OBJECTIVE To investigate the effects of basic fibroblast growth factor(bFGF) on repairing transected sciatic nerves in rats. METHODS The animal models of the transected sciatic nerve of 40 SD rats were established, which divided into 4 groups: normal saline (NS) group, nerve growth factor (NGF) group, bFGF group and normal control group. The epineurium of the transected sciatic nerve was sutured under microscope, then bFGF or NGF was dropped into local sites and injected intramuscularly once a day for 30 days after operation. Functional repair for the transected sciatic nerves was studied by nerve conductive velocity (NCV) and sciatic nerve function index (SFI). RESULTS As a criterion, the level of the normal control group was regarded as zero, SFI of NS group, NGF group and bFGF group were -114.30 +/- 10.34, -70.50 +/- 11.01, -50.45 +/- 7.82 respectively at 1 month after operation, and they were -54.96 +/- 16.46, -35.21 +/- 10.80, -27.53 +/- 11.23 respectively in 3 months after operation. NCV of bFGF group was significantly faster than NS group and NGF group. CONCLUSION bFGF can significantly promote the functional repair of injured peripheral nerve, and its effects are better than NGF.
OBJECTIVE The biological effects of recombinant human epidermal growth factor (rhEGF) and recombinant human fibroblast growth factor (rhFGF) were evaluated on the model of incised wounds in mini pigs. METHODS Total of 160 incised wounds in 16 mini pigs were divided into two groups (rhEGF group and rhFGF group), each containing 80 wounds. In rhEGF group, 60 incised wounds were treated with different dosages of rhEGF (50, 10 and 0.5 micrograms/wound), and another 20 wounds were treated with solvent as control group. In rhFGF group, all wounds were treated in the same way as described in rhEGF group, the dosages of rhFGF were 150, 90 and 30 U/cm2 respectively. The measurements of cavity volume and area in wound, histological examination were used to evaluate the results of wound healing. RESULTS The results showed that wound healing was accelerated in all wounds treated with rhEGF and rhFGF. In rhEGF group, the velocity of re-epithelialization was faster than that of rhFGF group, however, new granulation tissue in rhFGF was more than that of rhEGF group. CONCLUSION The results indicate that rhEGF and rhFGF can stimulate wound healing, however, the mechanisms and the biological effects involved in these processes are quite different. It suggests that it is better to use rhFGF in those wounds which need more granulation tissue formation and use rhEGF in the wounds which mainly need re-epithelialization.
The basic fibroblastic growth factor (bFGF) was employed to stimulate the earlyrevascularization of the autogenous free fat grafts. In the experimental group the fibrin containingbFGF was mixed to the fat to be implanted, and the fat containing the fibrin only was used as thecontrol. The animals were perfused with Chenese ink through intubation to the aorta via the heart at 5 ,7, and 10 days after operation. The vascularizarion was significantly increased at the bFGF side ascompared with ...
Human fibroblasts and human epidermal keratinocytes were used for culture. Chitosan solution were added in the culture solution(DMEM). After 72 hours, the fibroblasts showed rapid growth in the control culture without Chitosan, But the numbers of human fibroblasts from growth was decreased as the concentration of Chitosan was increasing. On the contrary the human epidermal keratinocytes growed more rapidly in the culture with Chitosan than in the culture without Chitosan. The results showed that Chitosan inhibited the growwth of human fibroblast and stimulated the growth of human epidermal keratinocyte .
The ultrastructures of 14 keloids and 7 hypertrophic scars were examined by electron micrascopy.Both lesions were found to be comprised of fibroblasts, macrophages, microfi brils of collagen andmicrovessels which were partly or completely obliterated. Most fibroblasts were of active cell types.They contained abundant coarse endoplasmic reticulum and prominent Golgi complexes. The fibrils inthe lesions were irtegularly arranged. Meanwhile myofibroblasts were often seen in the keloid.In the cytoplasm of the myofibroblasts, in addition to coarse endoplasmic reticulum and Golgi complexes, many fine myofilaments, dense bodies, dense patches and distrupted basal lamina were present. These characteristic features might help to differentiate keloid from hypertrophic sacr.
Objective To observe the proliferation and migration of endothelial cells after 30% total burn surface area (TBSA) of deep partial thickness scald, and the effect of basic fibroblast growth factor (bFGF) on angiogenesis during wound healing.Methods A total of 133 male Wistar ratswere divided randomly into normal control (n=7), injured control group (n=42), bFGF group (n=42) andanti-c-fos group (n=42). The apoptosis expression of fibroblasts was determinedwith in situ hybridization and the changes of proliferation cell nuclear antigen(PCNA), focal adhesion rinase(FAK), c-fos and extracellular signalregulated kinase(ERK) proteins expression were detected with immunohistochemistry staining technique after 3 hours, 6 hours, 1 day, 3 days, 7 days, 14 days and 21 days of scald.Results In injured control group and bFGF group, theproliferation rate of the vascular endothelial had evident changes 7 days and14 days after scald； the expression of FAK was increased 14 days after scald. ERK proteins expression was different between injury control group and bFGF group at initial stage after scald. Stimulation of ERKs by bFGF led to up-regulation of c-fos and b expression of FAK. Conclusion Exogenous bFGF extended the influence on wound healing process by ERK signaling pathway, affecting migration cascade of vascular endothelial cell. The oncogene proteins play an important role on accelerating angiogenesis duringwound healing.
