OBJECTIVE: To determine the influence of basic fibroblast growth factor (bFGF) on endothelial cell (EC) proliferation in vitro and its possible mechanisms, and to examine the effect of both TNP-470 and dexamethasone (Dex) on the EC proliferation induced by bFGF. METHODS: Human umbilical vein endothelial cells were cultured and the proliferation of EC was quantified by a colorimetric assay using MTT reagent. The expression of nuclear factor-kappa B (NF-kappa B) and ki-67 was detected with SABC immunohistochemical method. RESULTS: bFGF stimulated the EC proliferation and enhanced the expression of NF-kappa B and ki-67 in nucleus; TNP-470 and Dex suppressed EC proliferation induced by bFGF, and reduced the expression of NF-kappa B and ki-67 in nucleus. CONCLUSION: The above results indicate that the possible mechanisms of EC proliferation stimulated by bFGF come from that bFGF can activate NF-kappa B to promote the synthesis of DNA and EC mitosis. TNP-470 and Dex inhibited EC proliferation stimulated by bFGF by inhibiting NF-kappa B.
Objctive To explore the relationship between the expression of Fas/FasL and the apoptosis occurs in retinal ischemia/reperfusion injury of rats , as well as the therapeutic effects of bFGF on the ischemic retina.Methods Th emodels of retinal ischemia/reperfusion injury was made by transient elevating introcular pressure. A total of 28 rats were divided into normal and operation group.The latter were subdivided into 1 hour, 6, 12, 24, 48 and 72 hours after reperfusion group, in which the left eyes of the rats were in the ischemia/reper fusion groups and the right ones were in the treatment groups (bFGF intracameral injection). Apoptosis was assessed by the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labelling (TUNEL) method, and the expression of Fas and Fas ligand was studied by strept avidin-biotin complex （SABC）immunohistochemistry. Results No positive cells were observed in the normal rats′retinae, but there was a significant number of TUNEL positive cells in 6-24 hours after transient ischemia followed by a decrease at the 48th hour. The number of TUNEL positive cells reached a maximum at the 24th hour after ischemia. The expression of Fas gradually increased as early as when it was at the 6th hour, reached a peak at the 24th hour, and then decreased at the 48th hour. Similarly, the expression of Fas ligand was at peak in 24-48 hours in GCL and INL of retina. Conclusions Retinal ischemia-reperfusion after transient elevated IOP induced apoptosis of cells in the retina. Fas/FasL may play an important role in the early events of the apoptotic pathways. bFGF can rescue RGCs from retinal ischemia/reperfusion injury through downregulation of the expression of Fas/FasL and may represent an important mechanism for therapeutic neuroprotection. (Chin J Ocul Fundus Dis，2003，19：160-163)
OBJECTIVE: To evaluate the effect of vascular endothelial growth factor(VEGF) 165 or basic fibroblast growth factor (bFGF), which was slowly-released in fibrin glue patch, on expanded prefabricated flaps in rabbits to facilitate the neoangiogenesis process. METHODS: A total of 53 rabbits were divided randomly into 6 groups. The central auricular vascular bundle of the ear was implanted into the expanded prefabricated flap as the pedicle. Fibrin glue, sandwiched between the expander and the implanted vessels, was adopted for topical delivering and slow-releasing of VEGF(625 ng) or bFGF(2880U). After 14 days, the island flap with the implanted vascular bundles as the pedicle was elevated, sutured back to its original position and then harvested more 3 days later. Neoangiogenesis was measured by digital recording of survival area, laser Doppler flowmetry, PCNA immunohistochemistry, TUNEL, ink and PbO infusions. RESULTS: When compared with the other groups, flap survival improved; neoangiogenesis of flaps increased, together with the blood flow enhanced in the groups applied growth factors. The reduced cellular apoptosis and the increased proliferation were also observed. CONCLUSION: VEGF or bFGF slowly-released by fibrin glue shows the potential to facilitate neoangiogenesis and accelerate maturation of the expanded prefabricated flap.
