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| 1 | Quantitative analysis of vascular endothelial growth factor, microvascular density and their clinicopathologic features in human hepatocellular carcinoma显示文摘BACKGROUND: Angiogenesis is known to be essential to the survival, growth, invasion, and metastasis of tumor cells. Vascular endothelial growth factor (VEGF) are an important angiogenic factor regulating tumor angiogenesis, but its significance and tumor pathologic features are un- clear in hepatocellular carcinoma (HCC). In the present study, we analyzed expression of tissue VEGF, alteration of microvascular density (MVD) in microvessel angiogenesis, development and metastasis of HCC, and level of serum VEGF in differential diagnosis of benign and malignant liv- er diseases. METHODS: Tumor specimens were prospectively collected from HCC patients undergoing resection. Total RNAs were extracted and the expression levels were detected from different parts of HCC tissues. The cellular distributions of VEGF and MVD of liver tumors and their paracancerous and distal cancerous tissues were investigated by streptavi- din peroxidase (S-P) immunohistochemistry, respectively. The VEGF levels of circulating blood and hepatoma tissues were measured by enzyme-linked immunosorbent assay. RESULTS: The incidence of VEGF expression was 63.9% in HCCs (23/36 cases), 78.3% in non-encapsulated HCCs (18/23), and 90.9% in HCCs with extrahepatic metastasis (10/11), respectively. The VEGF expression was tightly correlated with MVD (P <0.01). The MVD in HCC with metastasis, low differentiation or non-encapsulation was significantly higher than that in HCC with intact capsule, high differentiation, or no metastasis. No significant diffe- rence was found between VEGF, MVD, tumor size, and hepatitis virus infection. The level of total RNA in HCC tis- sues was significantly lower but the VEGF level significantly higher than those in paracancerous or distal cancerous ones (P<0.01). The abnormal expression levels of VEGF in sera of HCC patients were directly correlated with the me- tastasis and recurrence of tumors. CONCLUSION: The high expression of VEGF and abnor- mality of tissue MVD are useful predictors for vascular inva- sion and metastasis of liver tumors. | Deng-Fu Yao, Xin-Hua Wu, Yong Zhu, Gong-Sheng Shi, Zhi-Zhen Dong, Deng-Bing Yao, Wei Wu, Li-Wei Qiu and Xian-Yong Meng Nantong, China Research Center of Clinical Molecular Biology , Department of Pathology and Department of Gastroenterology , Affiliated Hos- pital of Nantong University Department of Diagnostics , and Institute of Neurosciences , Nantong University Nantong 226001, China | 2005 | Hepatobiliary & Pancreatic Diseases International2005，4，2： | 81 |
| 2 | Expression of vascular endothelial growth factor and its role in oncogenesis of human gastric carcinoma显示文摘AIM To establish the role of vascular endothelial growth factor (VEGF) in the oncogenesisof 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 VEGF165 complimentary DNA in either the sense or antisense orientation. The biological changes of the cells were observed in which VEGF was up-regulated or downregulated.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 VEGF165 antisense into human gastric cancer cells ( SGC-7901, immunofluorescence intensity,31.6%)) resulted in a significant reduction in VEGFspecific messenger RNA and total and cell surface VEGF protein ( immunofluorescence intensity, 8.9%)(P<0.05). Conversely, stable integration of VEGF165 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, tomor volume: 345.40 ± 136.31 mm3) (P<0.05 vs control SGC7901 group: 1534.40 ± 362.88 mm3), whereas up-regulation of VEGF resulted in increased xenografted tumor size (at 33 days postimplantation, tomor volume: 2350.50 ± 637.70mm3) (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. | 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 | 2001 | World Journal of Gastroenterology2001，7，4： | 37 |
