATIVE STRESS; LUNG FIBROSIS; MAST-CELLS; TGF-BETA; PALMITOYLETHANOLAMIDE ANALOG; SUPEROXIDE-DISMUTASE; CHRONIC INFLAMMATION; GROWTH-FACTOR; BLEOMYCIN;
D O I
10.3390/antiox9070601
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: Chronic pulmonary diseases are characterized by airway remodeling due to complex multicellular responses and the production of free oxygen radicals. They lead to a progressive decline of pulmonary functions. Adelmidrol is an analogue of palmitoylethanolamide (PEA), which is a well-known anti-inflammatory and anti-oxidant compound. In this study, we investigated the efficacy of adelmidrol (10 mg/Kg) for bleomycin-induced pulmonary fibrosis in mice. Methods: Bleomycin intratracheal administration was performed on the first day and for the following twenty-one days, mice were treated with adelmidrol (10 mg/Kg). Results: The survival rate and body weight gain were recorded daily. At the end of the experiment, adelmidrol-administered animals showed reduced airway infiltration by inflammatory cells, Myeloperoxidase (MPO) activity, and pro-inflammatory cytokine overexpression (IL,6 IL-1 beta, TNF-alpha, and TGF-1 beta). Moreover, adelmidrol treatment was able to manage the significant incapacity of antioxidants and elevation of the oxidant burden, as shown by the MDA, SOD, and GSH levels and decreased nitric oxide production. It was also able to significantly modulate the JAK2/STAT3 and I kappa B alpha/NF-kB pathway. Histologic examination of the lung tissues showed reduced sample injury, mast cell degranulation, chymase activity, and collagen deposition. Conclusions: In sum, our results propose adelmidrol as a therapeutic approach in the treatment of pulmonary fibrosis.
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页码:1 / 14
页数:14
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