Objoctive To investigate the effects of quercetin and X-ray on collagen synthesis of cultured human keloid-derived fibroblast and the mechanism. Methods Collagen synthesis of cultured human keloid and normal fibroblas...Objoctive To investigate the effects of quercetin and X-ray on collagen synthesis of cultured human keloid-derived fibroblast and the mechanism. Methods Collagen synthesis of cultured human keloid and normal fibroblasts were detected by hydroxyproline colorimetric analysis. Immunocytochemical staining was used to investigate collagen I and III expression, mRNA expression of collagen Ⅰ and Ⅲ, and transforming growth factor （ TGF）-β1 were assayed by reverse transcription-polymerase chain reaction （RT-PCR） and real-time PCR. Results Quercetin inhibited the collagen synthesis of both keloid and normal fibroblasts in a dose-dependent man- ner. Immunocytochemical staining indicated that collagenⅠ and Ⅲ were down-regulated by quercetin and X-ray （P 〈 0.05 ）, particularly collagen I （ P 〈 0. 05 ）. mRNA expression of both collagen I and III in quercetin groups significantly decreased compared with that in control group （ P 〈 0. 05 ）, especially in the group treated with both quercetin and X-ray （ P 〈 0. 01 ）. mRNA level of TGF-[31 gene was down-regulated by quercertin （ P 〈 0. 05 ）. Conclusions Quercetin will probably be one of the new medicines which could effectively treat keloid. Quercetin combined with X-ray could reduce the dose of radiation.展开更多
Objective: To explore the effects of connective tissue growth factor (CTGF) on the pathogenesis of human keloid. Methods: CTGF antisense oligonucleotides (ASODN) conjugated with isothiocyananate fluorescence was encap...Objective: To explore the effects of connective tissue growth factor (CTGF) on the pathogenesis of human keloid. Methods: CTGF antisense oligonucleotides (ASODN) conjugated with isothiocyananate fluorescence was encapsulated by liposome, and then added into the human keloid fibroblasts (HKFs) culture media. The intracellular distribution of CTGF ASODN was observed by fluorescence microscopy in the fixed HKFs. The proliferation of HKFs was measured by MTT test. The collagen synthesis of HKFs was measured by 3H-proline incorporation method. Results: Compared with control group, the CTGF ASODN can inhibit the proliferation and collagen synthesis of the HKFs (P<0.01). Conclusion: CTGF ASODN has anti-fibrotic effects on keloid in vitro, and CTGF play an important role in promoting the fibrosis of keloid.展开更多
Objective.To explore the expression characteristic of fibronectin gene in hypertr ophic scars and diabetic ul-cer tissues.Methods.The biopsies from normal skins,hypertrophic scars and diabetic foot ulc ers were taken....Objective.To explore the expression characteristic of fibronectin gene in hypertr ophic scars and diabetic ul-cer tissues.Methods.The biopsies from normal skins,hypertrophic scars and diabetic foot ulc ers were taken.The tech-nique of quantitative polymerase ch ain reaction(PCR)was used to evaluate the gene express ion of fibronectin in the above biopsies.Results.Fibronectin gene expression was enhanced in hypertrophic scars and decreased in diabetic foot ul-cers compared with that in normal ski ns.Quantitative comparison showed about 2-fold increase of fibronectin mR-NA level in hypertrophic scars and ab out 3-fold decrease of fibronectin mRNA level in diabetic ulcers as com-pared with that in normal skins.Conclusions.Fibronectin gene expression is influenced by the tissue environment.Di fferent expression and synthesis of fibronectin may cause d ifferent outcomes in wound healing.展开更多
Objective： The present study was designed to use an in vivo rabbit ear scar model to investigate the efficacy of systemic administration of endostatin in inhibiting scar formation. Methods： Eight male New Zealand wh...Objective： The present study was designed to use an in vivo rabbit ear scar model to investigate the efficacy of systemic administration of endostatin in inhibiting scar formation. Methods： Eight male New Zealand white rabbits were randomly assigned to two groups. Scar model was established by making six full skin defect wounds in each ear. For the intervention group, intraperitoneal injection of endostatin was performed each day after the wound healed （about 15 d post wounding）. For the control group, equal volume of saline was injected. Thickness of scars in each group was measured by sliding caliper and the scar microcirculatory perfusion was assessed by laser Doppler flowmetry on Days 15, 21, 28, and 35 post wounding. Rabbits were euthanatized and their scars were harvested for histological and proteomic analyses on Day 35 post wounding. Results： Macroscopically, scars of the control group were thicker than those