Regulation of Transplantation of Human Umbilical Cord Blood Derived Mesenchymal Stem Cells on Secretion of Neural Biochemistry Marker after Traumatic Brain Injury in Rats_Journal of Biomedical Engineering

Authors：

ZHAOJunjian ¹ ,  SHIJun ¹ , SHAOKun ¹ , WANGYi ¹ , MENGAiguo ¹ , ZENGXiaofang ² , CHENNaiyao ¹

1. The Affiliated Hospital, Hebei United University, Tangshan 063000, China;
2. Tangshan Twenty-two Metallurgical Construction Group Hospital, Tangshan 063000, China;

Corresponding author：

SHIJun, Email: mytsmyts@126.com

Keywords：

human umbilical cord blood mesenchymal stem cell; traumatic brain injury; S100βprotein; neuron specific enolase

DOI：

10.7507/1001-5515.20150028

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This research was to study the regulation of intravenous administration of human umbilical cord blood mesenchymal stem cells (HUCBMSCs) on secretion of neural specific protein in rats after traumatic brain injury (TBI), and to explore its mechanisms promoting the recovery of neurological function. The TBI models of rats were established. We then injected HUCBMSCs, labelled by Brdu (5-bromo-2-deoxyuridine), into the TBI rats via the tail vein using modified Feeney free-falling method. The levels of neural biochemical indicators (serum S100βprotein, NSE, LDH, CK) of rats were detected in shamed group, injury group and HUCBMSCs-transplanted group. And the morphological changes of brain tissue of rats in the three groups were observed by using HE staining under light microscope. During the whole experiment no immunosuppressant was used for the four groups. From the research, transplant-related death of the rats was not found in transplantation group. In the injury group, rises were found in contents of serum S100βprotein, NSE, LDH, CK in the early stage after the rats were injured, which were much higher than those in shamed group at correspondent time point(P < 0.01). In HUCBMSCs-transplanted group, although these biochemistry indexes were found rising for a short period in the early stage, along with the time, these indexes were obviously lower than in those injury group (P < 0.05). Under light microscopy pathological changes of rats in HUCBMSCs-transplanted group were much slighter than those in injury group. It was well concluded that in the situation of no immuno-suppressants, the intravenous-injected HUCBMSCs could reduce the secretion of serum S100βprotein, NSE, LDH, CK, promote the repair of tissue injury effectively, and promote the functional recovery of neurons.

Citation： ZHAOJunjian, SHIJun, SHAOKun, WANGYi, MENGAiguo, ZENGXiaofang, CHENNaiyao. Regulation of Transplantation of Human Umbilical Cord Blood Derived Mesenchymal Stem Cells on Secretion of Neural Biochemistry Marker after Traumatic Brain Injury in Rats. Journal of Biomedical Engineering, 2015, 32(1): 152-156. doi: 10.7507/1001-5515.20150028 Copy

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10.	SHENG J G, ITO K, SKINNER R D, et al. In vivo and in vitro evidence supporting a role for the inflammatory cytokine interleukin-1 as a driving force in Alzheimer pathogenesis[J]. Neurobiol Aging, 1997, 17(5): 761-766.
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12.	RAGHUPATHI R. Cell death mechanisms following traumatic brain injury[J]. Brain Pathol, 2004, 14(2): 215-222.
13.	HAUSMANN R, BIERMANN T, WIEST I, et al. Neuronal apoptosis following human brain injury[J]. Int J Legal Med, 2004, 118(1): 32-36.
14.	BIANCHI R, GIAMBANCO I, DONATO R. S100B/RAGE-dependent activation of microglia via NF-kappaB and AP-1 Co-regulation of COX-2 expression by S100B, IL-1beta and TNF-alpha[J]. Neurobiol Aging, 2010, 31(4): 665-677.
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19.	ZHAO J J, CHEN N Y, SHEN N, et al. Transplantation of human umbilical cord blood mesenchymal stem cells to treat a rat model of traumatic brain injury[J]. Neural Regen Res, 2012, 7(10): 741-748.

