Sleep deprivation alters prostaglandin and anti-oxidant enzymes in rats induced with neuropathic pain

Abstract

Human studies of sleep and pain are particularly challenging and must confront potential confounds such as co-existing disease and poly pharmacy. As an example of co-existing disorders, more than 40% of individuals with symptoms of insomnia report at least one chronic painful physical condition. The effects of 72 hours Rapid eye movement sleep deprivation (REMSD) was investigated on serum levels of nociceptive mediator (Prostagladin E2-PGE2) and oxidative stress markers (Malondialdehyde-MDA & Super oxide dismutase-SOD) in rats with neuropathic pain. Twenty male Wistar rats were divided into 4 groups (un-ligated control, ligated control, sham control and test), each containing 5 rats. All the animals were ligated by chronic constriction injury (CCI) of the sciatic nerve except those in sham and un-ligated control groups. This was followed by 72 hours of REMSD using the multiple platform method, after which the serum level of PGE2, SOD and MDA were assessed. The induction of 72 hours REMSD led to a significant (P<0.05) decrease in serum PGE2 in test group compared with ligated control. This study also showed that REMSD reduced production of reactive oxygen species as shown by a significant (P<0.05) decrease in serum MDA and an insignificant decrease in serum SOD compared with ligated control group. In conclusion, 72 hours REMSD showed a decrease in serum levels of PGE2, MDA, and insignificant decrease in SOD in sciatic nerve-ligated Wistar rats. It can be deduced from this study that 72 hours REMSD has hypoalgesic effect on rats with neuropathic pain.