| 3 | Reduction of tumorigenicity of SMMC-7721 hepatoma cells by vascular endothelial growth factor antisense gene therapy显示文摘AIM To test the hypothesis to block VEGFexpression of SMMC-7721 hepatoma cells mayinhibit tumor growth using the rat hepatomamodel.METHODS Amplifiy the 200 VEGF cDNAfragment and insert it into human U6 genecassette in the reverse orientation transcribingsmall antisense RNA which could specificallyinteract with VEGF165, and VEGF121 mRNA.Construct the retroviral vector containing thisantisense VEGF U6 cassette and package thereplication-deficient recombinant retrovirus.SMMC-7721 cells were transduced with thesevirus and positive clones were selected withG418. PCR and Southern blot analysis wereperformed to determine if U6 cassette integratedinto the genomic DNA of positive clone.Transfected tumor cells were evaluated for RNAexpression by ribonuclease protection assays.The VEGF protein in the supernatant of parentaltumor cells and genetically modified tumor cellswas determined with ELISA. In vitro and in vivogrowth properties of antisense VEGF cell clonein nude mice were analyzed.RESULTS Restriction enzyme digestion andPCR sequencing verified that the antisense VEGFRNA retroviral vector was successfullyconstructed. After G418 selection, resistantSMMC-7721 cell clone was picked up. PCR andSouthern blot analysis suggested that U6cassette was integrated into the cell genomicDNA. Stable SMMC-7721 cell clone transducedwith U6 antisense RNA cassette could express200bp small antisense VEGF RNA and secretereduced levels of VEGF in culture condition.Production of VEGF by antisense transgeneexpressing cells was 65 ± 10 ng / L per 106 cells,420 ± 45 ng/L per 106 cells in sense group and 485± 30 ng/L per 106 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 VEGFRNA in SMMC-7721 cells could decrease thetumorigenicity, and antisense-VEGF genetherapy may be an adjuvant treatment forhepatoma. | Yu Cheng Tang Yu Li Guan Xiang Qian Department of Biochemistry, Shanghai Second Medical University, Shanghai 200025, China | 2001 | World Journal of Gastroenterology2001，7，1： | 33 |
| 4 | Delayed hepatocarcinogenesis through antiangiogenic intervention in the nuclear factor-kappa B activation pathway in rats显示文摘BACKGROUND:The active form of nuclear factor-kappa B(NF- κB)is involved in the initiation,generation,and development of hepatocellular carcinoma(HCC),and is up-regulated in inflammation-associated malignancies.We investigated the dynamic expression of NF-κB and its influences on the occurrence of HCC through antiangiogenic(thalidomide) intervention in NF-κB activation. METHODS:Hepatoma models were induced with 2-fluorenyl- acetamide(2-FAA,0.05%)in male Sprague-Dawley rats,and thalidomide(100 mg/kg body weight)was administered intragastrically to intervene in NF-κB activation.The pathological changes in the liver of sacrificed rats were assessed after hematoxylin and eosin staining.NF-κB mRNA was amplified by RT-nested PCR.The alterations of NF-κB and vascular endothelial growth factor(VEGF)expression were analyzed by enzyme-linked immunosorbent assay,immunohistochemistry,and Western blotting. RESULTS:Rat hepatocytes showed denatured,precancerous,and cancerous stages in hepatocarcinogenesis,with an increasing tendency of hepatic NF-κB,NF-κB mRNA,and VEGF expression,and their values in the HCC group were higher than those in controls(P<0.001).In the thalidomide- treated group,the morphologic changes generated only punctiform denaturation and necrosis at the early or middle stages,and nodular hyperplasia or a little atypical hyperplasia at the final stages,with the expression of NF-κB (χ2=9.93,P<0.001)and VEGF(χ2=8.024,P<0.001)lower than that in the 2-FAA group. CONCLUSION:NF-κB is overexpressed in hepatocarcinogenesis and antiangiogenic treatment down-regulates the expression of NF-κB and VEGF,and delays the occurrence of HCC. | Dong, Zhi-Zhen Yao, Deng-Fu Wu, Wei Yao, Min Yu, Hong-Bo Shen, Jun-Jun Qiu, Li-Wei Yao, Ning-Hua Sai, Wen-Li Yang, Jun-Ling | 2010 | Hepatobiliary & Pancreatic Diseases International2010，9，2： | 31 |
| 5 | Pyrrolizidine alkaloids-induced hepatic sinusoidal obstruction syndrome: Pathogenesis, clinical manifestations, diagnosis,treatment, and outcomes显示文摘Hepatic sinusoidal obstruction syndrome (HSOS) can be caused by the intake of pyrrolizidine alkaloids (PAs). To date, PAs-induced HSOS has not been extensively studied. In view of the difference in etiology of HSOS between the West and China, clinical profiles, imaging findings, treatment, and outcomes of HSOS associated with hematopoietic stem cell transplantation or oxaliplatin might be hardly extrapolated to PAs-induced HSOS. Reactive metabolites derived from PAs form pyrrole-protein adducts that result in toxic destruction