期刊文献+
共找到12篇文章
< 1 >
每页显示 20 50 100
Effects of endostatin on expression of vascular endothelial growth factor and its receptors and neovascularization in colonic carcinoma implanted in nude mice 被引量:17
1
作者 Yun-HeJia Xin-ShuDong Xi-ShanWang 《World Journal of Gastroenterology》 SCIE CAS CSCD 2004年第22期3361-3364,共4页
AIM:To investigate the antiangiogenic effects of endostatin on colonic carcinoma cell line implanted in nude mice and its mechanism. METHODS:Nude mice underwent subcutaneous injection with LS-174t colonic carcinoma ce... AIM:To investigate the antiangiogenic effects of endostatin on colonic carcinoma cell line implanted in nude mice and its mechanism. METHODS:Nude mice underwent subcutaneous injection with LS-174t colonic carcinoma cell line to generate carcinoma and were randomly separated into two groups.Mice received injection of vehicle or endostatin every day for two weeks. After the tumor was harvested,the tumor volumes were determined,and the expressions of CD34,VEGF and FIk-1 were examined by immunohistochemical method. RESULTS:Tumor volume was significantly inhibited in the endostatin group(84.17%)and tumor weight was significantly inhibited in the endostatin group(0.197±0.049) compared to the control group(1.198±0.105)(F=22.56, P=0.001),microvessel density(MVD)was significantly decreased in the treated group(31.857±3.515)compared to the control group(100.143±4.290)(F=151.62,P<0.001). Furthermore,the expression of FIk-1 was significantly inhibited in the treated group(34.29%) ompared to the control group(8.57%)(X^2=13.745,P=0.001).However no significant decrease was observed in the expression of vascular endothelial growth factor(VEGF)between these two groups(X^2=0.119,P=0.730). CONCLUSION:Endostatin can inhibit tumor growth and angiogenesis by blocking Vegf/FIk-1 pathway.This experiment provides the theory basis for developing a new anti-carcinoma drug through studying the properties of anti-angiogenesis inhibitors. 展开更多
关键词 Angiogenesis Inhibitors Animals Antigens CD34 Cell Line Tumor Colonic Neoplasms ENDOSTATINS MICE Mice Nude neovascularization Pathologic Research Support Non-U.S. Gov't Vascular Endothelial Growth Factor A Vascular Endothelial Growth Factor Receptor-2 Xenograft Model Antitumor Assays
下载PDF
The prognostic molecular markers in hepatocellular carcinoma 被引量:163
2
作者 Lun-Xiu Qin Zhao-You Tang,Liver Cancer Institute and Zhongshan Hospital,Fudan University,Shanghai,China 《World Journal of Gastroenterology》 SCIE CAS CSCD 2002年第3期385-392,共8页
The prognosis of hepatocellular carcinoma (HCC) still remains dismal, although many advances in its clinical study have been made. It is important for tumor control to identify the factors that predispose patients to ... The prognosis of hepatocellular carcinoma (HCC) still remains dismal, although many advances in its clinical study have been made. It is important for tumor control to identify the factors that predispose patients to death. With new discoveries in cancer biology, the pathological and biological prognostic factors of HCC have been studied quite extensively. Analyzing molecular markers (biomarkers) with prognostic significance is a complementary method. A large number of molecular factors have been shown to associate with the invasiveness of HCC, and have potential prognostic significance. One important aspect is the analysis of molecular markers for the cellular malignancy phenotype. These include alterations in DNA ploidy, cellular proliferation markers (PCNA, Ki-67, Mcm2, MIB1, MIA, and CSE1L/CAS protein), nuclear morphology, the p53 gene and its related molecule MD M2, other cell cycle regulators (cyclin A, cyclin D, cyclin E, cdc2, p27, p73), oncogenes and their receptors (such as ras, c-myc, c-fms, HGF, c-met, and erb-B receptor family members), apoptosis related factors (Fas and FasL), as well as telomerase activity. Another important aspect is the analysis of molecular markers involved in the process of cancer invasion and metastasis. Adhesion molecules (E-cadherin, catenins, serum intercellular adhesion molecule-1, CD44 variants), proteinases involved in the degradation of extracellular matrix (MMP-2, MMP-9, uPA, uPAR, PAI), as well as other molecules have been regarded as biomarkers for the malignant phenotype of HCC, and are related to prognosis and therapeutic outcomes. Tumor angiogenesis is critical to both the growth and metastasis of cancers including HCC, and has