目的:通过戊四氮癫痫持续状态大鼠模型,观察外源性碱性成纤维细胞生长因子(bFGF)对癫痫大鼠海马组织内c-fos表达的影响。方法:建立SD大鼠戊四氮(PTZ)诱导癫痫持续状态模型,生理盐水(NS)注射作为对照,皮下注射bFGF进行干预,分4纽:即NS组...目的:通过戊四氮癫痫持续状态大鼠模型,观察外源性碱性成纤维细胞生长因子(bFGF)对癫痫大鼠海马组织内c-fos表达的影响。方法:建立SD大鼠戊四氮(PTZ)诱导癫痫持续状态模型,生理盐水(NS)注射作为对照,皮下注射bFGF进行干预,分4纽:即NS组、NS+bFGF组、PTZ组、PTZ+bFGF组。选择处理后第3、7、14天3个时间点进行观察,采用免疫组化SABC法检测c-fos。结果:发作后3、7、14 d PTZ组海马组织c-fos较NS组有显著升高(P<0.01),以发作后14 d升高更为明显,PTZ+bFGF组各时间点c-fos较PTZ组下降(P<0.05);c-fos含量在PTZ组各时间点亦大于NS组(P<0.05),以发作后14 d升高较为显著;NS+bFGF组发作后各时间点c-fos较PTZ组差异无统计学意义(P>0.05)。结论:大鼠癫痫持续状态后一定时间内c-fos表达增加,bFGF能够降低大鼠癫痫发作后c-fos表达,减少神经元的损害。展开更多
Objectives To observe the effect of basic fibroblast growth factor (bFGF) slow-release microcapsules on angiogenesis in infarcted myocardial regions. Methods.Myocardial infarction was induced in 24 New Zealand rabbits...Objectives To observe the effect of basic fibroblast growth factor (bFGF) slow-release microcapsules on angiogenesis in infarcted myocardial regions. Methods.Myocardial infarction was induced in 24 New Zealand rabbits by ligating the root of left anterior descending coronary artery.Group Ⅰ(n=8) served as control, group Ⅱ(n=8) as a blank microcapsule group, group Ⅲ(n=8, each microcapsule contains 1μg bFGF) as micrpcapsule group.In group Ⅱ and Ⅲ, 5 blank microcapsules or bFGF slow-release microcapsules were implanted into myocardium underneath the epicardium between the left anterior descending coronary artery and left circumflex artery.Infarct size was evaluated by infarcted weight/left ventricle weight ratio and angiogenesis was evaluated by immunohistochemical examinations 5 weeks later. [WT5”BX] Results.As compared with group Ⅰ and Ⅱ, rabbits treated with bFGF slow-release microcapsules showed higher microvessel counts (group Ⅰ3775±450, group Ⅱ3837±498,vs.group Ⅲ 13550±481,P<0001) and less infarcted weight /left ventricle weight (group Ⅰ168%±04%,group Ⅱ167%±05%,vs.group Ⅲ 70%±02%,P<0001). Conclusions.Subepicardial administration of bFGF slow-release microcapsule in the infarcted rabbit model results in effective angiogenesis and reduction in infarct size.展开更多
Accumulating data suggest that FGFs/FGFR1 plays essential roles in the bone development and human skeletal diseases. Conditional inactivation of fgfrl caused different phenotypes displaying in different cells or speci...Accumulating data suggest that FGFs/FGFR1 plays essential roles in the bone development and human skeletal diseases. Conditional inactivation of fgfrl caused different phenotypes displaying in different cells or specific organs and revealed some novel functions of FGFR1 in bone development. Fgfrl mutation mainly induced 2 types of human skeletal diseases, craniosynostosis syndrome and dysplasias. Similar mutation of fgfrl in mouse model just mimicked the phenotype that happened in human. These fa- cilitate the investigation on the underlying mechanism of the diseases. Here we mainly focused on the ad- vance of FGFR1 function in the bone development and its mutation caused skeletal diseases.展开更多
Objective. This study was to investigate the effects of transforming growth factor-β(TGFβ) and fi- broblast growth factor (FGF) in the subcapsular opacification formation of the lens. Methods. Lens epithelial explan...Objective. This study was to investigate the effects of transforming growth factor-β(TGFβ) and fi- broblast growth factor (FGF) in the subcapsular opacification formation of the lens. Methods. Lens epithelial explants from 10-day-old rats were cultured with TGFβ1 or TGFβ2 in the presence of FGF for 5 days, then were examined by light and electron microscopy, and by immunolocal- ization of smooth muscle(α-sm) actin and type I collagen. Results. In TGFβ/FGF-treated explants,extensive proliferation occured, with formation of spindle and star-shaped cells. These cells showed ultrastructure and biochemical features of fibroblast or myofibroblast. Prominent Golgi apparatus and rough endoplaic reticulum were observed in some cells. Intracellular micro- filaments with cytoplasmic dense babies and membrane associated dense bodies, features of smooth muscle cells, were also observed. Some cells showed reactivity to -sin actin antibody. TGFβ/FGF-treated ex- plants were strongly stained with type I collagen antibody. Condusion. In the presence of FGF, TGFβ1 and TGFβ2 induced lens epithelial cell (LEC ) proliferation and transformation into fibroblast or myofibroblast-like cells, with producing of abundant collagen matrix in the explants. The changes are similar to the metaplasia that occurrs in subcapsular opacification of the lens. The findings suggest that TGFβ and FGF plays a role in the pathogenesis of subcapsular opacification of the lens.展开更多