of hepatic sinusoidal endothelial cells. PAs-induced HSOS typically manifests as painful hepatomegaly, ascites, and jaundice. Laboratory tests revealed abnormal liver function tests were observed in most of the patients with PAs-induced HSOS. In addition, contrast computed tomography and magnetic resonance imaging scan show that patients with PAs-induced HSOS have distinct imaging features, which reveal that radiological imaging provides an effective noninvasive method for the diagnosis of PAs-induced HSOS. Liver biopsy and histological examination showed that PAs-induced HSOS displayed distinct features in acute and chronic stages. Therapeutic strategies for PAs-induced HSOS include rigorous fluid management, anticoagulant therapy, glucocorticoids, transjugular intrahepatic portosystemic shunt, liver transplantation, etc. The aim of this review is to describe the pathogenesis, clinical profiles, diagnostic criteria, treatment, and outcomes of PAs-induced HSOS. | Xiao-Qian Yang Jin Ye Xin Li Qian Li Yu-Hu Song | 2019 | World Journal of Gastroenterology2019，25，28： | 29 |
| 6 | Association between vascular endothelial growth factor and metastasis after transcatheter arterial chemoembolization in patients with hepatocellular carcinoma显示文摘BACKGROUND: Hypoxia up-regulates vascular endothelialgrowth factor (VEGF) and stimulates the growth of hepa-tocellular carcinoma (HCC) cells. This study was designedto investigate the association between changes in plasmaVEGF levels after transcatheter arterial chemoembolization(TACE) and HCC progression, especially in relation tometastasis.METHODS: Plasma VEGF levels were measured by quati-tative sandwich enzyme-linked immunosorbent assay(ELISA R&D system). Plasma VEGF levels were measuredbefore, 3 days and 4 weeks after TACE in 30 patients withHCC. The development of metastasis was evaluated at theend of the third month after TACE.RESULTS: The plasma VEGF levels of the 30 patients withHCC were 154.47±90.17 pg/ml. The total plasma VEGFlevels after TACE increased compared with their basal levels(P<0.05), and the plasma VEGF levels had a tendency toincrease in patients with heterogenous uptake of iodizdoiland portal vein thrombosis. Follow-up for six monthsshowed metastatic foci in 20 patients (74%) with increasedplasma VEGF, but none of the patients with decreased plas-ma VEGF developed metastasis.CONCLUSION: Increased plasma VEGF expression is asso-ciated with the development of metastasis in HCC after TA-CE. | Zheng-Ping Xiong, Shu-Ren Yang, Zhao-Yu Liang, En-Hua Xiao, Xiao-Ping Yu,Shen-Ke Zhou and Zi-Shu Zhang, Department of Radiology , Hunan Provincial TumorHospital. Changsha 410006, China Department of Radiology, Xiangya Second Hospital of Central South Uni-versity, Changsha 410011, China | 2004 | Hepatobiliary & Pancreatic Diseases International2004，3，3： | 27 |
| 7 | Coronary microvascular dysfunction in diabetes mellitus:A review显示文摘The exploration of coronary microcirculatory dysfunction in diabetes has accelerated in recent years.Cardiac function is compromised in diabetes.Diabetic patients manifest accelerated atherosclerosis in coronary arteries.These data are confirmed in diabetic animal mod-els,where lesions of small coronary arteries have been described.These concepts are epitomized in the classic microvascular complications of diabetes,i.e.blindness,kidney failure and distal dry gangrene.Most importantly,accumulating data indicate that insights gained from the link between inflammation and diabetes can yield predictive and prognostic information of considerable clinical utility.This review summarizes the evidence for the predisposing factors and the mechanisms involved in diabetes,and assesses the current state of knowledge regarding the triggers for inflammation in this disease.We evaluate the roles of hyperglycemia,oxidative stress,polyol pathway,protein kinase C,advanced glycation end products,insulin resistance,peroxisome proliferator-activated receptor-γ,inflammation,and diabetic cardiomyopathy as a 'stem cell disease'.Furthermore,we discuss the mechanisms responsible for impaired coronary arteriole function.Finally,we consider how new insights in diabetes may provide innovative therapeutic strategies. | Andrea Picchi Stefano Capobianco Marta Focardi | 2010 | World Journal of Cardiology2010，2，11： | 24 |