drawn much attention in recent years. Many angiogenesis-related markers, such as vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), platelet-derived endothelial cell growth factor (PD-ECGF), thrombospondin (TSP), angiogenin, pleiotrophin, and endostatin (ES) levels, as well as intratumor microvessel density (MVD) have been evaluated and found to be of prognostic significance. Body fluid (particularly blood and urinary) testing for biomarkers is easily accessible and useful in clinical patients. The prognostic significance of circulating DNA in plasma or serum, and its genetic alterations in HCC are other important trends. More attention should be paid to these two areas in future. As the progress of the human genome project advances, so does a clearer understanding of tumor biology, and more and more new prognostic markers with high sensitivity and specificity will be found and used in clinical assays. However, the combination of some items, i.e., the pathological features and some biomarkers mentioned above, seems to be more practical for now. 展开更多
关键词 Apoptosis CARCINOGENS Carcinoma Hepatocellular Cell Adhesion Cell Division Cell Nucleus Extracellular Matrix Genes p53 Humans Liver Neoplasms neovascularization Pathologic PLOIDIES Prognosis Proteome TELOMERASE Tumor Markers Biological
下载PDF
Analysis of p53 and vascular endothelial growth factor expression in human gallbladder carcinoma for the determination of tumor vascularity 被引量:13
3
作者 Yu Tian Ren-Yu Ding +2 位作者 Ying-Hui Zhi Ren-Xuan Guo Shuo-Dong Wu 《World Journal of Gastroenterology》 SCIE CAS CSCD 2006年第3期415-419,共5页
AIM: To examine the expression of p53 and vascular endothelial growth factor (VEGF) as well as microvessel count (MVC) and to investigate the role of VEGF as an angiogenic marker and the possible role of p53 in t... AIM: To examine the expression of p53 and vascular endothelial growth factor (VEGF) as well as microvessel count (MVC) and to investigate the role of VEGF as an angiogenic marker and the possible role of p53 in the regulation of angiogenesis in human gallbladder carcinoma. METHODS: Surgically resected specimens of 49 gallbladder carcinomas were studied by immunohistochemical staining for p53 protein, VEGF, and factor VIII-related antigen. VEGF expression and mutant p53 expression were then correlated with Nevin stage, differentiation grade, MVC, and lymph node metastasis. RESULTS: Positive p53 protein and VEGF expressions were found in 61.2% and 63.3% of tumors, respectively. p53 and VEGF staining status was identical in 55.1% of tumors. The Nevin staging of p53- or VEGF-positive tumors was significantly later than that of negative tumors. The MVC in p53- or VEGF-positive tumors was significantly higher than that in negative tumors, and MVC in both p53- and VEGF-negative tumors was significantly lower than that in the other subgroups. CONCLUSION: Our findings suggest that pS3-VEGF pathway can regulate tumor angiogenesis in human gallbladder carcinoma. Combined analysis of p53 and VEGF expression might be useful for predicting the tumor vascularity of gallbladder cancer. 展开更多
关键词 Gallbladder neoplasms Protein p53 neovascularization Pathology
下载PDF
Reduction of tumorigenicity of SMMC-7721 hepatoma cells by vascular endothelial growth factor antisense gene therapy 被引量:33
4
作者 Yu Cheng Tang Yu Li Guan Xiang Qian Department of Biochemistry, Shanghai Second Medical University, Shanghai 200025, China 《World Journal of Gastroenterology》 SCIE CAS CSCD 2001年第1期22-27,共6页
AIM: To test the hypothesis to block VEGF expression of SMMC-7721 hepatoma cells may inhibit tumor growth using the rat hepatoma model. METHODS: Amplify the 200 VEGF cDNA fragment and insert it into human U6 gene cass... AIM: To test the hypothesis to block VEGF expression of SMMC-7721 hepatoma cells may inhibit tumor growth using the rat hepatoma model. METHODS: Amplify the 200 VEGF cDNA fragment and insert it into human U6 gene cassette in the reverse orientation transcribing small antisense RNA which could specifically interact with VEGF165, and VEGF121 mRNA. Construct the retroviral vector containing this antisense VEGF U6 cassette and package the replication-deficient recombinant retrovirus. SMMC-7721 cells were transduced with these virus and positive clones were selected with G418. PCR and Southern blot analysis were performed to determine if U6 cassette integrated into the genomic DNA of positive clone. Transfected