The aim of the present study was investigate the impact of seawater immersion on peripheral nerve injury and the underlying mechanisms. A total of 234 specific pathogen-free Sprague-Dawley male rats were randomly divided into a sham group, injury control group and seawater immersion + injury group. The Sciatic Functional Index (SFI) was used to assess nerve function for 6 weeks after injury. Compound muscle action potentials were measured and hematoxylin and eosin (H&E) staining of nerve specimens was carried out at week 6. Levels of reactive oxygen species (ROS) and malondialdehyde (MDA) in nerve tissues were measured by enzyme-linked immunosorbent assay (ELISA), and the expression levels of inducible nitric oxide synthase (iNOS) mRNA and protein were measured by reverse transcription-quantitative polymerase chain reaction and immunohistochemistry, respectively. The SFI value in the seawater immersion + injury group after 6 weeks was lower than that in the injury control group (P<0.05). The compound muscle action potential in the seawater immersion + injury group had a prolonged latency, and the amplitude and nerve conduction velocity were decreased compared with those in the other groups (P<0.05). H&E staining demonstrated that nerve fiber regeneration was worse in the seawater immersion + injury group. The ROS and MDA levels in the seawater immersion + injury group were higher than those in the other groups (P<0.05). The expression levels of iNOS mRNA and protein gradually increased in the injury and seawater immersion + injury groups and peaked at 48 h after surgery. Immersion in seawater further aggravated sciatic nerve injury and led to worse neuronal recovery. The mechanism may be associated with oxidative stress.
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| http://dx.doi.org/10.3892/etm.2015.2281 | DOI Listing |
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