| 8 | Role of bevacizumab in colorectal cancer growth and its adverse effects:A review显示文摘Angiogenesis affects both wound healing and malignant cell growth through nutrients and oxygen.Vascular endothelial growth factor(VEGF) is the most important element involved in this complex process.Inhibition of VEGF influences angiogenesis and may restrict tumor growth and metastatic ability.Modern antiangiogenic therapy is based on this theory.Bevacizumab is a recombinant humanized monoclonal antibody(immunoglobulin G1) which binds with VEGF-A forming a large molecule.It can not be bound with VEGF tyrosine kinase receptors preventing VEGF-A incorporation;thus its activity is inhibited inducing blockage of VEGFmediated angiogenesis.Bevacizumab,in combination with chemotherapy or other novel targeted therapeutic agents,is currently used more frequently in clinical practice,mainly for managing advanced colorectal cancer.It is also used for managing other malignancies,such as breast cancer,pancreatic cancer,prostate cancer,non small-cell lung cancer,metastatic renal carcinoma and ovarian tumors.Although it is generally considered a safe treatment,there are reports of some rare side effects which should be taken into account.Recent experiments in rats and mice show promising results with a wider therapeutic range. | Efstathios T Pavlidis Theodoros E Pavlidis | 2013 | World Journal of Gastroenterology2013，19，31： | 24 |
| 9 | Vascular endothelial dysfunction and pharmacological treatment显示文摘The endothelium exerts multiple actions involving regulation of vascular permeability and tone, coagulation and fibrinolysis, inflammatory and immunological reactions and cell growth. Alterations of one or more such actions may cause vascular endothelial dysfunction. Different risk factors such as hypercholesterolemia, homocystinemia, hyperglycemia, hypertension, smo-king, inflammation, and aging contribute to the development of endothelial dysfunction. Mechanisms underlying endothelial dysfunction are multiple, including impaired endothelium-derived vasodilators, enhanced endothelium-derived vasoconstrictors, over production of reactive oxygen species and reactive nitrogen species, activation of inflammatory and immune reactions, and imbalance of coagulation and fibrinolysis. Endothelial dysfunction occurs in many cardiovascular diseases, which involves different mechanisms, depending on specific risk factors affecting the disease. Among these mechanisms, a reduction in nitric oxide(NO) bioavailability plays a central role in the development of endothelial dysfunction because NO exerts diverse physiological actions, including vasodilation, anti-inflammation, antiplatelet, antiproliferation and antimigration. Experimental and clinical studies have demonstrated that a variety of currently used or investigational drugs, such as angiotensin-converting enzyme inhibitors, angiotensin AT1 receptors blockers, angiotensin-(1-7), antioxidants, beta-blockers, calcium channel blockers, endothelial NO synthase enhancers, phosphodiesterase 5 inhibitors, sphingosine-1-phosphate and statins, exert endothelial protective effects. Due to the difference in mechanisms of action, these drugs need to be used according to specific mechanisms underlying endothelial dysfunction of the disease. | Jin Bo Su | 2015 | World Journal of Cardiology2015，7，11： | 24 |
| 10 | Endothelial progenitor cells in cardiovascular diseases显示文摘Endothelial dysfunction has been associated with the development of atherosclerosis and cardiovascular diseases. Adult endothelial progenitor cells(EPCs) are derived from hematopoietic stem cells and are capable of forming new blood vessels through a process of vas-culogenesis. There are studies which report correlations between circulating EPCs and cardiovascular risk fac-tors. There are also studies on how pharmacotherapies may influence levels of circulating EPCs. In this review, we discuss the potential role of endothelial progenitor cells as both diagnostic and prognostic biomarkers. In addition, we look at the interaction between cardio-vascular pharmacotherapies and endothelial progenitor cells. We also discuss how EPCs can be used directly and indirectly as a therapeutic agent. Finally, we evalu-ate the challenges facing EPC research and how these may be overcome. | Poay Sian Sabrina Lee Kian Keong Poh | 2014 | World Journal of Stem Cells2014，6，3： | 22 |
