AIMTo investigate the effect of flavone on ocular blood flow in rabbit eyes and the formation of choroidal neovascularization (CNV) in rat model of age-related macular degeneration (AMD).
Purpose:Age-related macular degeneration(AMD)as a disease entity is "dry" at early stage and made up of two main components at late stage:atrophic AMD and exudative AMD.Quercetin acts as an anti-oxidant to p...Purpose:Age-related macular degeneration(AMD)as a disease entity is "dry" at early stage and made up of two main components at late stage:atrophic AMD and exudative AMD.Quercetin acts as an anti-oxidant to protect retinal pigment epithelial cells(RPE)from damaged by oxidative stress,but its effect on formation of choroidal neovascularization(CNV)in AMD is unclear.The aim of this study is to investigate the effect of quercetin on the formation of CNV in AMD.Methods:The development of CNV induced by laser was detected.by fluorescein angiography(FA).Colored microsphere technique was used to determine the choroidal blood flow in ocular hypertensive rabbit eyes.In in vitro studies,HUVECs were treated with NaIO3,H2O2 and NaN3 to induce oxidative cell damages.The effect of quercetin on various oxidations-induced injuries in HUVECs was measured by MTT assay.HUVECs migration was assessed using a wound healing assay.Results:Quercetin significantly inhibited the formation of laser-induced CNV.The choroidal blood flow in rabbit eyes was significantly increased after quercetin instillation.In vitro results showed quercetin enhanced various oxidations-induced injuries in HUVECs and inhibited migration of HUVECs during wound healing.Conclusion:Quercetin inhibited the formation of CNV both in vivo and in vitro and increased choroidal blood flow.It could become a promising candidate for the treatment of AMD.展开更多
AIM： To study the effects of cytokeratin 17 （CK17） on sodium iodate （NalOs） induced rat retinal pigment epithelium （RPE） degeneration, laser induced rat choroidal neovascularization （CNV）, and oxidative stres...AIM： To study the effects of cytokeratin 17 （CK17） on sodium iodate （NalOs） induced rat retinal pigment epithelium （RPE） degeneration, laser induced rat choroidal neovascularization （CNV）, and oxidative stress of human retinal pigment epithelium cells （ARPE-19） and human umbilical vein endothelial cell （HUVEC）. METHODS： Thirty 8-week-old male Brown Norway rats were randomly divided into 3 groups, 10 rats in control group treated with solvent alone; 10 rats in NalOs group treated with solvent and 35 mg/kg NalO3 injection through hypoglossal vein and 10 rats in CK17 ＋NaIOs group treated with 1% CK17 eye drop 3 times a day for lwk before and 4wk after NalOs injection. RPE function was measured with c-wave of electroretinogram （ERG）. Another 20 rats were randomly divided into 2 groups. Of them 10 rats in CK17 group were anesthetized to receive Nd：YAG laser and given 1% CK17 eye drop before same as above; 10 rats in control were received Nd：YAG and treated with solvent. The development of choroidal neovascularization （CNV） was determined by fundus fluorescein angiography （FFA） performed on 4wk after laser. Methylthiazoly tetrazolium （MTT） assay was used to study effect of CK17 on various oxidants induced injury in ARPE-19 and HUVEC /n vitro RESULTS： Four weeks after NalOs injection, the c- wave amplitude of ERG was 0.393±0.02 V in the control group, 0.184±0.018 V in NalOs group and 0.3±0.01 V in CK17＋NalOs group. There was a significant reversal of the c-wave by CK17 as compared to NalOs group （P〈0.01）. Four weeks after laser, the size of the CNV lesion was 2.57±0.27 mm2 in control group and 1.64 ±0.08 mm2 in CK17 group. The lesion size significantly diminished in CK17 group （P〈0.01）. The inn vitro results showed CK17 also reversed the various oxidants induced injuries in ARPE-19 at the dose of 100 μg/mL and enhanced the injury in HUVECs at different concentrations. CONCLUSION： CK17 can significantly protect RPE from NalOs induced degeneration in vivo and /n vito and also could reverse the various oxidants induced injuries in vitro. It inhibits the development of CNV in rat model, interfered with vascular endothelial cell proliferation in ivtro.展开更多
OBJECTIVE The objective was to study the relationship between the tumor factor of cancer MATLT and the catalytic subunit of telomerase. The function of telomerase in the blockade of cell differentiation and in the pro...OBJECTIVE The objective was to study the relationship between the tumor factor of cancer MATLT and the catalytic subunit of telomerase. The function of telomerase in the blockade of cell differentiation and in the protection of DNA MT resembles closely the function of the tumor factor of cancer MATKw. Because of this close similarity we made an attempt to examine the possibility that the tumor factor of MATKT might be the catalytic subunit of telomerase. METHODS We used purified MAT isozymes, telomerase antibody, immunoprecipitation, and a selective inhibitor of the tumor factor of MATLT from urine to study the relationship between the tumor factor of MATLT and telomerase. RESULTS We were able to show that the tumor MATcw, but not the liver MATL, was selectively inhibited by the telomerase antibody, and the tumor MATLT, but not the liver MATL, was preferentially immunoprecipitated with the telomerase antibody. The catalytic subunit of telomerase was detectable in the tumor MATLT preparation by immunoblotting, but was undetectable in the liver MATc preparation and the tumor MATc preparation stripped off of the tumor factor. In addition, PP-0.39, which is an effective differentiation inducer purified from urine previously found to selectively antagonize the tumor factor of MATLT, was found in this study to be a potent inhibitor of telomerase. The inhibition of telomerase by PP-0.39 was far more sensitive than the elimination of the tumor factor from MATLT. CONCLUSION All results are consistent with the hypothesis that the tumor factor of MATLT is the catalytic subunit of telomerase. Thus, the blockade of cell differentiation by telomerase is mediated through its interaction with MAT to affect methylation enzymes, so that hypomethylation of nucleic acids necessary for the cell to undergo differentiation cannot take place.展开更多
文摘AIMTo investigate the effect of flavone on ocular blood flow in rabbit eyes and the formation of choroidal neovascularization (CNV) in rat model of age-related macular degeneration (AMD).
