Bone marrow mesenchymal stem cell transplantation inhibits apoptosis in the rat spinal cord injured by acrylamide
10.3969/j.issn.2095-4344.0435
- VernacularTitle:骨髓间充质干细胞移植对丙烯酰胺中毒大鼠脊髓组织细胞凋亡的影响
- Author:
Jing-Song SUN
1
;
Xue-Ying ZHOU
;
Shu-Xian QU
;
Tong-Jing BU
;
Shuang-Yue LI
Author Information
1. 大连医科大学附属第一医院
- From:
Chinese Journal of Tissue Engineering Research
2018;22(5):680-685
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND: Until now, there is no effective treatment for peripheral neuropathy caused by acrylamide. Therefore, it is necessary to explore new treatment methods. OBJECTIVE: To explore the protection role and its mechanism of bone marrow mesenchymal stem cells (BMSCs) against acrylamide-induced intoxication in the spinal cords of rats. METHODS: BMSCs were cultured by the whole bone marrow adherence method and identified by morphological observation and flow cytometry detection. Thirty Sprague-Dawley rats, clean grade, were randomly divided into three groups (n=10 for each group): normal control group, acrylamide group and BMSCs transplantation group. The latter two groups received acrylamide by gavage, 50 mg/(kg?d), 5 days per week, for 2 weeks with an interval of 2 days. Then, in the BMSCs transplantation group, 3×106BMSCs were transplanted by the caudal vein, 5 days per week, for 3 consecutive weeks. Hematoxylin-eosin staining was utilized to observe the morphological changes of the spinal cord. Tunel assay was used to detect cell apoptosis. Western blot assay was adopted to detect the expression levels of Bcl-2 and Bax. RESULTS AND CONCLUSION: In the acrylamide-exposed rats, the damage to the structure was found in the spinal cords by morphological observation, which was significantly alleviated after BMSCs transplantation. The disturbed expression levels of Bax and Bcl-2 were also significantly inversed after BMSCs transplantation (P < 0.05). These results suggest that BMSCs transplantation can inhibit cell apoptosis in the spinal cords of acrylamide-intoxicated rats, probably by up-regulating expression of Bcl-2 and down-regulating expression of Bax.
