6533b83afe1ef96bd12a70e7

RESEARCH PRODUCT

Does granulocyte-colony stimulating factor stimulate peripheral nerve regeneration? An experimental study on traumatic lesion of the sciatic nerve in rats.

Clemens SommerOliver KempskiHarald Von PeinAxel HeimannJacek SzczygielskiJoachim OertelAndreas KramerDoerthe Keiner

subject

Traumatic brain injuryLesionGranulocyte Colony-Stimulating FactormedicineAnimalsHumansbiologybusiness.industrySciatic nerve injuryNerve injurymedicine.diseaseSpinal cordSciatic NerveGranulocyte colony-stimulating factorNerve RegenerationRatsDisease Models Animalmedicine.anatomical_structureAnesthesiabiology.proteinSurgeryNeurology (clinical)Sciatic nervemedicine.symptomSciatic NeuropathybusinessNeurotrophinGranulocytes

description

Aim of the study. To analyse the therapeutic potential of granulocyte-colony stimulating factor (G-CSF) treatment using a rat model of traumatic sciatic nerve lesion. Clinical rationale for the study. G-CSF has proven strong neurotrophic properties in various models of ischaemic and traumatic brain injury. Fewer studies exist regarding the influence of G-CSF on posttraumatic peripheral nerve regeneration. Currently, the possibilities of pharmacological prevention or treatment of mechanical nerve injury are limited, and there is an urgent need to find new treatment strategies applicable in clinical situations. Material and methods . A controlled traumatic right sciatic nerve lesion was set using a waterjet device. Three treatment groups were created. In the first group, G-CSF was administered after sciatic nerve injury. The second group received G-CSF before and after trauma, while the third group was treated with glucose 5%-solution. Sciatic nerve function was assessed clinically and electrophysiologically at day 1, and after weeks 1, 2, 4 and 6. Additionally, α-motoneurons of the spinal cord and sciatic nerve fibres were counted at week 6. Results. Clinically, rats in both G-CSF groups improved faster compared to the control group. Additionally, animals treated with G-CSF had a significantly better improvement of motor potential amplitude and motor nerve conduction velocity at week 6 (p < 0.05). Histologically, G-CSF treatment resulted in a significantly higher number of α-motoneurons and small myelinated nerve fibres compared to placebo treatment (p < 0.05). Conclusions and clinical implications. Under G-CSF treatment, the recovery of motor nerve conduction velocity and amplitude was enhanced. Further, signs of nerve regeneration and preservation of α-motoneurons were observed. These results indicate that G-CSF might accelerate and intensify the recovery of injured nerves. Thus, treatment with G-CSF may be beneficial for patients with peripheral nerve damage, and should be explored in further clinical studies.

10.5603/pjnns.a2021.0075https://pubmed.ncbi.nlm.nih.gov/34664711