BACKGROUND:Recent studies have found that stem cels can directly differentiate into mature myocardial cels or promote their regeneration, providing a new therapeutic strategy for the treatment of myocardial infarction. However, the low cel transplantation rate reduces the myocardial differentiation ability and myocardial repair.
OBJECTIVE: To study the role of heat shock treatment in Sca-1+ cel transplantation for treatment of myocardial infarction in mice.
METHODS:Sca-1+ cels were isolated from the bone marrow of mice using magnetic bead sorting method, and were subjected to heat shock treatment. Animal models of myocardial infarction were made in mice, and then randomized into two groups: heat shock group and non-heat shock group, which were given 1 mL heat shock-treated Sca-1+ cels and 1 mL non-heat shock-treated Sca-1+ celsvia the tail vein, respectively. After transplantation, cel survival, heart function, myocardial cel apoptosis and myocardial fibrosis were detected. Meanwhile, the expressions of heat shock factor (HSP), HSP70 and miR-34a in the left ventricle were measured.
RESULTS AND CONCLUSION:(1) The expression of sry gene in the heat shock group was significantly higher than that in the non-heat shock group. (2) The left ventricular ejection fraction and fractional shortening in the heat shock group were significantly higher than those in the non-heat shock group. The left ventricular end-diastolic diameter and systolic diameter in the heat shock group were significantly lower than those in the non-heat shock group. (3) The cardiac fibrosis and myocardial cel apoptosis in the heat shock group were significantly lower than those in the non-heat shock group. (4) The HSF and HSP70 expression in the left ventricle was significantly higher in the heat shock group than the non-heat shock group, and the miR-34a expression in the left ventricle was significantly lower in the heat shock group than the non-heat shock group. These findings indicate that heat shock-treated Sca-1+ cel transplantation can reduce myocardial apoptosis and infarct size, and improve heart function of mice with myocardial infarction.

Objective:To investigate the promotive effect of 4,5,6,7-tetrabromobenzotriazole (TBB) on the apoptosis of the human cervical cancer HeLa cells,and to clarify its effect mechanism in related signaling pathways.Methods:The human cervical cancer HeLa cells at logarithmic growth phase were divided into control group(without TBB) and experiment group(with TBB).MTT assay was used to detect the survival rate of the HeLa cells;the morphology of HeLa cells was observed under inverted microscope;Annexin Ⅴ-FITC/PI double staining and flow cytometry(FCM) were used to determine the apoptotic rates of the HeLa cells;the expression levels of apoptosis-related proteins p-Akt,Akt,Bcl-2,Bax,cleaved-caspase-3,and Pro-caspase-3 were detected by Western blotting method.Results:The MTT results showed that the survival rates of the HeLa cells in experiment group were significantly decreased(P<0.01) in a dose-dependent manner compared with control group.The apoptotic morphology of the HeLa cells in experiment group were found as cell shrinkage and karyopyknosis under inverted microscope.The Annexin Ⅴ-FITC/PI double staining and FCM results showed that the apoptotic rates of the HeLa cells in experiment group (3,6,12 and 24 h) were higher than that in control group (P<0.05 or P<0.01).The Western blotting results showed that compared with control group,the expression levels of the anti-apoptotic proteins p-Akt and Bcl-2 in HeLa cells in experiment group were decreased obviously,whereas the expression levels of the pro-apoptotic proteins Bax and cleaved-caspase-3 were increased and the expression levels of Pro-caspase-3 were decreased.Conclusion:TBB may promote the apoptosis of human cervical cancer HeLa cells by inhibiting the Akt signaling pathway.