OBJECTIVE To observe the effects of basic fibroblast growth factor(bFGF) on the healing of cutaneous chronic wounds. METHODS Twenty-eight cases with thirty-three wounds from trauma, diabetes, pressure and radiation injuries were locally treated with bFGF in a dosage of 150 U/cm2 wounds. The healing time of wounds was used to evaluate the treatment results. RESULTS The healing time in all of chronic wounds were accelerated. All wounds from trauma, diabetes and pressure were healed within 4 weeks and another 2 wounds from radiation injuries were healed over 4 weeks. The healing rate within 4 weeks was 93.9%. CONCLUSION The results indicate that bFGF can be used as a promoter to accelerate the healing of chronic wounds in clinic.
To evaluate the effects of bFGF on wound healing and the side-effects of bFGF, a multi-centers and controlled clinical trial were carried out in 32 hospitals in China. One thousand and twenty-four cases with acute wounds such as burn, donor site or operative wound and chronic wounds such as bed sore, draining sinus, ulcer were treated with bFGF. Another 826 cases with the similar wounds were used as control. The results showed: 1. The duration of wound healing was shorted 3-4 days in trial group when compared with the contorl; 2. The successful rates from bFGF on promoting the wound healing for burns, operative wounds and chronic dermal ulcers was 95.2%, 96.5% and 93.5%, respectively; 3. No adverse reaction was found. CONCLUSION: 1. bEGF can make the "silent" reparative cells dividing and proliferating. 2. bFGF can improve the quality and the velocity of wound healing.
To investigate the effects of basic fibroblast growth factor (bFGF) on necrosis rate, succinate dehydrogenase level and oxygen consumption of the skin flap, 18 Wistar rats were divided into 2 groups. Caudally based skin flap was raised on the back of each rat. Nine micrograms bFGF or normal saline with heparin was instilled under the flaps respectively after closure of the wounds. After 7 days, the necrosis rate of each wound was measured. The result showed that in bFGF group, the average necrosis rate of skin flap was 18.2%, less than that of the control group (37.14%). Succinate dehydrogenase content and oxygen consumption in bFGF group were higher than those of the corresponding sites in the control group (P lt; 0.05). It was suggested that the use of bFGF resulted in the decrease rate of necrosis of skin flap, and it maintained higher succinale dehydrogenase level and oxygen consumption. It was concluded that bFGF would probably be valuable for clinical use.
ObjectiveTo investigate the effects of 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole (YC-1), a hypoxia-inducible factor-1α (HIF-1α) inhibitor, on hypoxia induced rat pulmonary arterial adventitial fibroblasts (AFs) proliferation and collagen synthesis, and explore the molecular mechanism.MethodsUnder hypoxic condition, rat AFs were cultured in DMEM medium supplemented with 10% fetal bovine serum in vitro. The cells were divided into five groups, ie. a normoxia group, a hypoxia group and three hypoxia+YC-1 groups (treated with YC-1 at concentration of 0.01, 0.05 and 0.1 mmol/L, respectively). The cells proliferation was determined by MTT method. Collagen synthesis of AFs was measured by 3H-proline incorporation assay. The expression of HIF-1α in AFs in different conditions was measured by Western blot, and the mRNA expression of transforming growth factor-β1 (TGF-β1) was measured by reverse-transcription polymerase chain reaction.ResultsThe proliferation rate and the incorporation data of 3H-proline in the hypoxia group were significantly increased as compared with those in the control group (both P<0.01). YC-1 significantly reduced the proliferation rate and incorporation data of3H-proline induced by hypoxia in a dose-dependent manner. YC-1 could also down-regulate the expressions of HIF-1α and TGF-β1 mRNA significantly (both P<0.01). Compared with the hypoxia group, the expressions of HIF-1α and TGF-β1 mRNA decreased respectively by 65% and 61% in the hypoxia+YC-1 (0.1 mmol/L) group (bothP<0.01).ConclusionsYC-1 can inhibit hypoxia-induced AFs proliferation and collagen synthesis in a dose-dependent manner. The mechanism may relate to YC-1’s inhibitory effect on expressions of HIF-1α and TGF-β1 mRNA.