| 11 | TSH抑制疗法对分化型甲状腺癌患者术后血清Tg、VEGF、TSGF、CD44V6、sIL-2R及T淋巴细胞亚群水平的影响显示文摘目的:探讨促甲状腺激素(thyroid stimulating hormone,TSH)抑制疗法对分化型甲状腺癌(differentiated thyroid carcinoma,DTC)患者术后血清甲状腺球蛋白(thyroglobulin,Tg)、血管内皮生长因子(vascular endothelial growth factor,VEGF)、肿瘤特异性生长因子(tumors pecific growth factor,TSGF)、白细胞分化抗原44变异型6(CD44V6)、可溶性白细胞介素-2受体(soluble interleukin-2receptor,sIL-2R)及T淋巴细胞亚群水平的影响。方法:选择2014年1月~2017年1月我院收治的接受甲状腺全切手术治疗的100例DTC患者,随机分为对照组和实验组,各50例。对照组患者常规给予甲状腺素替代治疗,实验组患者给予TSH抑制疗法(口服左甲状腺素钠片,控制血清TSH水平低于0.1mU/L),两组患者均给予治疗1个月。比较两组患者治疗前后血清Tg、VEGF、TSGF、CD44V6、sIL-2R水平及外周血CD3^+、CD4^+、CD8^+水平。结果:两组治疗前的血清Tg、VEGF、TSGF、CD44V6、sIL-2R水平比较,均无显著性差异(P>0.05);两组治疗后的血清Tg、VEGF、TSGF、CD44V6、sIL-2R水平相比治疗前均较低,且实验组治疗后血清Tg、VEGF、TSGF、CD44V6、sIL-2R水平变化均显著优于对照组(P<0.05)。两组治疗前的外周血CD3^+、CD4^+、CD8^+水平比较,均无显著性差异(P>0.05);两组治疗后的外周血CD3^+、CD4^+水平相比治疗前均较高、CD8^+水平相比治疗前均较低,且实验组治疗后血外周血CD3^+、CD4^+、CD8^+水平变化均优于对照组,具有显著性差异(P<0.05)。结论:DTC行甲状腺全切手术治疗后接受TSH抑制疗法能够有效降低血清Tg、VEGF、TSGF、CD44V6、sIL-2R水平,改善细胞免疫功能,值得在临床上推广应用。 | 张力丹 席永昌 尤立强 张建阳 张建媛 | 2018 | 海南医学院学报2018，24，2： | 23 |
| 12 | Activation of SIRT1 ameliorates LPS-induced lung injury in mice via decreasing endothelial tight junction permeability显示文摘The integrity of the endothelial barrier is a determinant of the prognosis of lipopolysaccharide (LPS)-induced acute lung injury (ALI). In this study, we investigated whether and how Sirtuin 1 (SIRT1) maintained the vascular integrity during ALI. An experimental model of ALI was established in mice through intratracheal administration of LPS (10 mg/kg). LPS stimulation significantly increased the pulmonary permeability and decreased the expression of SIRT1 and tight junction proteins (TJs), including occludin, claudin-5, tight junction protein 1 and tight junction protein 2. Morphological studies showed that LPS induced obvious lung injury with inammatory cell infiltration in the interstitial and alveolar space, hemorrhage, edema, and the thickened alveolar wall compared to the control mice. Intratracheal administration of the selective SIRT1 activator SRT1720 (6.25 mg/kg) significantly attenuated LPS- induced lung injury, lung hyper-permeability and increased TJs expression, whereas intratracheal administration of the selective SIRT1 inhibitor EX527 (6.25 mg/kg) aggravated LPS-induced ALI. Similar protective effects of SIRT1 on pulmonary cellular permeability were observed in primary human pulmonary microvascular endothelial cells treated with LPS (2 mg/mL) in vitro. We further demonstrated that the RhoA/ROCK signaling pathway was activated in SIRT1 regulation of tight junction permeability. The RhoA/ROCK inhibitor Y-27632 (10 μM) increased the expression of TJs and reversed LPS- or EX527-induced hyper-permeability. In conclusion, SIRT1 ameliorates LPS-induced lung injury via decreasing endothelial tight junction permeability, possibly via RhoA/ ROCK signaling pathway. This finding may contribute to the development of new therapeutic approaches for lung injury. | Cui-ping Fu Sheng-yu Hao Xiao-bo Xu Jian Zhou Zi-long Liu Huan Lu Li-min Wang Wei-zhong Jin Shan-qun Li | 2019 | Acta Pharmacologica Sinica2019，40，5： | 22 |
| 13 | Constraint-induced movement therapy enhances angiogenesis and neurogenesis after cerebral ischemia/reperfusion显示文摘Constraint-induced movement therapy after cerebral ischemia stimulates axonal growth by decreasing expression levels of Nogo-A,RhoA,and Rho-associated kinase(ROCK)in the ischemic boundary zone.However,it remains unclear if there are any associations between the Nogo-A/RhoA/ROCK pathway and angiogenesis in adult rat brains in pathological processes such as ischemic stroke.In addition,it has not yet been reported whether constraint-induced movement therapy can promote angiogenesis in stroke in adult rats by overcoming Nogo-A/RhoA/ROCK signaling.Here,a stroke model was established by middle cerebral artery occlusion and reperfusion.Seven days after stroke,the following treatments were initiated and continued for 3 weeks:forced limb use in constraint-induced movement therapy rats(constraint-induced movement therapy group),intraperitoneal infusion of fasudil(a ROCK inhibitor)in fasudil rats(fasudil group),or lateral ventricular injection of NEP1-40(a specific antagonist of the Nogo-66 receptor)in NEP1-40 rats(NEP1-40 group).Immunohistochemistry and western blot assay results showed that,at 2 weeks after middle cerebral artery occlusion,expression levels of RhoA and ROCK were lower