Abstract
BackgroundRoot avulsion of the brachial plexus causes an oxidative stress reaction in the spinal cord and induces dramatic spinal motoneuron death, while EGb761 is a natural free radical cleaning agent. This study was designed to investigate the protective effects of intraperitoneally injected EGb761 against neural damage following brachial root avulsion.MethodsThe effect of EGb761 on avulsion-induced motoneuron injury was studied in 26 total groups of (n) rats, treated as follows. Animals in singular number groups received EGb761(50 mg/kg.d) and those in complex number groups received normal saline solution (i.p.), serving as controls. Groups 1-8 were used for the determination of nitric oxide (NO) levels in the serum and injured spinal cord at the 5 d, 2 w, 4 w, and 6 w time points. Groups 9-16 were used for determination of constitutive nitric oxide synthase (cNOS) and inducible nitric oxide synthase (iNOS) levels in injured spinal cord at the 5 d, 2 w, 4 w, and 6 w time points. Groups 17-26 were used for determination of the number of neuronal nitric oxide synthase (nNOS)-positive and surviving motoneurons in injured C7 ventral horn at the 5 d, 2 w, 4 w, 6 w and 8 w time points.ResultsCompared to control groups, the EGb761 treatment group not only had significant decreased levels of NO in serum at 2 w and 6 w after avulsion, but also had reduced levels of NO specifically in the spinal cord at 2 w, 4 w and 6 w. The cNOS activity in the spinal cord was also significant decreased at 2 w and 4 w, while the iNOS activity in injured C6-T1 spinal segments was reduced at 2 w, 4 w and 6 w. All together, the percentages of NADPH-d positive motoneurons in an injured C7 segment were down-regulated and the number of surviving motoneurons in injured C7 ventral horn was increased at 2 w, 4 w, 6 w and 8 w in treated versus untreated animals.ConclusionsIntraperitoneal administration of EGb761 after root avulsion of the brachial plexus exerted protective effects by decreasing the level of NO in spinal cord and serum and the activity of cNOS and iNOS, easing the delayed motoneurons death. EGb761 should be considered in the treatment of brachial plexus nerve injuries.
Highlights
Brachial plexus injuries in adults are commonly caused by auto or motorcycle accidents
Our present study found that EGb761 protects motoneurons against avulsion injury and that this neuroprotective effect was related to the reduction of both nitric oxide (NO) and NOS in the injured spinal cord
Treatment with EGb761 regulated constitutive nitric oxide synthase (cNOS) and inducible nitric oxide synthase (iNOS) activity in injured C6-T1 spinal segments Root avulsion resulted in a change in cNOS and iNOS activity in injured C6-T1 spinal segments
Summary
Brachial plexus injuries in adults are commonly caused by auto or motorcycle accidents. De novo expression of neuronal NOS (nNOS) was observed in injured motoneurons, and the time course and density of nNOS expression both correlated well with the severity of motoneuron death following brachial root avulsion, in which the oxidant peroxynitrite played an important role [15,16]. This raises the question of whether EGb761 has a similar neuroprotective effect on avulsion-injured motoneurons. Our present study found that EGb761 protects motoneurons against avulsion injury and that this neuroprotective effect was related to the reduction of both NO and NOS in the injured spinal cord. This study was designed to investigate the protective effects of intraperitoneally injected EGb761 against neural damage following brachial root avulsion
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