Paracrine action of bone marrow mesenchymal stem cells and cell apoptosis following cerebral ischemia
10.3969/j.issn.1673-8225.2010.01.001
- VernacularTitle:骨髓间充质干细胞旁分泌作用与脑缺血后的细胞凋亡
- Author:
Feng CHENG
;
Lixin LI
;
Huaiyong HAO
;
Heping TIAN
;
Xueliang DAI
;
Weixing HU
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2010;14(1):1-5
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND: One of mechanisms involved in treating cerebral ischemia with bone marrow mesenchymal stem cells (BMMSCs) implantation is paracrine action. However, few studies have reported this mechanism.OBJECTIVE: To observe the inhibitory effect of BMMSCs paracrine action on apoptosis and its mechanism after cerebral ischemia. METHODS: BMMSCs were isolated from rats with adherent culture. Rat cerebral ischemia model was established by the middle cerebral artery occlusion. A total of 24 rats were divided into 4 groups, with 6 animals in each group. Cell implantation medication group: rats were received U0126 medication after BMMSCs implantation; Non-implantation medication group: rats were received U0126 medication after PBS injection; Cell implantation control group: received solvent medication after BMMSCs implantation; Non-implantation control group: received solvent medication after PBS injection. At 7 days after operation, the expressions of vascular endothelial cell growth factor (VEGF) and p-ERK1/2 protein were measured by Western blot analysis, and the apoptosis cells in the area of ischemic penumbra and cortex were examined by TUNEL. RESULTS AND CONCLUSION: The VEGF protein content in the brain tissue was significantly greater in the cell implantation groups than that of the non-implantation group, with increased p-ERK1/2 and decreased apoptosis cells. The expression of p-ERK1/2 was down-regulated in rats which were administrated U0126 while the number of the apoptosis cells was increased, but the VEGF protein expression had no statistical difference. It suggested that BMMSCs can paracrine VEGF in the striatum of brain and play an inhibitory effect on apoptosis in the ischemia area via activating ERK1/2.