of the intervention group. Significant differences between the two groups were observed on Days 21 and 35 （p〈0.05）. Scar thickness, measured by scar elevation index （SEI） at Day 35 post wounding, was significantly reduced in the intervention group （1.09±0.19） compared with the controls （1.36±0.28）. Microvessel density （MVD） observed in the intervention group （1.73±0.94） was significantly lower than that of the control group （5.63±1.78） on Day 35. The distribution of collagen fibers in scars treated with endostatin was relatively regular, while collagen fibers in untreated controls were thicker and showed disordered alignment. Western blot analysis showed that the expressions of type I collagen and Bcl-2 were depressed by injection of endostatin. Conclusions： Our results from the rabbit ear hypertrophic scar model indicate that systemic application of endostatin could inhibit local hypertrophic scar formation, possibly through reducing scar vascularization and angiogenesis. Our results indicated that endostatin may promote the apoptosis of endothelial cells and block their release of platelet-dedved growth factor （PDGF） and fibroblast growth factor （FGF）, thereby controlling collagen production by fibroblasts. Blood vessel-targeted treatment may be a promising strategy for scar therapy.展开更多
Objective: To explore the inhibitory effect of He Ne laser irradiation on fibroblast growth of hypertrophic scars in culture. Methods: He Ne laser with wavelength of 632.8 nm, power density of 50 mW/cm 2 and doses of ...Objective: To explore the inhibitory effect of He Ne laser irradiation on fibroblast growth of hypertrophic scars in culture. Methods: He Ne laser with wavelength of 632.8 nm, power density of 50 mW/cm 2 and doses of 3 J/cm 2, 30 J/cm 2 , 90 J/cm 2 and 180 J/cm 2 was used to irradiate human scar fibroblasts in culture 1, 3 and 5 times respectively, and then the cell count and cell cycle analysis were done. Results: Repeated irradiation with He Ne laser at dose of 180 J/cm 2 three and five times led to an evident decrease in total cell number compared with that of the control group and there was a significant difference (P< 0.05 ). The cell cycle analysis showed after three and five times of irradiation with 180 J/cm 2 He Ne laser the cell number in S phase decreased from 51% to 20% and 14% respectively, the cell number in G 0/G 1 phase increased from 28% to 55% and 60% respectively, and the cell percentage in Sub G1 phase was 6.7 % and 9.8 % respectively.Conclusions: Repeated irradiation with 180 J/cm 2 He Ne laser can inhibit scar fibroblasts growth in culture. It may be that He Ne laser irradiation causes cell stagnation in G 0/G 1 phase and apoptosis.展开更多
文摘Objoctive To investigate the effects of quercetin and X-ray on collagen synthesis of cultured human keloid-derived fibroblast and the mechanism. Methods Collagen synthesis of cultured human keloid and normal fibroblasts were detected by hydroxyproline colorimetric analysis. Immunocytochemical staining was used to investigate collagen I and III expression, mRNA expression of collagen Ⅰ and Ⅲ, and transforming growth factor （ TGF）-β1 were assayed by reverse transcription-polymerase chain reaction （RT-PCR） and real-time PCR. Results Quercetin inhibited the collagen synthesis of both keloid and normal fibroblasts in a dose-dependent man- ner. Immunocytochemical staining indicated that collagenⅠ and Ⅲ were down-regulated by quercetin and X-ray （P 〈 0.05 ）, particularly collagen I （ P 〈 0. 05 ）. mRNA expression of both collagen I and III in quercetin groups significantly decreased compared with that in control group （ P 〈 0. 05 ）, especially in the group treated with both quercetin and X-ray （ P 〈 0. 01 ）. mRNA level of TGF-[31 gene was down-regulated by quercertin （ P 〈 0. 05 ）. Conclusions Quercetin will probably be one of the new medicines which could effectively treat keloid. Quercetin combined with X-ray could reduce the dose of radiation.
文摘Objective: To explore the effects of connective tissue growth factor (CTGF) on the pathogenesis of human keloid. Methods: CTGF antisense oligonucleotides (ASODN) conjugated with isothiocyananate fluorescence was encapsulated by liposome, and then added into the human keloid fibroblasts (HKFs) culture media. The intracellular distribution of CTGF ASODN was observed by fluorescence microscopy in the fixed HKFs. The proliferation of HKFs was measured by MTT test. The collagen synthesis of HKFs was measured by 3H-proline incorporation method. Results: Compared with control group, the CTGF ASODN can inhibit the proliferation and collagen synthesis of the HKFs (P<0.01). Conclusion: CTGF ASODN has anti-fibrotic effects on keloid in vitro, and CTGF play an important role in promoting the fibrosis of keloid.
