Effects and mechanism of the transplantation of human umbilical cord blood msenchymal stem cells to treat spinal cord injury
SUN Li, YU Li, ZHANG Hua-Fang, WANG Li, WEI Zhi-Xin
Chinese Journal of Clinical Anatomy ›› 2011, Vol. 29 ›› Issue (2) : 202-207.
Effects and mechanism of the transplantation of human umbilical cord blood msenchymal stem cells to treat spinal cord injury
Objective To explore the therapeutic effect and mechanism of mesenchymal stem cells (MSCs) derived from human umbilical cord blood on rat spinal cord injury. Methods MSCs were separated and purified from human umbilical cord blood. The spinal cord semi-transection was done on adult rats and then the animals were randomly divided into three groups which were treated with BrdU labeled MSCs, culture medium or saline respectively. Functional outcome was measured using the Basso-Beattie-Bresnehan (BBB) score method periodically up to 28 days post-surgery. MSCs survival and migration were observed by immunofluorescence double labeling techniques. The expression pattern of HMGB1 and NF-κB were detected by immunohistochemical techniques. Results BBB score showed that locomotor improvement in MSCs transplantation groups was much better than that of normal saline group and culture medium group at 28 days post-transplantation (P<0.05). BrdU-labeled MSCs could be detected in the lesion area at 7, 14 and 21 days post-transplantation. 53.3% of transplanted BrdU-positive cells were GFAP-positive, and 22.15% of them were NSE-positive. The positive rate of HMGB1 and NF-κB expression in MSCs transplantation group were lower than that in saline group and culture medium group, and there was a significant differences among three groups (P<0.05). Conclusions MSCs could promote functional recovery of the injuried spinal cord by replacing damaged nerve cells and alleviating inflammatory reaction.
Human umbilical cord blood / Mesenchymal stem cells / Spinal cord injury / Regeneration
[1] 李德华,单伟,韩静,等
[G2]. 人脐静脉间充质干细胞向胰岛β样细胞诱导分化的实验研究
[J].中国临床解剖学杂志，2007，25（4）：424-426.
[2] 张炳强,于丽,张雪莉,等.丹参素联合生长因子体外诱导人脐血间充质干细胞分化为神经细胞的研究
[J].神经解剖学杂志,2009,25（1）:63-67.
[3] Cho SR, Kim YR, Kang HS, et al.Functional recovery after the transplantation of neurally differentiated mesenchymal stem cells derived from bone barrow in a rat model of spinal cord injury
[J]. Cell Transplant,2009,18(12):1359-1368.
[4] Lee JK, Jin HK, Endo S, et al. Intracerebral transplantation of bone marrow-derived mesenchymal stem cells reduces amyloid-beta deposition and rescues memory deficits in Alzheimer's disease mice by modulation of immune responses
[J]. Stem Cells, 2010, 28(2):329-343.
[5] Lee HJ, Lee JK, Lee H, et al. The therapeutic potential of human umbilical cord blood-derived mesenchymal stem cells in Alzheimer's disease
[J]. Neurosci Lett, 2010, 481(1):30-35.
[6] Lee HJ, Lee JK, Lee H, et al. Human umbilical cord blood-derived mesenchymal stem cells improve neuropathology and cognitive impairment in an Alzheimer's disease mouse model through modulation of neuroinflammation
[J]. Neurobiol Aging, 2010,3(24)
[Epub ahead of print]
[7] Cizkova D, Rosocha J, Vanicky I, et al. Transplants of human mesenchymal stem cells improve functional recovery after spinal cord injury in the rat
[J]. Cell Mol Neurobiol,2006, 26(7-8): 1165-1178.
[8] Bae JS, Carter JE, Jin HK. Adipose tissue-derived stem cells rescue Purkinje neurons and alleviate inflammatory responses in Niemann-Pick disease type C mice
[J]. Cell Tissue Res,2010,340(2):357-369.
[9] Erlandsson H, Andersson U. The nuclear protein HMGB1 as a proinflammatory mediator
[J].Eur J Immunol,2004,34(6):1503-1512.
[10]Palmubo R，Binaehi ME. High mobility group boxl，a cue for stem cell recruitment
[J].Biochem Pharmacol, 2004, 68(6):1165-1170.
[11]Degryse B, Virgilio MD. The nuclear Protein HMGBI，a new kind of chemokine
[J] . FEBS Lett, 2003, 553(l-2):11-17.
[12]Palumbo R, Sampaolesi M, Marchis FD. Extracellular HMGB1,a signal of tissue damage, induces mesoangioblast migration and proliferation
[J].Cell Biol, 2004,164(3):441-449.
[13]Compagno M, Lim WK, Grunn A. Mutations of multiple genes cause deregulation of NF-kappaB in diffuse large B-cell lymphoma
[J]. Nature, 2009, 459(7247):717-721.
[14]Huttunen HJ, Fages C, Rauvala H. Receptor for advanced glycation end products(RAGE)-mediated neurite outgrowth and activation of NF-kappaB require the cytoplasmic domain of the receptor but different downstream signaling pathways
[J].J Biol Chem,1999,274(28):19919-19924.
[15]Bachis A, Colangelo AM, Vicini S, et al. Interleukin-10 prevents glutamate-mediated cerebellar granule cell death by blocking caspase-3-like activity
[J].J Neurosci ,2001,21(9):3104-3012.
/
| 〈 |
|
〉 |
