Objective To study the mechanisms and treatment of ischemia /reperfusion injury, expression of intracellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) were measured, the effect on suppression of ICAM-1 and VCAM-1 by the pyrrolidine dithiocarbamate (PDTC) were investigated. Methods Endothelial cells were divided into 3 groups, hypoxia group: endothelial cells were exposed in hypoxia condition, then returned to reoxygenation condition; the PDTC group: PDTC was added to the endothelial cells in the culture media before exposing to hypoxia condition; control group: endothelial cells underwent treatment. Confocal microscopy was used to detect expression of ICAM-1 and VCAM-1. Results ICAM-1 and VCAM-1 expression were low in endothelial cells of control group, and increased in hypoxia group . ICAM-1 and VCAM-1 expression of endothelial cells in PDTC group werelower than those in hypoxia group , but higher than those in control group. Conclusions It seems that hypoxia/ reoxygenation can activate the endothelial cells and increase the expression of cell adhesion molecules. PDTC can decrease the expression of ICAM-1 and VCAM-1. PDTC may prove benificial in the treatment of ischemia /reperfusion injury.
Objective To explore the effects of calcitonin gene-related peptide (CGRP) on the migration of bone marrow mesenchymal stem cells (BMSCs) and vascular endothel ial growth factor (VEGF) expression in vitro. Methods TheBMSCs were isolated from Sprague Dawley rats using whole bone marrow adherence method. At 1, 2, and 3 weeks after culture, the expressions of CGRP receptor (CGRPR) was detected by Western blot. The BMSCs were treated with CGRP at concentration 1 × 10-8 mol/L (experimental group) and did not treated (control group), and the efficacy of BMSCs migration was analyzed by Transwell chamber assay after 72 hours; at 1, 3, 5, and 7 days, the mRNA expressions of vascular cell adhesion molecule 1 (VCAM-1) were detected by real-time fluorescent quantitative PCR; the protein expressions of VEGF were examined using immunohistochemistry and Western blot. Results CGRPR expressed stably in the cultured BMSCs and reached the peak at 2 weeks. CGRP had a significantly enhanced role in promoting cell migration. The number of cell migration was (3.20 ± 1.77) cells/HP in experimental group and (1.11 ± 0.49) cells/HP in control group, showing significant difference (t=4.230, P=0.001). In experimental group, the expressions of VCAM-1 mRNA increased with time and reached the peak at 7 days. There were significant differences in the expressions of VCAM-1 mRNA between control group and experimental group at 3, 5, and 7 days (P lt; 0.05). Immunocytochemistry results showed positive DAB staining for VEGF at 5 and 7 days in experimental group. Western blot results showed that the protein expressions of VEGF increased significantly at 5 and 7 days in experimental group when compared with control group (P lt; 0.05), which was signfiantly higher at 5 days than at 7 days in experimental group (P lt; 0.05). Conclusion CGRP can promote the migration of BMSCs and stimulate the protein expression of VEGF, which may plays an important role in regulating bone metabol ism by increasing angiogenesis.