in the ischemic boundary zone in rats treated with NEP1-40 compared with rats treated with ischemia/reperfusion or constraint-induced movement therapy alone.However,at 4 weeks after middle cerebral artery occlusion,expression levels of RhoA and ROCK in the ischemic boundary zone were markedly decreased in the NEP1-40 and constraint-induced movement therapy groups,but there was no difference between these two groups.Compared with the ischemia/reperfusion group,modified neurological severity scores and foot fault scores were lower and time taken to locate the platform was shorter in the constraint-induced movement therapy and fasudil groups at 4 weeks after middle cerebral artery occlusion,especially in the constraint-induced movement therapy group.Immunofluorescent staining demonstrated that fasudil promoted an immune response of nerve-regeneration-related markers(BrdU in combination with CD31(platelet endothelial cell adhesion molecule),Nestin,doublecortin,NeuN,and glial fibrillary acidic protein)in the subventricular zone and ischemic boundary zone ipsilateral to the infarct.After 3 weeks of constraint-induced movement therapy,the number of regenerated nerve cells was noticeably increased,and was accompanied by an increased immune response of tight junctions(claudin-5),a pericyte marker(a-smooth muscle actin),and vascular endothelial growth factor receptor 2.Taken together,the results demonstrate that,compared with fasudil,constraint-induced movement therapy led to stronger angiogenesis and nerve regeneration ability and better nerve functional recovery at 4 weeks after cerebral ischemia/reperfusion.In addition,constraint-induced movement therapy has the same degree of inhibition of RhoA and ROCK as NEP1-40.Therefore,constraint-induced movement therapy promotes angiogenesis and neurogenesis after cerebral ischemia/reperfusion injury,at least in part by overcoming the Nogo-A/RhoA/ROCK signaling pathway.All protocols were approved by the Institutional Animal Care and Use Committee of China Medical University,China on December 9,2015(approval No.2015 PS326 K). | Zhi-Yong Zhai Juan Feng | 2019 | Neural Regeneration Research2019，14，10： | 22 |
| 14 | Serum vascular endothelial growth factor is a potential biomarker of metastatic recurrence after curative resection of hepatocellular carcinoma显示文摘INTRODUCTIONHepatocellular carcinoma(HCC)is one of the mostcommon malignancies in China.To date,surgery is stillthe best solution to it.However,metastatic recurrencesafter curative hepatic resections are very common.Tang etal have reported that recurrence rate within 5 years | Qi Niu Zhao You Tang Zeng Chen Ma Lun Xiu Qin Lian Hai Zhang | 2000 | World Journal of Gastroenterology2000，6，4： | 20 |
| 15 | Repurposing vitamin D for treatment of human malignancies via targeting tumor microenvironment显示文摘Tumor cells along with a small proportion of cancer stem cells exist in a stromal microenvironment consisting of vasculature, cancer-associated fibroblasts, immune cells and extracellular components.Recent epidemiological and clinical studies strongly support that vitamin D supplementation is associated with reduced cancer risk and favorable prognosis. Experimental results suggest that vitamin D not only suppresses cancer cells, but also regulates tumor microenvironment to facilitate tumor repression. In this review, we have outlined the current knowledge on epidemiological studies and clinical trials of vitamin D. Notably, wesummarized and discussed the anticancer action of vitamin D in cancer cells, cancer stem cells and stroma cells in tumor microenvironment, providing a better understanding of the role of vitamin D in cancer. We presently re-propose vitamin D to be a novel and economical anticancer agent. | Xu Wu Wei Hu Lan Lu Yueshui Zhao Yejiang Zhou Zhangang Xiao Lin Zhang Hanyu Zhang Xiaobing Li Wanping Li Shengpeng Wang Chi Hin Cho Jing Shen Mingxing Li | 2019 | Acta Pharmaceutica Sinica B2019，9，2： | 20 |
