7 research outputs found

    Royal jelly can diminish secondary neuronal damage after experimental spinal cord injury in rabbits

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    PubMed: 22538080The aim of this experimental study was to investigate the neuroprotective effect of Royal jelly (RJ) on traumatic spinal cord injury (SCI). Twenty-one New Zealand male rabbits, weighing between 2.5 and 3.0. kg were divided into three groups: Sham (no drug or operation, n= 7), Control (laminectomy. +. single dose of 1. ml/kg saline orally, after trauma; n= 7) and RJ (laminectomy. +. 100. mg/kg RJ, orally, after trauma, n= 7). Laminectomy was performed at T10 and balloon catheter was applied extradurally for traumatic SCI. Four and 24. h after surgery, rabbits were evaluated according to the Tarlov scoring system. Blood, cerebrospinal fluid and tissue sample from spinal cord were taken for measurements of antioxidant status or detection of apoptosis. Four hours after SCI, all animals in control or RJ treated groups became paraparesic. Significant improvement was observed in RJ treated group, 24. h after SCI, with respect to control. Traumatic SCI led to increase in the lipid peroxidation and decrease enzymic or non-enzymic endogenous antioxidative defense systems, and increase in apoptotic cell numbers. RJ treatment mostly prevented lipid peroxidation and also augmented endogenous enzymic or non-enzymic antioxidative defense systems. Again, RJ treatment significantly decreased the apoptotic cell number induced by SCI. © 2012 Elsevier Ltd.Traumatic SCI was found to lead an increase in the lipid peroxidation and a decrease in enzymatic or nonenzymatic endogenous antioxidative defense systems. Furthermore, it was observed that SCI led to apoptosis in spinal cord tissue. A preliminary study was performed to investigate the neuroprotective effect of Royal jelly in spinal cord injury. This work demonstrates for the first time the effect of RJ on SCI. RJ treatment mostly prevented lipid peroxidation, augmented endogenous antioxidative defense systems and prevented apoptosis or neurodeficite following a traumatic SCI. Thus, neuroprotective effect of RJ in the SCI was supported by behavioral, biochemical and histopathological tests. Inhibition of oxidative stress or apoptosis by RJ may have potential therapeutic benefits for reducing secondary damage and improving the outcome after a traumatic SCI. The authors believe that further studies are necessitated about the effect of different doses of RJ or the effect of RJ at different terms after SCI
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