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Low‐Level Laser Therapy Restores the Oxidative Stress Balance in Acute Lung Injury Induced by Gut Ischemia and Reperfusion
Author(s) -
Lima Flávia Mafra,
Albertini Regiane,
Dantas Yvana,
MaiaFilho Antonio Luis,
Loura Santana Cristiano,
CastroFariaNeto Hugo Caire,
França Cristiane,
Villaverde Antonio Balbin,
Aimbire Flávio
Publication year - 2012
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.2012.01214.x
Subject(s) - bronchoalveolar lavage , lung , extravasation , myeloperoxidase , oxidative stress , chemistry , hsp70 , inflammation , edema , evans blue , pathology , immunology , medicine , endocrinology , heat shock protein , biochemistry , gene
It remains unknown if the oxidative stress can be regulated by low‐level laser therapy ( LLLT ) in lung inflammation induced by intestinal reperfusion (i‐ I/R ). A study was developed in which rats were irradiated (660 nm, 30 mW, 5.4 J) on the skin over the bronchus and euthanized 2 h after the initial of intestinal reperfusion. Lung edema and bronchoalveolar lavage fluid neutrophils were measured by the Evans blue extravasation and myeloperoxidase ( MPO ) activity respectively. Lung histology was used for analyzing the injury score. Reactive oxygen species ( ROS ) was measured by fluorescence. Both expression intercellular adhesion molecule 1 ( ICAM ‐1) and peroxisome proliferator‐activated receptor‐y ( PPARy ) were measured by RT‐PCR . The lung immunohistochemical localization of ICAM ‐1 was visualized as a brown stain. Both lung HSP 70 and glutathione protein were evaluated by ELISA . LLLT reduced neatly the edema, neutrophils influx, MPO activity and ICAM ‐1 mRNA expression. LLLT also reduced the ROS formation and oppositely increased GSH concentration in lung from i‐ I/R groups. Both HSP 70 and PPARy expression also were elevated after laser irradiation. Results indicate that laser effect in attenuating the acute lung inflammation is driven to restore the balance between the pro‐ and antioxidants mediators rising of PPARy expression and consequently the HSP 70 production.