| 16 | Effect of Fuzhenghuayu decoction on vascular endothelial growth factor secretion in hepatic stellate cells显示文摘Objective: To investigate the effect of Fuzhenghuayudecoction on autocrine activation of hepatic stellatecell (HSC).Methods: The drug serum containing Fuzhenghuayudecoction was collected from normal rats, and cul-tured with activated HSC in vitro. The conditionedmedium from the drug serum treated HSC was addedto primary cultured quiescent HSC. Cell prolifera-tion was assayed by tetrazolium colorimetric test,and the contents of type Ⅰ collagen and vascular endo-thelial growth factor (VEGF) in the supernatantwere measured with ELISA.Results: The conditioned medium from activatedHSC could stimulate the quiescent HSC proliferationand type Ⅰ collagen secretion. The drug serum inhibi-ted this stimulating action and VEGF secretion fromthe activated HSC.Conclusion: Fuzhenghuayu decoction acts effectivelyagainst the autocrine activation pathway of HSC.The mechanism may be associated with the inhibitionof the secretion of VEGF by activated HSC. | Cheng Liu Cun-Meng Jiang Cheng-Hai Liu Ping Liu Yi-Yang Hu From the Institute of Liver Diseases and Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China | 2002 | Hepatobiliary & Pancreatic Diseases International2002，1，2： | 19 |
| 17 | Bevacizumab for the management of diabetic macular edema显示文摘Diabetic retinopathy (DR) is a leading cause of vision loss in the working-age population and is relatedto 1%-5% of cases of blindness worldwide. Diabetic macular edema (DME) is the most frequent cause of DR vision loss and is an important public health problem. Recent studies have implicated vascular endothelial growth factor (VEGF) in DR and DME pathogenesis, as well as provided evidence of the benefits of anti-VEGF agents for the management of such conditions. Despite the benefits of intravitreal ranibizumab injection for the management of DME, the cost-effectiveness of intravitreal bevacizumab therapy has gained increasing interest in the scientific community. This review summarizes the studies examining bevacizumab for the management of DME, focusing on the efficacy and duration of the clinical benefits of decreasing DME and the improvement of best-corrected visual acuity (BCVA). There is strong evidence that intravitreal bevacizumab injection therapy has a good cost-effective profile in the management of DME and may be associated with laser photocoagulation; however, its clinical superiority in terms of the duration of DME regression and the improvement of BCVA compared with intravitreal ranibizumab and other intravitreal anti-VEGF therapies remains unclear and deserves further investigation. | Francisco Rosa Stefanini J Fernando Arevalo Maurício Maia | 2013 | World Journal of Diabetes2013，4，2： | 18 |
| 18 | Circulating endothelial and progenitor cells:Evidence from acute and long-term exercise effects显示文摘Circulating bone-marrow-derived cells,named endothelial progenitor cells(EPCs),are capable of maintaining,generating,and replacing terminally differentiated cells within their own specific tissue as a consequence of physiological cell turnover or tissue damage due to injury.Endothelium maintenance and restoration of normal endothelial cell function is guaranteed by a complex physiological procedure in which EPCs play a significant role.Decreased number of peripheral blood EPCs has been associated with endothelial dysfunction and high cardiovascular risk.In this review,we initially report current knowledge with regard to the role of EPCs in healthy subjects and the clinical value of EPCs in different disease populations such as arterial hypertension,obstructive sleep-apnea syndrome,obesity,diabetes mellitus,peripheral arterial disease,coronary artery disease,pulmonary hypertension,and heart failure.Recent studies have introduced the novel concept that physical activity,either performed as a single exercise session or performed as part of an exercise training program,results in a significant increase of circulating EPCs.In the second part of this review we provide preliminary evidence from recent studies investigating the effects of acute and long-term exercise in healthy subjects and athletes as well as in disease populations. | Matina Koutroumpi Stavros Dimopoulos Katherini Psarra Theodoros Kyprianou Serafim Nanas | 2012 | World Journal of Cardiology2012，4，12： | 18 |
