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Dimethyl Sulfoxide Attenuates Acute Lung Injury Induced by Hemorrhagic Shock/Resuscitation in Rats.

Authors :
Tsung, Yu-Chi
Chung, Chih-Yang
Wan, Hung-Chieh
Chang, Ya-Ying
Shih, Ping-Cheng
Hsu, Han-Shui
Kao, Ming-Chang
Huang, Chun-Jen
Source :
Inflammation. Apr2017, Vol. 40 Issue 2, p555-565. 11p.
Publication Year :
2017

Abstract

Inflammation following hemorrhagic shock/resuscitation (HS/RES) induces acute lung injury (ALI). Dimethyl sulfoxide (DMSO) possesses anti-inflammatory and antioxidative capacities. We sought to clarify whether DMSO could attenuate ALI induced by HS/RES. Male Sprague-Dawley rats were allocated to receive either a sham operation, sham plus DMSO, HS/RES, or HS/RES plus DMSO, and these were denoted as the Sham, Sham + DMSO, HS/RES, or HS/RES + DMSO group, respectively ( n = 12 in each group). HS/RES was achieved by drawing blood to lower mean arterial pressure (40-45 mmHg for 60 min) followed by reinfusion with shed blood/saline mixtures. All rats received an intravenous injection of normal saline or DMSO immediately before resuscitation or at matching points relative to the sham groups. Arterial blood gas and histological assays (including histopathology, neutrophil infiltration, and lung water content) confirmed that HS/RES induced ALI. Significant increases in pulmonary expression of tumor necrosis factor-α (TNF-α), malondialdehyde, nuclear factor-kappa B (NF-κB), inducible nitric oxide synthase (iNOS), and cyclooxygenase 2 (COX-2) confirmed that HS/RES induced pulmonary inflammation and oxidative stress. DMSO significantly attenuated the pulmonary inflammation and ALI induced by HS/RES. The mechanisms for this may involve reducing inflammation and oxidative stress through inhibition of pulmonary NF-κB, TNF-α, iNOS, and COX-2 expression. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
03603997
Volume :
40
Issue :
2
Database :
Academic Search Index
Journal :
Inflammation
Publication Type :
Academic Journal
Accession number :
121918925
Full Text :
https://doi.org/10.1007/s10753-016-0502-4