Objective To explore the glycation of basic fibroblast grow th factor( bFGF) in diabetic skin.Methods The abdom inal full-thickness skin tissues from 58 patients( 29 diabetic and 29 non-diabetic) aged 40 to69 years an...Objective To explore the glycation of basic fibroblast grow th factor( bFGF) in diabetic skin.Methods The abdom inal full-thickness skin tissues from 58 patients( 29 diabetic and 29 non-diabetic) aged 40 to69 years and granulation tissues from 15 patients( 8 diabetic and 7 non-diabetic) aged 50 to 59 were analyzed.The proportion of advanced glycation end products( AGEs)-b FG F intotal b FGF was measured with co-immunoprecipitation and the histological characteristics of wound skin were detected with hem atoxylin and eosin staining. The cell viability, apoptosis, and angiogenesis of human derm al m icrovascular endothelial cells( HDMECs) after exposure to AG Es-b FG For bFGF were measured with cell counting kit-8, flow cytom etry,and tube form ation assay, respectively. Results The proportion of AG Es-b FG F in total b FG F showed agedependent increaseboth in diabetic and non-diabetic skin. As com pared with non-diabetic skin, the constituent ratio in diabetic skin increased significantly in the equal age-group, and the same result could be obtained in granulation tissues from patients aged 50 to 59. The proportion of AG Es-b FG F in diabetic granulation was low er than that in diabetic skin from patients aged 50 to 59. H istological analysis show ed few er vessels in diabetic skin wound. In vitro, the viability and vascularization of H D M EC s were promoted by b FG F and inhibited after exposure to AGEs-bFGF for 7d. Conclusion The present study indicates that one cause for im paired wound healing in diabetic skin could be the glycated b FG F and its changed angiogenic function.展开更多
The purpose of the present study was to determine protectivie effects of basic fibroblast growth factor (bFGF) on cochlear neurons and hair cells in vitro and in vivo. In experiment I, cultured spiral ganglion neurons...The purpose of the present study was to determine protectivie effects of basic fibroblast growth factor (bFGF) on cochlear neurons and hair cells in vitro and in vivo. In experiment I, cultured spiral ganglion neurons (SGNs) prepared from P3 mice were exposed to 20mM glutamate for 2 hours before the culture medium was replaced with fresh medium containing 0, 25, 50, and 100 ng/ml bFGF, respectively. Fourteen days later, all cultures were fixed with 4% paraformaldehyde, and stained with 1% toluidine blue. The number of surviving SGNs were counted and the length of SGNs neurites were measured. Exposure to 20 mM glutamate for 24 hours resulted in an inhibition on neurite outgrowth of SGNs and elevated cell death. Treatment of the cultures with bFGF led to promotion of neurite outgrowth and elevated number of surviving SGNs. Effects of bFGF were dose dependent with the highest potency at 100 ng/ml. In experiment Ⅱ, in vivo studies were carried out with guinea pigs in which bFGF or artificial perilymph was perfused into the cochlea to assess possible protective effects of bFGF on cochlear hair cells and compound action potentials(CAP). The CAPs were measured before, immediatly and 48 hours after exposure to noise. Significant differences in CAP were observed (p＜0. 05 ) among the bFGF perfused group, control group(t =3. 896 ) and artificial perilymph perfused group (t =2. 520) at 48 hours after noise exposure, Cochleae were removed and hair cell Loss was analyzed in surface preparations prepared from all experimental animals. Acoustic trauma caused loss of 651 and 687 inner hair cells in the control and artificial perilymph perfused group, respectively. In sharp contrast, only 31 inner hair cells were lost in the bFGF perfused ears. Similarly, more outer hair cells died in the control and perilymph perfuesed group (41830 and 41968, respectively) than in the group treated with bFGF (34258). Our results demonstrate that bFGF protected SGNs against glutmate neurotoxicity in vitro. In addition, treatment with bFGF also protected hair cells from acoustic trauma.展开更多
基金National Natural Science Foundation of China(81071568,81272111)National Science and Technology Support Plan(2012BAI11B00)
文摘Objective To explore the glycation of basic fibroblast grow th factor( bFGF) in diabetic skin.Methods The abdom inal full-thickness skin tissues from 58 patients( 29 diabetic and 29 non-diabetic) aged 40 to69 years and granulation tissues from 15 patients( 8 diabetic and 7 non-diabetic) aged 50 to 59 were analyzed.The proportion of advanced glycation end products( AGEs)-b FG F intotal b FGF was measured with co-immunoprecipitation and the histological characteristics of wound skin were detected with hem atoxylin and eosin staining. The cell viability, apoptosis, and angiogenesis of human derm al m icrovascular endothelial cells( HDMECs) after exposure to AG Es-b FG For bFGF were measured with cell counting kit-8, flow cytom etry,and tube form ation assay, respectively. Results The proportion of AG Es-b FG F in total b FG F showed agedependent increaseboth in diabetic and non-diabetic skin. As com pared with non-diabetic skin, the constituent ratio in diabetic skin increased significantly in the equal age-group, and the same result could be obtained in granulation tissues from patients aged 50 to 59. The proportion of AG Es-b FG F in diabetic granulation was low er than that in diabetic skin from patients aged 50 to 59. H istological analysis show ed few er vessels in diabetic skin wound. In vitro, the viability and vascularization of H D M EC s were promoted by b FG F and inhibited after exposure to AGEs-bFGF for 7d. Conclusion The present study indicates that one cause for im paired wound healing in diabetic skin could be the glycated b FG F and its changed angiogenic function.
文摘The purpose of the present study was to determine protectivie effects of basic fibroblast growth factor (bFGF) on cochlear neurons and hair cells in vitro and in vivo. In experiment I, cultured spiral ganglion neurons (SGNs) prepared from P3 mice were exposed to 20mM glutamate for 2 hours before the culture medium was replaced with fresh medium containing 0, 25, 50, and 100 ng/ml bFGF, respectively. Fourteen days later, all cultures were fixed with 4% paraformaldehyde, and stained with 1% toluidine blue. The number of surviving SGNs were counted and the length of SGNs neurites were measured. Exposure to 20 mM glutamate for 24 hours resulted in an inhibition on neurite outgrowth of SGNs and elevated cell death. Treatment of the cultures with bFGF led to promotion of neurite outgrowth and elevated number of surviving SGNs. Effects of bFGF were dose dependent with the highest potency at 100 ng/ml. In experiment Ⅱ, in vivo studies were carried out with guinea pigs in which bFGF or artificial perilymph was perfused into the cochlea to assess possible protective effects of bFGF on cochlear hair cells and compound action potentials(CAP). The CAPs were measured before, immediatly and 48 hours after exposure to noise. Significant differences in CAP were observed (p＜0. 05 ) among the bFGF perfused group, control group(t =3. 896 ) and artificial perilymph perfused group (t =2. 520) at 48 hours after noise exposure, Cochleae were removed and hair cell Loss was analyzed in surface preparations prepared from all experimental animals. Acoustic trauma caused loss of 651 and 687 inner hair cells in the control and artificial perilymph perfused group, respectively. In sharp contrast, only 31 inner hair cells were lost in the bFGF perfused ears. Similarly, more outer hair cells died in the control and perilymph perfuesed group (41830 and 41968, respectively) than in the group treated with bFGF (34258). Our results demonstrate that bFGF protected SGNs against glutmate neurotoxicity in vitro. In addition, treatment with bFGF also protected hair cells from acoustic trauma.