tumor cells were evaluated for RNA expression by ribonuclease protection assays. The VEGF protein in the supernatant of parental tumor cells and genetically modified tumor cells was determined with ELISA. In vitro and in vivo growth properties of antisense VEGF cell clone in nude mice were analyzed. RESULTS: Restriction enzyme digestion and PCR sequencing verified that the antisense VEGF RNA retroviral vector was successfully constructed.After G418 selection, resistant SMMC-7721 cell clone was picked up. PCR and Southern blot analysis suggested that U6 cassette was integrated into the cell genomic DNA. Stable SMMC-7721 cell clone transduced with U6 antisense RNA cassette could express 200 bp small antisense VEGF RNA and secrete reduced levels of VEGF in culture condition. Production of VEGF by antisense transgene-expressing cells was 65+/-10 ng/L per 10(6) cells, 42045 ng/L per 10(6) cells in sense group and 485+/-30 ng/L per 10(6) cells in the negative control group, (P【 0.05). The antisense-VEGF cell clone appeared phenotypically indistinguishable from SMMC-7721 cells and SMMC-7721 cells transfected sense VEGF. The growth rate of the antisense-VEGF cell clone was the same as the control cells. When S.C. was implanted into nude mice, growth of antisense-VEGF cell lines was greatly inhibited compared with control cells. CONCLUSION: Expression of antisense VEGF RNA in SMMC-7721 cells could decrease the tumorigenicity, and antisense-VEGF gene therapy may be an adjuvant treatment for hepatoma. 展开更多
关键词 Gene Therapy Animals Carcinoma Hepatocellular Cell Division DNA Polymerase III Endothelial Growth Factors Endothelium Vascular Enzyme-Linked Immunosorbent Assay Gene Expression Humans Liver Neoplasms LYMPHOKINES MICE Mice Nude neovascularization Pathologic Promoter Regions (Genetics) RNA Antisense Research Support Non-U.S. Gov't Transduction Genetic Tumor Cells Cultured Vascular Endothelial Growth Factor A Vascular Endothelial Growth Factors
下载PDF
Expression of vascular endothelial growth factor and its role in oncogenesis of human gastric carcinoma 被引量:37
5
作者 Du-Hu Liu Xue-Yong Zhang Dai-Ming Fan Yu-Xin Huang Jin-Shan Zhang Wei-Quan Huang Yuan-Qiang Zhang Qing-Sheng Huang Wen-Yu Ma Yu-Bo Chai Ming Jin Institute of Digestive Disease,Xijing Hospital,~2 Department of Gastroenterology,Tangdu Hospital,~3Department of Histology and Embryology,~4 Department of Microbiology,~5 Department of Biochemistry,Fourth Military Medical University,Xi’an 710033,Shaanxi Province,China 《World Journal of Gastroenterology》 SCIE CAS CSCD 2001年第4期500-505,共6页
AIM: To establish the role of vascular endothelial growth factor (VEGF) in the oncogenesis of human gastric carcinoma more directly. METHODS: The expression of VEGF and its receptor kinase-domain insert containing rec... AIM: To establish the role of vascular endothelial growth factor (VEGF) in the oncogenesis of human gastric carcinoma more directly. METHODS: The expression of VEGF and its receptor kinase-domain insert containing receptor (KDR) in human gastric cancer tissue were observed by immunohistochemical staining. VEGF levels were manipulated in human gastric cancer cell using eukaryotic expression constructs designed to express the complete VEGF(165) complimentary DNA in either the sense or antisense orientation. The biological changes of the cells were observed in which VEGF was up-regulated or down-regulated. RESULTS: VEGF-positive rate was 50%, and VEGF was mainly localized in the cytoplasm and membrane of the tumor cells, while KDR was mainly located in the membrane of vascular endothelial cells in gastric cancer tissues and peri-cancerous tissue. In 2 cases of 50 specimens, the gastric cancer cells expressed KDR, localized in both the cytoplasm and membrane. Introduction of VEGF(165) antisense into human gastric cancer cells (SGC-7901, immunofluorescence intensity, 31.6%)) resulted in a significant reduction in VEGF-specific messenger RNA and total and cell surface VEGF protein (immunofluorescence intensity, 8.9%) (P【0.05). Conversely, stable integration of VEGF(165) in the sense orientation resulted in an increase in cellular and cell surface VEGF (immunofluorescence intensity, 75.4%) (P【0.05). Lowered VEGF levels were associated with a marked decrease in the growth of nude mouse xenografted tumor (at 33 days postimplantation, tumor volume: 345.40 +/- 136.31 mm3)(P【0.05 vs control SGC-7901 group: 1534.40 +/- 362.88 mm3), whereas up-regulation of VEGF resulted in increased xenografted tumor size (at 33 days postimplantation, tumor volume: 2350.50 +/- 637.70 mm3) (P【0.05 vs control SGC-7901 group). CONCLUSION: This study provides direct evidence that VEGF plays an important role in the oncogenesis of human gastric cancer. 展开更多
