Abstract
Objective To investigate the efficacy of the combination of bone marrow stromal cells （BMSCs） and bcl-2 gene in the treatment cerebral ischemia and its effect on the expression of basic fibroblast growth factor （bFGF） in rats. Methods Forty Wistar rats were used to establish middle cerebral artery occlusion model. They were randomly divided into 4 groups： saline control, hcl-2, BMSCs and BMSCs ＋ bcl-2 groups （n = 10 in each group）. Every group was redivided into 3- and 14-day after reperfusion subgroups （n = 5 in each subgroup）. Neurological scores of the experimental rats were assessed. BMSCs were labeled with bromodeoxyuridine （BrdU）. The distribution and numbers of BMSCs, the expressions of Bcl-2 and bFGF were detected by immunohistochemistry, and apoptotic cells were detected with TUNEL staining in rat brain.Rsults The neurological score at day 3 after reperfusion in the BMSCs ＋ bcl-2 group was significantly lower than that in the saline control group （P 〈 0. 05）, and at day 14, it was significantly lower than that in the other 3 groups （all P 〈0. 05）. A large number of BrdU-positive BMSCs were observed in the infarcted hemisphere in the BMSCs ＋ bcl-2 and BMSCs groups. The numbers of BrdU-positive BMSCs at day 3 and 14 after reperfusion in the BMSCs ＋ bel-2 group were significantly higher than those in the BMSCs group （all P 〈0. 05）. The expressions of Bcl-2 in the infarcted hemisphere at day 3 and 14 after reperfusion in BMSCs ＋bcl-2 group were significantly higher than those in the other 3 groups （all P 〈0.05）. The expressions of Bcl-2 at all time points were increased more significantly than those in the other 3 groups （all P 〈0. 05）. The numbers of apoptosis in brain at all time points in the BMSCs ＋ bcl-2 group were decreased more significantly than those in the other 3 groups （all P 〈0. 05）. Conclusions Both BMSCs and bcl-2 genes have the therapeutic effect on cerebral ischemia. The efficacy of combination of bothof them is significantly superior to monotherapy. They may significantly improve the neurological function and increase the expression of bFGF in rats. Its mechanism may be that bcl-2 genes have inhibited BMSCs apoptosis at the same time of anti-apoptosis in brain. Key words: bone marrow stromal cell; bcl-2; cerebral ischemia; apoptosis; basic fibroblast growth factor
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