RESUMO
BACKGROUND: At present, cell patch technology has been widely used in the repair of various tissues and organs such as periodontal ligament, cornea, heart, cartilage, and esophagus. However, the effect and mechanism of basic fibroblast growth factor (bFGF) on the proliferation and osteogenic differentiation of bone marrow mesenchymal stem cell patches are still unknown. It is of great significance for understanding how to integrate growth factor with tissueengineered cell patch technology for the final use in tissue engineering repairing. OBJECTIVE: To investigate the expression of angiogenesis-related factors in rat bone marrow mesenchymal stem cell patch during bFGF-induced osteogenic differentiation. METHODS: After isolation, purification and identification, rat bone marrow mesenchymal stem cell patches were constructed by continuous induction of vitamin C and divided into two groups: bFGF group (20 µg/L bFGF+osteoinductive medium) and control group (osteoinductive medium). The expression of angiogenesis-related genes was detected by alizarin red staining at 7 and 14 days of osteogenic induction and by fluorescence quantitative PCR method at 10 days of osteogenic induction. RESULTS AND CONCLUSION: The results of alizarin red staining showed that the number of calcified nodules in the bFGF group was significantly higher than that in the control group. The expression of transforming growth factor Β1 mRNA in the bFGF group was significantly higher than that in the control group, while the expression of vascular endothelial growth factor, angiopoietin 1 and platelet-derived factor BB was lower than that in the control group. Together, these results demonstrate that bFGF can induce the osteogenic differentiation of rat bone marrow mesenchymal stem cell patches, and increase the expression of transforming growth factor Β1 in the late osteogenic stage.
RESUMO
Aim To investigate the antiarrhythmic mechanism of taurine-magnesium coordination com-pound on abnormal sodium current channel ( INa ) in-duced by hypoxia-reoxygenation in ventricular myocytes of rats. Methods Single ventricular myocytes were i-solated from each rat heart using enzymatic dissociation through Langendorff retrograde aortic perfusion. Whole-cell patch clamp was applied in voltage clamp mode to record INa both in normal ventricular myocytes and single ventricular myocytes of arrhythmia induced by hypoxia-reoxygenation. Results The peak density of INa was changed from ( 56. 89 ± 2. 07 ) pA/pF to (35. 05 ± 1. 52) pA/pF( n=6, P 0. 05), in a concentration-dependent manner, while amioda-rone restored it to (39. 44 ± 1. 24) pA/pF (n=6,P<0. 01 ) . Both high concentration of TMCC and amioda-rone could shift the I-V curve downward. In addition, TMCC and amiodarone could restore the INa inactivation curve and slow down its inactivation, whereas the acti-vation curves showed no significant differences among groups. Conclusion TMCC(200,400 μmol·L-1) could restore the H/R induced INa reduction and shift the I-V curve downward by inhibiting steady-state inac-tivation, which is suggested to be one of the mecha-nisms of the antiarrhythmic effects of TMCC in hypoxia-reoxygenation model.