关键词 Gene Expression Regulation Neoplastic Adult Aged Animals Cell Division Cloning Molecular DNA Antisense DNA Complementary Endothelial Growth Factors Endothelium Vascular Female Humans LYMPHOKINES Male MICE Mice Nude Middle Aged neovascularization Pathologic Receptor Protein-Tyrosine Kinases Receptors Growth Factor Receptors Vascular Endothelial Growth Factor Stomach Neoplasms Transfection Tumor Cells Cultured Vascular Endothelial Growth Factor A Vascular Endothelial Growth Factors
下载PDF
Effect of endothelial progenitor cells in neovascularization and their application in tumor therapy 被引量:11
6
作者 DONG Fang HA Xiao-qin 《Chinese Medical Journal》 SCIE CAS CSCD 2010年第17期2454-2460,共7页
Objective To review the effect of endothelial progenitor cells in neovascularization as well as their application to the therapy of tumors.Data sources The data used in this review were mainly from PubMed for relevant... Objective To review the effect of endothelial progenitor cells in neovascularization as well as their application to the therapy of tumors.Data sources The data used in this review were mainly from PubMed for relevant English language articles published from 1997 to 2009. The search term was "endothelial progenitor cells".Study selection Articles regarding the role of endothelial progenitor cells in neovascularization and their application to the therapy of tumors were selected.Results Endothelial progenitor cells isolated from bone marrow, umbilical cord blood and peripheral blood can proliferate, mobilize and differentiate into mature endothelial cells. Experiments suggest endothelial progenitor cells take part in forming the tumor vascular through a variety of mechanisms related to vascular endothelial growth factor, matrix metalloproteinases, chemokine stromal cell-derived factor 1 and its receptor C-X-C receptor-4, erythropoietin, Notchsignal pathway and so on. Evidence demonstrates that the number and function change of endothelial progenitor cells in peripheral blood can be used as a biomarker of the response of cancer patients to anti-tumor therapy and predict the prognosis and recurrence. In addition, irradiation temporarily increased endothelial cells number and decreased the endothelial progenitor cell counts in animal models. Meanwhile, in preclinical experiments, therapeutic gene-modified endothelial progenitor cells have been approved to attenuate tumor growth and offer a novel strategy for cell therapy and gene therapy of cancer.Conclusions Endothelial progenitor cells play a particular role in neovascularization and have attractively potential prognostic and therapeutic applications to malignant tumors. However, a series of problems, such as the definitive biomarkers of endothelial progenitor cells, their interrelationship with radiotherapy and their application in cell therapy and gene therapy of tumors, need further investigation. 展开更多
关键词 endothelial progenitor cells pathological neovascularization tumor therapy
原文传递
Extracellular domain of kinase domain region mediated by adeno-associated virus inhibits growth and angiogenesis of bladder cancer in Balb-c mice
7
作者 张志超 张智清 +3 位作者 曾革非 张立国 徐春晓 郭应禄 《Chinese Medical Journal》 SCIE CAS CSCD 2002年第8期1209-1212,154,共4页
OBJECTIVE: To verify whether the extracellular domain of kinase domain region (KDR) has anti-angiogenesis activity in vivo. METHODS: cDNA was cloned into adeno-associated virus (AAV) vector pSNAV and transfected to ba... OBJECTIVE: To verify whether the extracellular domain of kinase domain region (KDR) has anti-angiogenesis activity in vivo. METHODS: cDNA was cloned into adeno-associated virus (AAV) vector pSNAV and transfected to baby hamster kidney (BHK) cells. Recombinant AAV was obtained from the cell culture supernatant after adding helper virus. Recombinant AAV-infected human bladder cancer EJ cell line (EJ cells) were injected subcutaneously into Balb-c nude mice. Tumor specimens were removed from the mice, paraffin-embedded and sliced, then stained by immunohistochemistry. Microvessel density (MVD) was determined under a microscope. RESULTS: The tumor volume developed by EJ cells transfected with the extracellular domain of KDR was significantly smaller (1.70 +/- 0.18 cm(3)) compared with that in the control (5.62 +/- 0.67 cm(3)) (P 展开更多
