AIM:To evaluate celastrol's effect on choroidal neovascularization(CNV).METHODS:In this study,neovascular formation in vitro(tube formation and aortic ring culture)and in vivo(laser induced neovascular in mice)was...AIM:To evaluate celastrol's effect on choroidal neovascularization(CNV).METHODS:In this study,neovascular formation in vitro(tube formation and aortic ring culture)and in vivo(laser induced neovascular in mice)was treated with celastrol to evaluate this natural compound's impact on CNV.Western blot was applied to explore the possible mechanism for it.For in vitro assay,triplicate for each group was repeated at least three times.For in vivo assay,each group contains 5 mice.RESULTS:Celastrol supressed tube formation and aortic ring sprout neovascularization.In vitro assay exhibited that celastrol inhibiting vascular endothelial growth factor(VEGF)-induced proliferation and migration of human umbilical vein endothelial cells and human choroidal endothelial cells,and by blocking VEGF signaling.Furthermore,intraperitoneal administration of celastrol significantly reduced the area of laser-induced CNV in an in vivo mouse model.By day 14,the area of CNV had decreased by 49.15%and 80.26%in the 0.1 mg/kg celastrol-treated group(n=5)and in the 0.5 mg/kg celastrol treated group(n=5),respectively,compared to the vehicle-treated group(n=5).CONCLUSION:Celastrol inhibits CNV by inhibiting VEGF-induced proliferation and migration of vascular endothelial cells,indicating that celastrol is a potent,natural therapeutic compound for the prevention of CNV.展开更多
AIM:To investigate the effect of Staphylococcus aureus(S.aures)lysates(SALs)on herpes simplex virus type-Ⅰ(HSV1)infection in human corneal epithelial(HCE)cells and in a mouse model of HSV1 keratitis.METHODS:HCE,Vero,...AIM:To investigate the effect of Staphylococcus aureus(S.aures)lysates(SALs)on herpes simplex virus type-Ⅰ(HSV1)infection in human corneal epithelial(HCE)cells and in a mouse model of HSV1 keratitis.METHODS:HCE,Vero,HeLa,and BV2 cells were infected with HSV1[HSV1f strain,HSV1f;HSV-1-H129 with green fluorescent protein(GFP)knock-in,HSV1g].Pre-or post-infection,SAL at various concentrations was added to the culture medium for 24 h.GFP fluorescence in HSV1g or plaque formation by HSV1f were examined.The effects of heat-treated SAL,precooled acetone-precipitated SAL,and SAL subjected to ultrafiltration(100 kDa)were evaluated.The effects of other bacterial components and lysates on HSV1 infection were also tested,including lipoteichoic acid(LTA),peptidoglycan(PGN),staphylococcal protein A(SPA),andα-hemolysin from S.aureus(α-toxin)as well as lysates from a wild-type S.aureus strain,S.epidermidis,and Escherichia coli(W-SAL,SEL,and ECL,respectively).In addition,SAL eye drops were applied topically to BALB/c mice with HSV1 keratitis,followed by in vivo observations.RESULTS:The cytopathic effect,plaque formation(HSV1f),and GFP expression(HSV1g)in infected cells were inhibited by SAL in a dose-dependent manner.The active component of SAL(≥100 kDa)was heat-sensitive and retained activity after acetone precipitation.In HSV1ginfected cells,treatment with LTA-sa,α-toxin,PGN-sa,or SPA did not inhibit GFP expression.SAL,W-SAL,and SEL(but not ECL)decreased GFP expression.In mice with HSV1 keratitis,SAL reduced corneal lesions by 71%.CONCLUSION:The results of this study demonstrate that SAL can be used to inhibit HSV1 infection,particularly keratitis.Further studies are needed to determine the active components and mechanism underlying the effects of SAL.展开更多
基金Supported by National Natural Science Foundation of China(No.81570826)。
文摘AIM:To evaluate celastrol's effect on choroidal neovascularization(CNV).METHODS:In this study,neovascular formation in vitro(tube formation and aortic ring culture)and in vivo(laser induced neovascular in mice)was treated with celastrol to evaluate this natural compound's impact on CNV.Western blot was applied to explore the possible mechanism for it.For in vitro assay,triplicate for each group was repeated at least three times.For in vivo assay,each group contains 5 mice.RESULTS:Celastrol supressed tube formation and aortic ring sprout neovascularization.In vitro assay exhibited that celastrol inhibiting vascular endothelial growth factor(VEGF)-induced proliferation and migration of human umbilical vein endothelial cells and human choroidal endothelial cells,and by blocking VEGF signaling.Furthermore,intraperitoneal administration of celastrol significantly reduced the area of laser-induced CNV in an in vivo mouse model.By day 14,the area of CNV had decreased by 49.15%and 80.26%in the 0.1 mg/kg celastrol-treated group(n=5)and in the 0.5 mg/kg celastrol treated group(n=5),respectively,compared to the vehicle-treated group(n=5).CONCLUSION:Celastrol inhibits CNV by inhibiting VEGF-induced proliferation and migration of vascular endothelial cells,indicating that celastrol is a potent,natural therapeutic compound for the prevention of CNV.
基金the National Natural Science Foundation of China(No.81770896,No.81970848)the Guangzhou Science Technology and Innovation Commission(No.201607020011)。
文摘AIM:To investigate the effect of Staphylococcus aureus(S.aures)lysates(SALs)on herpes simplex virus type-Ⅰ(HSV1)infection in human corneal epithelial(HCE)cells and in a mouse model of HSV1 keratitis.METHODS:HCE,Vero,HeLa,and BV2 cells were infected with HSV1[HSV1f strain,HSV1f;HSV-1-H129 with green fluorescent protein(GFP)knock-in,HSV1g].Pre-or post-infection,SAL at various concentrations was added to the culture medium for 24 h.GFP fluorescence in HSV1g or plaque formation by HSV1f were examined.The effects of heat-treated SAL,precooled acetone-precipitated SAL,and SAL subjected to ultrafiltration(100 kDa)were evaluated.The effects of other bacterial components and lysates on HSV1 infection were also tested,including lipoteichoic acid(LTA),peptidoglycan(PGN),staphylococcal protein A(SPA),andα-hemolysin from S.aureus(α-toxin)as well as lysates from a wild-type S.aureus strain,S.epidermidis,and Escherichia coli(W-SAL,SEL,and ECL,respectively).In addition,SAL eye drops were applied topically to BALB/c mice with HSV1 keratitis,followed by in vivo observations.RESULTS:The cytopathic effect,plaque formation(HSV1f),and GFP expression(HSV1g)in infected cells were inhibited by SAL in a dose-dependent manner.The active component of SAL(≥100 kDa)was heat-sensitive and retained activity after acetone precipitation.In HSV1ginfected cells,treatment with LTA-sa,α-toxin,PGN-sa,or SPA did not inhibit GFP expression.SAL,W-SAL,and SEL(but not ECL)decreased GFP expression.In mice with HSV1 keratitis,SAL reduced corneal lesions by 71%.CONCLUSION:The results of this study demonstrate that SAL can be used to inhibit HSV1 infection,particularly keratitis.Further studies are needed to determine the active components and mechanism underlying the effects of SAL.