1. WALKER P A, SHAH S K, HARTING M T, et al. Progenitor cell therapies for traumatic brain injury: barriers and opportunities in translation[J]. Dis Model Mech, 2009, 2(1/2): 23-38.
2. NASEF A, ASHAMMAKHI N, FOUILLARD L. Immunomodulatory effect of mesenchymal stromal cells: possible mechanisms[J]. Regen Med, 2008, 3(4): 531-546.
3. FEENEY D M, BOYESON M G, LINN R T, et al. Responses to cortical injury:Ⅰ. Methodology and local effects of contusions in the rat[J]. Brain Res, 1981, 211(1): 67-77.
4. SECCO M, ZUCCONI E, VIEIRA N M, et al. Multipotent stem cells from umbilical cord: cord is richer than blood![J]. Stem Cells, 2008, 26(1): 146-150.
5. BAKSH D, YAO R, TUAN R S. Comparison of proliferative and multilineage differentiation potential of human mesenchymal stem cells derived from umbilical cord and bone marrow[J]. Stem Cells, 2007, 25(6): 1384-1392.
6. LAMERS K J, VOS P, VERBEEK M M, et al. Protein S-100B, neuron-specific enolase (NSE), myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP) in cerebrospinal fluid (CSF) and blood of neurological patient4s[J]. Brain Res Bull, 2003, 61(3): 261-264.
7. SEN J, BELLI A. S100B in neuropathologic states: the CRP of the brain?[J]. Neurosci Res, 2007, 85(7): 1373-1380.
8. TIAINEN M, ROINE R O, PETTILA V, et al. Serum neuron-specific enolase and S-100B protein in cardiac arrest patients treated with hypothermia[J]. Stroke, 2003, 34(12): 2881-2886.
9. DERKACH D N, OKAMOTO H, TAKAHASHI S. Neuronal and astroglial injuries in patients undergoing coronary artery bypass grafting and aortic arch replacement during hypothermic cardiopulmonary bypass[J]. Anesth Analg, 2000, 91(5): 1066-1072.
10. SHENG J G, ITO K, SKINNER R D, et al. In vivo and in vitro evidence supporting a role for the inflammatory cytokine interleukin-1 as a driving force in Alzheimer pathogenesis[J]. Neurobiol Aging, 1997, 17(5): 761-766.
11. SCOTTO C, DELOULME J C, ROUSSEAU D, et al. Calcium and S100B regulation of p53-dependent cell growth arrest and apoptosis[J]. Mol Cell Biol, 1998, 18(7): 4272-4281.
12. RAGHUPATHI R. Cell death mechanisms following traumatic brain injury[J]. Brain Pathol, 2004, 14(2): 215-222.
13. HAUSMANN R, BIERMANN T, WIEST I, et al. Neuronal apoptosis following human brain injury[J]. Int J Legal Med, 2004, 118(1): 32-36.
14. BIANCHI R, GIAMBANCO I, DONATO R. S100B/RAGE-dependent activation of microglia via NF-kappaB and AP-1 Co-regulation of COX-2 expression by S100B, IL-1beta and TNF-alpha[J]. Neurobiol Aging, 2010, 31(4): 665-677.
15. HERRMANN M, JOST S, KUTZ S, et al. Temporal profile of release of neurobiochemical markers of brain damage after traumatic brain injury is associated with intracranial pathology as demonstrated in cranial computerized tomography[J]. J Neurotrauma, 2000, 17(2): 113-122.
16. SABARIRAJAN J, VIJAYARAJ P, NACHIAPPAN V. Induction of acute respiratory distress syndrome in rats by lipopolysaccharide and its effect on oxidative stress and antioxidant status in lung[J]. Indian J Biochem Biophys, 2010, 47(5): 278-284.
17. CAKIR B, KASIMAY O, KOLGAZI M, et al. Stress-induced multiple organ damage in rats is ameliorated by the antioxidant and anxiolytic effects of regular exercise[J]. Cell Biochem Funct, 2010, 28(6): 469-479.
18. ERARSLAN E, EKIZ F, UZ B, et al. Effects of erdosteine on cyclosporine-A-induced hepatotoxicity in rats[J]. Drug Chem Toxicol, 2011, 34(1): 32-37.
19. ZHAO J J, CHEN N Y, SHEN N, et al. Transplantation of human umbilical cord blood mesenchymal stem cells to treat a rat model of traumatic brain injury[J]. Neural Regen Res, 2012, 7(10): 741-748.

Journal of Biomedical Engineering

Regulation of Transplantation of Human Umbilical Cord Blood Derived Mesenchymal Stem Cells on Secretion of Neural Biochemistry Marker after Traumatic Brain Injury in Rats

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