关键词 Gene Therapy Animals Bladder Neoplasms Cloning Molecular CRICETINAE DEPENDOVIRUS Endothelial Growth Factors Female Intercellular Signaling Peptides and Proteins LYMPHOKINES MICE Mice Inbred BALB C Mice Nude neovascularization Pathologic Research Support Non-U.S. Gov't Vascular Endothelial Growth Factor A Vascular Endothelial Growth Factor Receptor-2 Vascular Endothelial Growth Factors
原文传递
Tumor blood vessels formation in osteosarcoma:vasculogenesis mimicry 被引量:45
8
作者 蔡宣松 贾永伟 +1 位作者 梅炯 汤如勇 《Chinese Medical Journal》 SCIE CAS CSCD 2004年第1期94-98,共5页
BACKGROUND: Osteosarcoma is characterized by high neovascularization and a high propensity for metastasis through bloodstream. This study was to examine whether there is evidence for vasculogenic mimicry in osteosarco... BACKGROUND: Osteosarcoma is characterized by high neovascularization and a high propensity for metastasis through bloodstream. This study was to examine whether there is evidence for vasculogenic mimicry in osteosarcoma and to illustrate mechanism of tumor blood vessels formation in osteosarcoma. METHODS: Osteosarcoma cell lines (U-2OS) were tested for their ability to form tubular networks in three-dimensional culture containing type I collagen. The structures of the tubular networks were observed with phase contrast microscope and transmission electron microscope (TEM). Morphometric studies using hematoxylin and eosin (HE) stain and CD31 immunohistochemical stain to show tumor-lined channels in human osteosarcoma were also performed. RESULTS: Observation with light microscope and TEM showed that highly aggressive osteosarcoma cell lines (U-2OS) formed networks containing channels when grown in three-dimensional culture containing type I collagen, in the absence of endothelial cells or fibroblasts. Morphometric observation using HE stain and CD31 immunohistochemical stain showed that tumor cell-lined channels were also detected in vivo in osteosarcoma; by comparison, all vascular areas in the pedicle of osteochondroma or outside osteochondroma were endothelial-lined. CONCLUSION: These observations strongly suggest that aggressive osteosarcoma cells may generate vascular channels that facilitate tumor perfusion independent of tumor angiogenesis and have the ability of vasculogenic mimicry. 展开更多
关键词 Bone Neoplasms Cell Line Tumor Collagen Humans IMMUNOHISTOCHEMISTRY neovascularization Pathologic OSTEOSARCOMA Research Support Non-U.S. Gov't
原文传递
Effect of endothelial PAS domain protein 1 and hypoxia inducible factor 1~ on vascular endothelial growth factor expression in human pancreatic carcinoma 被引量:14
9
作者 ZHU Dong-ming LI De-chun +1 位作者 ZHANG Zi-xiang ZHANG Xiao-yi 《Chinese Medical Journal》 SCIE CAS CSCD 2008年第22期2258-2264,共7页
Background Transcription factors hypoxia inducible factor 1α (HIF 1α) and endothelial PAS domain protein 1 (EPAS1) promote the transcription of vascular endothelial growth factor (VEGF). VEGF enhances angiogen... Background Transcription factors hypoxia inducible factor 1α (HIF 1α) and endothelial PAS domain protein 1 (EPAS1) promote the transcription of vascular endothelial growth factor (VEGF). VEGF enhances angiogenesis and vascular permeability of tumours, which promotes tumour growth and facilitates entry of cancer cells into blood circulation and metastasizing. This study examined whether HIF 1α and EPAS1 stimulated angiogenesis through activation of VEGF in human pancreatic carcinoma. Methods Specimens from pancreatic carcinoma and healthy parts of same pancreas were taken from 60 patients. Real time quantitative reverse transcription polymerase chain reaction estimated expression of HIF 1α, EPAS1, and VEGF mRNAs. Western blotting and immunohistochemical, streptavidin peroxidase method assessed expression of HIF 1α, EPAS1, and VEGF proteins. Microvessel density (MVD) was assessed. Results Highly significant increases in expression of EPAS1, VEGF, and MVD were found in pancreatic carcinoma tissue but not in normal pancreatic tissue: VEGF at mRNA and protein levels (t=17.32, P=-0.0001; t=98.41, P=0.0001); EPAS1 protein level (t=22.51, P=0.0001). Expression of HIF la was similar in pancreatic carcinoma and normal pancreatic tissues at both mRNA and protein levels. Significant correlations were