文摘目的:通过戊四氮癫痫持续状态大鼠模型,观察外源性碱性成纤维细胞生长因子(bFGF)对癫痫大鼠海马组织内c-fos表达的影响。方法:建立SD大鼠戊四氮(PTZ)诱导癫痫持续状态模型,生理盐水(NS)注射作为对照,皮下注射bFGF进行干预,分4纽:即NS组、NS+bFGF组、PTZ组、PTZ+bFGF组。选择处理后第3、7、14天3个时间点进行观察,采用免疫组化SABC法检测c-fos。结果:发作后3、7、14 d PTZ组海马组织c-fos较NS组有显著升高(P<0.01),以发作后14 d升高更为明显,PTZ+bFGF组各时间点c-fos较PTZ组下降(P<0.05);c-fos含量在PTZ组各时间点亦大于NS组(P<0.05),以发作后14 d升高较为显著;NS+bFGF组发作后各时间点c-fos较PTZ组差异无统计学意义(P>0.05)。结论:大鼠癫痫持续状态后一定时间内c-fos表达增加,bFGF能够降低大鼠癫痫发作后c-fos表达,减少神经元的损害。
文摘Objectives To observe the effect of basic fibroblast growth factor (bFGF) slow-release microcapsules on angiogenesis in infarcted myocardial regions. Methods.Myocardial infarction was induced in 24 New Zealand rabbits by ligating the root of left anterior descending coronary artery.Group Ⅰ(n=8) served as control, group Ⅱ(n=8) as a blank microcapsule group, group Ⅲ(n=8, each microcapsule contains 1μg bFGF) as micrpcapsule group.In group Ⅱ and Ⅲ, 5 blank microcapsules or bFGF slow-release microcapsules were implanted into myocardium underneath the epicardium between the left anterior descending coronary artery and left circumflex artery.Infarct size was evaluated by infarcted weight/left ventricle weight ratio and angiogenesis was evaluated by immunohistochemical examinations 5 weeks later. [WT5”BX] Results.As compared with group Ⅰ and Ⅱ, rabbits treated with bFGF slow-release microcapsules showed higher microvessel counts (group Ⅰ3775±450, group Ⅱ3837±498,vs.group Ⅲ 13550±481,P<0001) and less infarcted weight /left ventricle weight (group Ⅰ168%±04%,group Ⅱ167%±05%,vs.group Ⅲ 70%±02%,P<0001). Conclusions.Subepicardial administration of bFGF slow-release microcapsule in the infarcted rabbit model results in effective angiogenesis and reduction in infarct size.
基金the National Key Basic Research and Devel opment Plan of China(973 Projects,2005CB522604)the Research Project of Scientific Committee of Chongqing(2004BA5016)
文摘Accumulating data suggest that FGFs/FGFR1 plays essential roles in the bone development and human skeletal diseases. Conditional inactivation of fgfrl caused different phenotypes displaying in different cells or specific organs and revealed some novel functions of FGFR1 in bone development. Fgfrl mutation mainly induced 2 types of human skeletal diseases, craniosynostosis syndrome and dysplasias. Similar mutation of fgfrl in mouse model just mimicked the phenotype that happened in human. These fa- cilitate the investigation on the underlying mechanism of the diseases. Here we mainly focused on the ad- vance of FGFR1 function in the bone development and its mutation caused skeletal diseases.
文摘Objective. This study was to investigate the effects of transforming growth factor-β(TGFβ) and fi- broblast growth factor (FGF) in the subcapsular opacification formation of the lens. Methods. Lens epithelial explants from 10-day-old rats were cultured with TGFβ1 or TGFβ2 in the presence of FGF for 5 days, then were examined by light and electron microscopy, and by immunolocal- ization of smooth muscle(α-sm) actin and type I collagen. Results. In TGFβ/FGF-treated explants,extensive proliferation occured, with formation of spindle and star-shaped cells. These cells showed ultrastructure and biochemical features of fibroblast or myofibroblast. Prominent Golgi apparatus and rough endoplaic reticulum were observed in some cells. Intracellular micro- filaments with cytoplasmic dense babies and membrane associated dense bodies, features of smooth muscle cells, were also observed. Some cells showed reactivity to -sin actin antibody. TGFβ/FGF-treated ex- plants were strongly stained with type I collagen antibody. Condusion. In the presence of FGF, TGFβ1 and TGFβ2 induced lens epithelial cell (LEC ) proliferation and transformation into fibroblast or myofibroblast-like cells, with producing of abundant collagen matrix in the explants. The changes are similar to the metaplasia that occurrs in subcapsular opacification of the lens. The findings suggest that TGFβ and FGF plays a role in the pathogenesis of subcapsular opacification of the lens.
