Effects of intraperitoneal hydrogen injection on nitric oxide synthase mRNA and malondialdehyde following limb ischemia-reperfusion in rabbits
Abstract
Objective: To investigate the effects of intraperitoneal hydrogen (H2) injection on the mRNA expression levels of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) as well as the serum malondialdehyde (MDA) level in a rabbit model of limb ischemia-reperfusion (I/R)-induced skeletal muscle injury.
Methods: To establish the hind limb I/R animal model, 30 rabbits were randomly assigned to one of three groups: Sham, I/R and IRH. An intraperitoneal injection of H2 was given to the IRH group, while an equivalent amount of air was given to the Sham and I/R groups. At 3, 6, 12 and 24 h post reperfusion, the serum MDA level, as well as the skeletal muscle iNOS and eNOS mRNA expression levels, were determined
Results: Both iNOS mRNA expression and serum MDA levels were higher in the I/R group than the Sham group (P < 0.01) and lower in the IRH group than the I/R group (P < 0.01 or P < 0.05) at various time points after reperfusion. The eNOS mRNA expression level exhibited no significant difference between the I/R and Sham groups following reperfusion but was significantly higher in the IRH group than in the Sham group (P < 0.01 or P < 0.05).
Conclusions: During the I/R process, the expression of iNOS mRNA was up-regulated along with an increase in MDA. Intraperitoneal injection of H2 could down-regulate iNOS mRNA expression and up-regulate eNOS mRNA expression in the I/R process, suggesting a protective effect of H2 in I/R-induced skeletal muscle injury.
Keywords
References
- Baue AE. The horror autotoxicus and multiple-organ fail- ure. Arch Surg 1992;127:1451–62.
- Nanobashvili J, Neumayer C, Fuegl A, Sporn E, Prager M, Polterauer P, et al. Ischaemia/reperfusion injury of skeletal muscle: Mechanisms, morphology, treatment strategies, and clinical applications. European Surgery 2002;34:83–9.
- Guillot M, Charles AL, Chamaraux-Tran TN, Bouitbir J, Meyer A, Zoll J, et al. Oxidative stress precedes skeletal muscle mitochondrial dysfunction during experimental aortic cross-clamping but is not associated with early lung, heart, brain, liver, or kidney mitochondrial impairment. J Vasc Surg 2014;60:1043–51.e5.
- Palmer RM, Ferrige AG, Moncada S. Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor. Nature 1987;327:524–6.
- Moncada S, Palmer RM, Higgs EA. Nitric oxide: physiol- ogy, pathophysiology, and pharmacology. Pharmacol Rev 1991;43:109–42.
- Rochette L, Lorin J, Zeller M, Guilland JC, Lorgis L, Cot- tin Y, et al. Nitric oxide synthase inhibition and oxidative stress in cardiovascular diseases: possible therapeutic tar- gets? Pharmacol Ther 2013;140:239–57.
- Korkmaz A, Kolankaya D. Inhibiting inducible nitric oxide synthase with rutin reduces renal ischemia/reperfusion in- jury. Can J Surg 2013;56:6–14.
- Huang G, Zhou J, Zhan W, Xiong Y, Hu C, Li X, et al. The neuroprotective effects of intraperitoneal injection of hydrogen in rabbits with cardiac arrest. Resuscitation 2013;84:690–5.
Details
Primary Language
English
Subjects
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Journal Section
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Authors
Dai-jun Wang
This is me
Hua Tian
This is me
Bao-xiang Zhuang
This is me
Hong-juan Wu
This is me
Publication Date
September 24, 2015
Submission Date
June 23, 2015
Acceptance Date
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Published in Issue
Year 2015 Volume: 49 Number: 5