observed between EPAS1 and VEGF (r=0.736, P=0.0041), between VEGF and MVD (r=0.858, P=0.0001), and between EPAS1 and MVD (r=0.641, P=0.0003). No significant correlations were observed between HIF la and VEGF, or between HIF 1α and MVD. MVD and expression of EPAS1 and VEGF were significantly related with TNM staging, so was EPASI and VEGF with size of tumour. Conclusions EPAS1 and VEGF, but not HIFla, are overexpressed in pancreatic carcinoma. The expression of EPAS1 is correlated with that of VEGF and MVD. EPAS1 may be involved in the angiogenesis of pancreatic carcinoma by upregulating the expression of VEGE Targeting EPAS1 may be a new method of antiangiogenic tumour therapy for pancreatic carcinoma. 展开更多
关键词 endothelial PAS domain-containing protein 1 vascular endothelial growth factors hypoxia inducible factor l a pancreatic neoplasms neovascularization pathological basic helix-loop-helix transcription factors
原文传递
Circulating endothelial progenitor cells in traumatic brain injury: an emerging therapeutic target? 被引量:5
10
作者 尉辉杰 江荣才 +1 位作者 刘丽 张建宁 《Chinese Journal of Traumatology》 CAS 2010年第5期316-318,共3页
Traumatic brain injury (TBI) is a major cause of mortality and morbidity in the world. Recent clinical investigations and basic researches suggest that strategies to improve angiogenesis following TBI may provide pr... Traumatic brain injury (TBI) is a major cause of mortality and morbidity in the world. Recent clinical investigations and basic researches suggest that strategies to improve angiogenesis following TBI may provide promising opportunities to improve clinical outcomes and brain functional recovery. More and more evidences show that circulating endothelial progenitor cells (EPCs), which have been identified in the peripheral blood, may play an important role in the pathologic and physiological anglo-genesis in adults. Moreover, impressive data demonstrate that EPCs are mobilized from bone marrow to blood circula- tion in response to traumatic or inflammatory stimulations. In this review, we discussed the role of EPCs in the repair of brain injury and the possible therapeutic implication for func- tional recovery of TBI in the future. 展开更多
关键词 Brain injuries Stem cells ENDOTHELIALCELLS neovascularization pathologic
原文传递
Effect of FGF-BP on angiogenesis in squamous cell carcinoma
11
作者 李为民 陈文彬 《Chinese Medical Journal》 SCIE CAS CSCD 2004年第4期621-623,共3页
关键词 ADULT Aged Aged 80 and over Carcinoma Squamous Cell Carrier Proteins FEMALE Humans MALE Middle Aged neovascularization Pathologic von Willebrand Factor
原文传递
Verteporfin-mediated on/off photoswitching functions synergistically to treat choroidal vascular diseases
12
作者 Yahan Ju Xiaochan Dai +10 位作者 Zhimin Tang Zunzhen Ming Ni Ni Dongqing Zhu Jing Zhang Bo Ma Jiajing Wang Rui Huang Siyu Zhao Yan Pang Ping Gu 《Bioactive Materials》 SCIE 2022年第8期402-415,共14页
Choroidal vascular diseases,such as age-related macular degeneration,are the leading cause of vision impairment and are characterized by pathological angiogenesis.Verteporfin-mediated photodynamic therapy is a current... Choroidal vascular diseases,such as age-related macular degeneration,are the leading cause of vision impairment and are characterized by pathological angiogenesis.Verteporfin-mediated photodynamic therapy is a current strategy that selectively occludes choroidal neovasculature.However,the clinically used large-dose systemic administration increases the risk of systemic adverse events,such as phototoxicity to superficial tissues.In this study,we developed an in situ verteporfin delivery system with a photoswitching synergistic function that disassembles in response to intraocular inflammatory enzymes.Under light-on conditions,verteporfin-mediated photodynamic therapy effectively occurs and this leads to vascular occlusion.Under light-off conditions,non-photoactive verteporfin negatively regulates vascular endothelial growth factor-induced angiogenesis as a yes-associated protein inhibitor.Taken together,our system serves as an intraocular verteporfin reservoir to improve the bioavailability of verteporfin by innovatively exploiting its photochemical and biological functions.This work provides a promising strategy with synergistic antiangiogenic effects for the treatment of choroidal vascular diseases. 展开更多
关键词 pathological neovascularization Photodynamic therapy Bio-responsive release In situ drug delivery
原文传递
上一页 1 下一页 到第
使用帮助 返回顶部