文摘Purpose:Age-related macular degeneration(AMD)as a disease entity is "dry" at early stage and made up of two main components at late stage:atrophic AMD and exudative AMD.Quercetin acts as an anti-oxidant to protect retinal pigment epithelial cells(RPE)from damaged by oxidative stress,but its effect on formation of choroidal neovascularization(CNV)in AMD is unclear.The aim of this study is to investigate the effect of quercetin on the formation of CNV in AMD.Methods:The development of CNV induced by laser was detected.by fluorescein angiography(FA).Colored microsphere technique was used to determine the choroidal blood flow in ocular hypertensive rabbit eyes.In in vitro studies,HUVECs were treated with NaIO3,H2O2 and NaN3 to induce oxidative cell damages.The effect of quercetin on various oxidations-induced injuries in HUVECs was measured by MTT assay.HUVECs migration was assessed using a wound healing assay.Results:Quercetin significantly inhibited the formation of laser-induced CNV.The choroidal blood flow in rabbit eyes was significantly increased after quercetin instillation.In vitro results showed quercetin enhanced various oxidations-induced injuries in HUVECs and inhibited migration of HUVECs during wound healing.Conclusion:Quercetin inhibited the formation of CNV both in vivo and in vitro and increased choroidal blood flow.It could become a promising candidate for the treatment of AMD.
文摘AIM： To study the effects of cytokeratin 17 （CK17） on sodium iodate （NalOs） induced rat retinal pigment epithelium （RPE） degeneration, laser induced rat choroidal neovascularization （CNV）, and oxidative stress of human retinal pigment epithelium cells （ARPE-19） and human umbilical vein endothelial cell （HUVEC）. METHODS： Thirty 8-week-old male Brown Norway rats were randomly divided into 3 groups, 10 rats in control group treated with solvent alone; 10 rats in NalOs group treated with solvent and 35 mg/kg NalO3 injection through hypoglossal vein and 10 rats in CK17 ＋NaIOs group treated with 1% CK17 eye drop 3 times a day for lwk before and 4wk after NalOs injection. RPE function was measured with c-wave of electroretinogram （ERG）. Another 20 rats were randomly divided into 2 groups. Of them 10 rats in CK17 group were anesthetized to receive Nd：YAG laser and given 1% CK17 eye drop before same as above; 10 rats in control were received Nd：YAG and treated with solvent. The development of choroidal neovascularization （CNV） was determined by fundus fluorescein angiography （FFA） performed on 4wk after laser. Methylthiazoly tetrazolium （MTT） assay was used to study effect of CK17 on various oxidants induced injury in ARPE-19 and HUVEC /n vitro RESULTS： Four weeks after NalOs injection, the c- wave amplitude of ERG was 0.393±0.02 V in the control group, 0.184±0.018 V in NalOs group and 0.3±0.01 V in CK17＋NalOs group. There was a significant reversal of the c-wave by CK17 as compared to NalOs group （P〈0.01）. Four weeks after laser, the size of the CNV lesion was 2.57±0.27 mm2 in control group and 1.64 ±0.08 mm2 in CK17 group. The lesion size significantly diminished in CK17 group （P〈0.01）. The inn vitro results showed CK17 also reversed the various oxidants induced injuries in ARPE-19 at the dose of 100 μg/mL and enhanced the injury in HUVECs at different concentrations. CONCLUSION： CK17 can significantly protect RPE from NalOs induced degeneration in vivo and /n vito and also could reverse the various oxidants induced injuries in vitro. It inhibits the development of CNV in rat model, interfered with vascular endothelial cell proliferation in ivtro.
文摘OBJECTIVE The objective was to study the relationship between the tumor factor of cancer MATLT and the catalytic subunit of telomerase. The function of telomerase in the blockade of cell differentiation and in the protection of DNA MT resembles closely the function of the tumor factor of cancer MATKw. Because of this close similarity we made an attempt to examine the possibility that the tumor factor of MATKT might be the catalytic subunit of telomerase. METHODS We used purified MAT isozymes, telomerase antibody, immunoprecipitation, and a selective inhibitor of the tumor factor of MATLT from urine to study the relationship between the tumor factor of MATLT and telomerase. RESULTS We were able to show that the tumor MATcw, but not the liver MATL, was selectively inhibited by the telomerase antibody, and the tumor MATLT, but not the liver MATL, was preferentially immunoprecipitated with the telomerase antibody. The catalytic subunit of telomerase was detectable in the tumor MATLT preparation by immunoblotting, but was undetectable in the liver MATc preparation and the tumor MATc preparation stripped off of the tumor factor. In addition, PP-0.39, which is an effective differentiation inducer purified from urine previously found to selectively antagonize the tumor factor of MATLT, was found in this study to be a potent inhibitor of telomerase. The inhibition of telomerase by PP-0.39 was far more sensitive than the elimination of the tumor factor from MATLT. CONCLUSION All results are consistent with the hypothesis that the tumor factor of MATLT is the catalytic subunit of telomerase. Thus, the blockade of cell differentiation by telomerase is mediated through its interaction with MAT to affect methylation enzymes, so that hypomethylation of nucleic acids necessary for the cell to undergo differentiation cannot take place.