OBJECTIVE: To investigate the changes of fibroblast growth factor (FGF) in burn wounds. METHODS: The FGF expression in the center of wound granulation, the edge of wound, the healed part of wound, the normal skin of patients, and the heal course of second degree burn wounds were detected by immunohistochemical methods. RESULTS: The expression intensity of FGF was different in the different sites of third degree burn wounds. The highest contents of FGF was in the center granulation of burn wounds, the less was in the borderline of wound and healed skin, and the least was in the healed skin. FGF expression mainly concentrated in the middle layer of wound, and almost no FGF expression in normal skin. The most FGF expression was occurred at 14 days after injury in second degree of burn wound. CONCLUSION: The changes of FGF in wounds are closely related to the wound healing, and rational use of FGF can promote wound healing.
Abstract To observe the effect of fibroblast growth factor (FGF) on wound healing, 50 mice were divided into 5 groups. On the back of every mouse, 2 wounds were made by operative cuts, one for experiment and the other for control. The wounds of the experimental group were covered with 0.5ml FGF solution (contented FGF 300 μg/ml, heparin 100 μg/ml), whereas the wounds of the control group were covered with 0.5ml 0.9% NaCl solution. All of the wounds were dressed by sterilized gauze, and received the same treatment once a day. After 1,3,5,7,10 days, the mice in every group were sacrificed and the tissues of the wounds were collected and prepared for microscopic examination. The results showed that the capillaries and fibroblasts in the experimental group were markedly increased and reached the peak 2～3 days earlier than those in the control group. It was suggested that FGF promoted the formation of granulation tissue and the wound healing.
Objective To evaluate the effect of composite (bFGF/PDPB) of basic fibroblast growth factor（bFGF） and partially deproteinized bone (PDPB) on the repair of femoral head defect. Methods Forty-eight femoral heads with defect derived from 24 New Zealand rabbits were divided into 3 groups at random, which were implanted with bFGF/PDPB(group A), PDPB(group B) and nothing(group C) respectively.The rabbits were sacrificed at 2,4,and8 weeks after operation, and then the femoral heads were obtained. The specimens injected with Chinese ink were created. Then X-ray examination, histopathological and morphological examination of blood vessel, and image analysis were made. Results The bone defects healed completely 8 weeks after operation in group A. The implants in the repaired tissue were not substituted completely in group B. The bone defects did not heal completely in group C. Two weeks after operation, affluent newly formed vessels were seen in repaired areas in groupA. No significant difference between group A and group B was observed 8 weeks after operation. In group C, newly formed vessels were scarce 2, 4, and 8 weeks after operation. There were 3 sides rated excellent, 2 good and 1 fair in group A; 1 excellent, 2 good, 2 fair and 1 poor in group B; and 1 fair and 5 poor in group C according to the X-ray evaluation 8 weeks after operation. Eight weeks after operation, the volume fraction of bone trabecula in repaired tissue was higher in group A than that in group B (Plt;0.05), and the fraction in group C was thelowest among the 3 groups (Plt;0.05). Conclusion The composite ofbFGF and PDPB can effectively promote the repair of femoral head defect of rabbit.
OBJECTIVE To investigate the effect of acid fibroblast growth factor (aFGF) on guided bone regeneration (GBR), to study whether aFGF can promote the repairing ability of GBR in bone defect. METHODS 10 mm long segmental defects were created in the diaphyses of both radii in 16 New Zealand rabbits. The defect was bridged with a silicon tube. Human recombinant aFGF was instilled into the tube on the experimental side, while the contralateral tube was instilled with saline as control group. The radiographic, gross and histologic examination of the samples were analyzed at 2, 4, 6 and 8 weeks after operation. RESULTS On the experimental side, there was new bone formation in the bone medullary cavity, the endosteum and the section surface of the cortex at 2 weeks. At 4 weeks, at the center of the blood clot in the tube there was new bone formation and bone defect was completely healed at 8 weeks. On the control side, new bone formation was less in every period compared with that of the experimental side. At 8 weeks, there was only partial healing of the bone defect. CONCLUSION It can be concluded that aFGF can promote new bone formation and facilitate GBR in bone defect.