| 19 | Effects of hypoxia-inducible factor-1α silencing on the proliferation of CBRH-7919 hepatoma cells显示文摘AIM:To study the effects of hypoxia-inducible factor1α(HIF-1α) silencing on the proliferation of hypoxic CBRH-7919 rat hepatoma cells.METHODS:The CBRH-7919 rat hepatoma cell line was used in this study and the hypoxic model was constructed using CoCl2.The HIF-1α-specific RNAi sequences were designed according to the gene coding sequence of rat HIF-1α obtained from GeneBank.The secondary structure of the HIF-1α gene sequence was analyzed using RNA draw software.The small interfering RNA(siRNA) transfection mixture was produced by mixing the siRNA and Lipofectamine2000TM,and transfected into the hypoxic hepatoma cells.Real time reverse transcription-polymerase chain reaction(RTPCR) and Western blotting assay were used to detect the expression levels of mRNA and protein.HIF-1α and vascular endothelial growth factor(VEGF) mRNA was determined using real time RT-PCR;the protein expression levels of AKT,p-AKT,p21 and cyclinD1 were determined using Western blotting.The proliferation of hepatoma cells was observed using the methyl thiazolyl tetrazolium(MTT) assay and the bromodeoxyuridine(BrdU) incorporation cell proliferation assay.RESULTS:Under induced hypoxia,the viability of the hepatoma cells reached a minimum at 800 μmol/L CoCl2;the viability of the cells was relatively high at CoCl2 concentrations between 100 μmol/L and 200 μmol/L.Under hypoxia,the mRNA and protein expression levels of HIF-1α and VEGF were significantly higher than that of hepatoma cells that were cultured in normaxia.HIF-1α-specific RNAi sequences were successfully transfected into hepatoma cells.The transfection of specific siRNAs significantly inhibited the mRNA and protein expression levels of HIF-1α and VEGF,along with the protein expression levels of p-AKT and cyclinD1;the protein expression of p21 was significantly increased,and there was no significant difference in the expression of AKT.The MTT assay showed that the amount of hepatoma cells in S phase in the siRNA transfection group was obviously smaller than that in the control group;in the siRNA transfection group,the amount of hepatoma cells in G1 phase was more than that in the control group.The BrdU incorporation assay showed that the number of BrdU positive hepatoma cells in the siRNA transfection group was less than that in the control group.The data of the MTT assay and BrdU incorporation assay suggested that HIF-1α silencing using siRNAs significantly inhibited the proliferation of hepatoma cells.CONCLUSION:Hypoxia increases the expression of HIF-1α,and HIF-1α silencing significantly inhibits the proliferation of hypoxic CBRH-7919 rat hepatoma cells. | Lin-Feng Xu Jia-Yan Ni Hong-Liang Sun Yao-Ting Chen Yu-Dan Wu | 2013 | World Journal of Gastroenterology2013，19，11： | 18 |
| 20 | Simvastatin inhibits apoptosis of endothelial cells induced by sepsis through upregulating the expression of Bcl-2 and downregulating Bax显示文摘BACKGROUND: Many studies have showed that apoptosis of endothelial cells plays a curial role in the progress of sepsis. But the role of simvastatin in apoptosis of endothelial cells induced by sepsis is not clear. The present study aimed to investigate the role of simvastatin in apoptosis of endothelial cells induced by sepsis and its mechanism.METHODS: Human umbilical vein endothelial cells(HUVECs) were randomly divided into three groups: control group, sepsis serum intervention group(sepsis group) and simvastatin+sepsis serum intervention group(simvastatin group). After 24-hour incubation with corresponding culture medium, the relative growth rate of HUVECS in different groups was detected by MTT assay; the apoptosis of HUVECs was detected by Hoechst33258 assay and fl ow cytometry; and the expression of the Bcl-2 and Bax genes of HUVECs was detected by PCR.RESULTS: Compared with the sepsis group, HUVECs in the simvastatin group had a higher relative growth rate. Apoptotic HUVECs decreased significantly in the simvastatin group in comparison with the sepsis group. Expression of the Bcl-2 gene in HUVECs decreased obviously, but the expression of the Bax gene increased obviously after 24-hour incubation with sepsis serum; however, the expression of the Bcl-2 and Bax genes was just the opposite in the simvastatin group.CONCLUSIONS: Our study suggests that simvastatin can inhibit apoptosis of endothelial cells induced by sepsis through upregulating the expression of Bcl-2 and downregulating Bax. It may be one of the mechanisms for simvastatin to treat sepsis. | Hui Fu Qiao-sheng Wang Qiong Luo Si Tan Hua Su Shi-lin Tang Zheng-liang Zhao Li-ping Huang | 2014 | World Journal of Emergency Medicine2014，5，4： | 18 |
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