Transplantation of Human Amniotic Mesenchymal in the Treatment of Focal Cerebral IschemiaXue-Guang Zhang1*, Fang Li1, 2, Zong-Ning Miao3, Yun-Yun Xu 4, Shi-Ying Zheng5, Ming-De Qin1 and Yan-Zheng Gu1
- *Corresponding Author:
- Xue-Guang Zhang
Institute of Medical Biotechnology
Soochow University, Jiangsu Province Key Laboratory of Stem Cells
No. 1 Shixin, Street Canglang District
Suzhou, 215007, China
E-mail: [email protected]
Received date February 18, 2012; Accepted date June 20, 2012; Published date June 22, 2012
Citation: Zhang XG, Li F, Miao ZN, Xu YY, Zheng SY (2012) Transplantation of Human Amniotic Mesenchymal in the Treatment of Focal Cerebral Ischemia. Anat Physiol S3:001. doi:10.4172/2161-0940.S3-001
Copyright :© 2012 Zhang XG, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
This study examined the potential of human amniotic mesenchymal (hAMSC) transplantation in repairing neurological deficits in an experimental focal cerebral ischemia model. Following isolation of hAMSC, growth characteristics and surface antigen expression was observed. Butylated hydroxyanisole (BHA) was used to induce the cultured cells into neuron-like cells, identified by immunocytochemistry. The suture model was used to induce focal cerebral ischemia in the rats, which were subsequently randomly divided into experimental and control groups for treatment with BrdU-labeled hAMSCs or PBS, respectively. Neurological deficits were assessed after transplantation using the Neurological Severity Scores, Beam Balance Test, and Elevated Body Swing Test. Eight weeks later rat brain tissue was processed for hematoxylin-eosin staining and BrdU immunohistochemistry, and survival and spatial distribution of transplanted hAMSCs. hAMSCs proliferated in vitro, and neuron specific enolase expressed in neurons and glial fibrillary acidic protein in astrocytes. The focal ischemia model resulted in varying degrees of left limb hemiplegia accompanied by the right side of Horner’s sign. When examined 1, 3, 6 and 8 weeks later, significant recovery in the neurological behavior was detected in the rats treated with the hAMSC transplantation compared to the control (P<0.01). BrdU-labeled hAMSCs were concentrated near the graft site and surrounding areas, in some cases migrating towards the ischemic lesion. Local gliosis and lymphocytic infiltration were not detected. hAMSC exhibit great potential for proliferation, and can be induced to differentiate into NSE-expressing neuron-like cells following treatment with BHA. Moreover, hAMSC transplantation may improve neurological symptoms after focal cerebral ischemia.