文摘Objective.To explore the expression characteristic of fibronectin gene in hypertr ophic scars and diabetic ul-cer tissues.Methods.The biopsies from normal skins,hypertrophic scars and diabetic foot ulc ers were taken.The tech-nique of quantitative polymerase ch ain reaction(PCR)was used to evaluate the gene express ion of fibronectin in the above biopsies.Results.Fibronectin gene expression was enhanced in hypertrophic scars and decreased in diabetic foot ul-cers compared with that in normal ski ns.Quantitative comparison showed about 2-fold increase of fibronectin mR-NA level in hypertrophic scars and ab out 3-fold decrease of fibronectin mRNA level in diabetic ulcers as com-pared with that in normal skins.Conclusions.Fibronectin gene expression is influenced by the tissue environment.Di fferent expression and synthesis of fibronectin may cause d ifferent outcomes in wound healing.
基金supported by the National Natural Science Foundation of China (No.81272120)the Health Department of the Zhejiang Province (No.2007B086),China
文摘Objective： The present study was designed to use an in vivo rabbit ear scar model to investigate the efficacy of systemic administration of endostatin in inhibiting scar formation. Methods： Eight male New Zealand white rabbits were randomly assigned to two groups. Scar model was established by making six full skin defect wounds in each ear. For the intervention group, intraperitoneal injection of endostatin was performed each day after the wound healed （about 15 d post wounding）. For the control group, equal volume of saline was injected. Thickness of scars in each group was measured by sliding caliper and the scar microcirculatory perfusion was assessed by laser Doppler flowmetry on Days 15, 21, 28, and 35 post wounding. Rabbits were euthanatized and their scars were harvested for histological and proteomic analyses on Day 35 post wounding. Results： Macroscopically, scars of the control group were thicker than those of the intervention group. Significant differences between the two groups were observed on Days 21 and 35 （p〈0.05）. Scar thickness, measured by scar elevation index （SEI） at Day 35 post wounding, was significantly reduced in the intervention group （1.09±0.19） compared with the controls （1.36±0.28）. Microvessel density （MVD） observed in the intervention group （1.73±0.94） was significantly lower than that of the control group （5.63±1.78） on Day 35. The distribution of collagen fibers in scars treated with endostatin was relatively regular, while collagen fibers in untreated controls were thicker and showed disordered alignment. Western blot analysis showed that the expressions of type I collagen and Bcl-2 were depressed by injection of endostatin. Conclusions： Our results from the rabbit ear hypertrophic scar model indicate that systemic application of endostatin could inhibit local hypertrophic scar formation, possibly through reducing scar vascularization and angiogenesis. Our results indicated that endostatin may promote the apoptosis of endothelial cells and block their release of platelet-dedved growth factor （PDGF） and fibroblast growth factor （FGF）, thereby controlling collagen production by fibroblasts. Blood vessel-targeted treatment may be a promising strategy for scar therapy.
文摘Objective: To explore the inhibitory effect of He Ne laser irradiation on fibroblast growth of hypertrophic scars in culture. Methods: He Ne laser with wavelength of 632.8 nm, power density of 50 mW/cm 2 and doses of 3 J/cm 2, 30 J/cm 2 , 90 J/cm 2 and 180 J/cm 2 was used to irradiate human scar fibroblasts in culture 1, 3 and 5 times respectively, and then the cell count and cell cycle analysis were done. Results: Repeated irradiation with He Ne laser at dose of 180 J/cm 2 three and five times led to an evident decrease in total cell number compared with that of the control group and there was a significant difference (P< 0.05 ). The cell cycle analysis showed after three and five times of irradiation with 180 J/cm 2 He Ne laser the cell number in S phase decreased from 51% to 20% and 14% respectively, the cell number in G 0/G 1 phase increased from 28% to 55% and 60% respectively, and the cell percentage in Sub G1 phase was 6.7 % and 9.8 % respectively.Conclusions: Repeated irradiation with 180 J/cm 2 He Ne laser can inhibit scar fibroblasts growth in culture. It may be that He Ne laser irradiation causes cell stagnation in G 0/G 1 phase and apoptosis.
