Different Effect by Different Starting Time Point of Exercise of the Nerve Regeneration after the Peripheral Nerve Injury
AUTHORS
Jae Sung Park,Kongju National University
ABSTRACT
Starting time point of exercise intervention is a hot issue in the field of exercise therapy. Some researchers insist that the exercise interventions should started from early period of rehabilitation but the others insist that the exercise interventions should started from later period that followed the first step of recovery period. This hot issue spread to peripheral nerve injury patients and therapist too. After the peripheral nerve injury, injured nerve fibers degenerated from distal to lesion. This degenerating process is known as the Wallerian degeneration.During this Wallerian degeneration process, macrophages remove the debris of axon and myelin that were damaged from injury. Without this cleaning process by macrophages, axons could not reconnect well and the whole process of nerve regeneration can’t be perfect. So the recruitment of macrophages during this Wallerian degeneration process could be crucial to peripheral nerve regeneration whole process. Treadmill exercise is widely used for motor rehabilitation and general health control in many field of therapy. Especially for the peripheral nerve rehabilitation, treadmill exercise interventions used open. So we investigate the effects of treadmill exercise on Wallerian degeneration process and analyze the benefits of treadmill exercise on peripheral nerve regeneration. We had investigated the type of macrophages and biomarkers to analyze the beneficial effects of treadmill exercise intervention on the Wallerian degeneration models. The main goal of this experiment was to compare and analyze the effects of early started exercise group and later started exercise group. With our study results, we have conclude that the later started exercise had better beneficial effect to the peripheral nerve regeneration.
KEYWORDS
Treadmill exercise, Wallerian degeneration, Macrophage, Peripheral nerve regeneration.
REFERENCES
[1] Ghiani CA, Ying Z, de Vellis J, Gomez-Pinilla F. “Exercise decreases myelin-associated glycoprotein expression in the spinal cord and positively modulates neuronal growth”. Glia; Vol.55, pp.966-975. (2007)
[2] Van Praag H, Kempermann G, Gage FH. “Running increases cell proliferation and neurogenesis in the adult mouse dentate gyrus”. Nature Neuroscience; Vol.2, pp.266-270. (1999)
[3] Molteni R, Zheng JQ, Ying Z, Gomez-Pinilla F, Twiss JL. “Voluntary exercise increases axonal regeneration from sensory neurons”. Proceedings of the National Academy of Sciences U S A; Vol.101, pp.8473-8478. (2004)
[4] Edgerton VR, Tillakaratne NJ, Bigbee AJ, de Leon RD, Roy RR. “Plasticity of the spinal neural circuitry after injury”. Annual Review of Neuroscience; Vol.27, pp.145-167. (2004)
[5] Park JS, Hoke A. “Treadmill exercise induced functional recovery after peripheral nerve repair is associated with increased levels of neurotrophic factors”. PLoS One; Vol.9, e90245. (2014)
[6] Chen ZL, Yu WM, Strickland S. “Peripheral regeneration”. Annual Review of Neuroscience; Vol.30, pp.209-233. (2007)
[7] Mueller M, Leonhard C, Wacker K, Ringelstein EB, Okabe M, Hickey WF, Kiefer R. “Macrophage response to peripheral nerve injury: the quantitative contribution of resident and hematogenous macrophages”. Laboratory Investigation; Vol.83, pp.175-185. (2003)
[8] Fawcett JW, Keynes RJ. “Peripheral nerve regeneration”. Annual Review of Neuroscience; Vol.13, pp.43-60. (1990)
[9] Ancuta P, Liu KY, Misra V, Wacleche VS, Gosselin A, Zhou X, Gabuzda D. “Transcriptional profiling reveals developmental relationship and distinct biological functions of CD16+ and CD16- monocyte subsets”. BMC Genomics; Vol.10, pp. 403-2164-10-403. (2009)
[10] De Sousa JR, de Sousa RP, Aarao TL, Dias LB,Jr, Carneiro FR, Fuzii HT, Quaresma JA. “In situ expression of M2 macrophage subpopulation in leprosy skin lesions”. Acta Tropica; Vol.157, pp.108-114. (2016)
[11] Nishikawa K, Seo N, Torii M, Ma N, Muraoka D, Tawara I. “Interleukin-17 induces an atypical M2-like macrophage subpopulation that regulates intestinal inflammation”. PLoS One; Vol.9, e108494. (2014)
[12] Schug TT, Li X. “PPARdelta-mediated macrophage activation: a matter of fat”. Disease Models & Mechanisms; Vol.2, pp.421-422. (2009)
[13] Casella G, Garzetti L, Gatta AT, Finardi A, Maiorino C, Ruffini F. “IL4 induces IL6-producing M2 macrophages associated to inhibition of neuroinflammation in vitro and in vivo”. J Neuroinflammation; Vol.13, pp.139-016-0596-5. (2016)
[14] Yakeu G, Butcher L, Isa S, Webb R, Roberts AW, Thomas AW, “Low-intensity exercise enhances expression of markers of alternative activation in circulating leukocytes: roles of PPARgamma and Th2 cytokines”. Atherosclerosis; Vol.212, pp.668-673. (2010)
[15] Bouhlel MA, Derudas B, Rigamonti E, Dièvart R, Brozek J, Haulon S, Zawadzki C, Jude B, Torpier G, Marx N, Staels B, Chinetti-Gbaguidi G. “PPARgamma activation primes human monocytes into alternative M2 macrophages with anti-inflammatory properties”. Cell Metabolism. Aug; Vol. 6, No. 2, pp.137-43. (2007)