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Recombinant adeno-associated virus-mediated delivery of antisense angiotensin Ⅱ receptor 1 gene attenuates hypertension development

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Acta Pharmacologica Sinica 2007年第11期28卷 1737-1745页

作者： Xu-guang LI~2,Jiang-tao YAN~2,Xi-zheng XU,Jia-ning WANG,Li-ming CHENG,Tao WANG,Ping ZUO,Dao-wen WANG~3institute of hypertension and Department of Internal Medicine,Tongji Hospital,Tongji Medical College,Huazhong University of Science andTechnology,Wuhan 430030,China institute of hypertension and Department of Internal Medicine Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China

Aim:The renin-angiotensin system plays a crucial role in the development andestablishment of hypertension,and the pharmacological blockade of the systemresults in a reduction in blood pressure.In the present study,we investigatedwhether the effects of a novel,double-stranded,recombinant adeno-associatedvirus vector (rAAV)-mediated antisense angiotensin Ⅱ receptor 1 (AT1R) geneefficiently prevents the development of hypertension induced by a high-salt dietin adult,male Sprague-Dawley (SD) rats.Methods:A rAAV was prepared with acassette containing a cytomegalovirus promoter and partial cDNA (660 base pairs)for the AT1R inserted in the antisense direction (rAAV-AT1-AS).A single tail veininjection of the rAAV-AT1-AS or rAAV-GFP (green fluorescent protein,a reportergene) was performed in adult,male SD rats.Two weeks after injection,the animalswere fed a diet containing 8% NaCl,and the systolic blood pressure was measuredweekly using the tail-cuff method for 12 weeks.Results:The high-salt dietinduced a significant rise in systolic blood pressure in the rAAV-GFP-treatedanimals;however,the rAAV-AT1-AS treatment attenuated the rise in blood pres-sure (142.7±4.5 mmHg vs 117±3.8 mmHg,Phypertension,including cardiac dysfunction and renal injury com-pared to the rAAV-GFP group.Conclusion:These results suggest that rAAV-mediated anti-AT1delivery attenuates the development of hypertension and pro-tects against renal injury and cardiac remodeling.

关键词： hypertension gene therapy angiotensin Ⅱ receptor 1 antisense double-stranded recombinant adeno-associated virus vector

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Telmisartan Protects against Insulin Resistance by Attenuating Inflammatory Response in Rats

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2011年第3期31卷 317-323页

作者：徐西振殷晓明冯文静李耕汪道文凃玲 Department of Internal Medicine and the institute of hypertension Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology

This study investigated the effects of telmisartan on insulin resistance in high-fat diet-treated rats and the possible mechanism.A total of 40 male Sprague-Dawley rats enrolled in the study were divided into 4 groups at random：ND group（n=10） and HD group（n=10）,in which the rats were given a normal chow diet or a high-fat diet for 20 weeks following a one-week adaptation;ND＋telmisartan（n=10） group and HD＋telmisartan group（n=10）,in which the rats were initially administered in the same way as the ND or HD group,and then they were orally gavaged with telmisartan（5 mg/kg daily） additionally for 5 weeks.Related inflammatory factors were measured by ELISA.Monocyte chemotactic protein 1（MCP-1）,phosphorylated JNK and IκB-α expressions in both adipose and liver were detected by Western blotting.CRP and angiotensin Ⅱ receptor 1（AT1） mRNA expressions in both adipose and liver were determined by RT-PCR.The results showed that telmisartan administration in vivo reversed insulin resistance as evidenced by a decrease in plasma fasting glucose levels,plasma fasting insulin levels and homeostasis model of assessment-insulin resistance（HOMA-IR）.Furthermore,telmisartan administration significantly reduced serum CRP,TNF-α and IL-1β levels,and elevated serum IL-10 levels.It was also found to hamper the high-fat diet-induced increase in CRP mRNA,AT1 mRNA and MCP-1,and decrease in IκB-α in both adipose and liver.It was concluded that telmisartan administration in vivo may improve insulin resistance through attenuated inflammatory response pathways.

关键词： telmisartan insulin resistance inflammation obesity

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GTP Cyclohydrolase 1 Gene 3'-UTR C+243T Variant Predicts Worsening Outcome in Patients with First-Onset Ischemic Stroke

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2010年第6期30卷 694-698页

作者：汤陵张岚丁虎涂巍严江涛 institute of hypertension and Department of Internal Medicine Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology

Tetrahydrobiopterin (BH4) is an essential cofactor for all three nitric oxide synthase (NOS isoforms), which plays an important role in vascular diseases. GTP cyclohydrolase 1 (GCH 1) is the first-step and rate-limiting enzyme for BH4 biosynthesis in its de novo pathway. Common GCH1 gene variant C+243T in the 3’-untranslated region predicts NO excretion. The present study examined the predictive role of GCH 1 gene 3’-UTR C+243T variant in the long-term outcome of ischemic stroke. A total of 142 patients with first-onset ischemic stroke were recruited and detected for genotype of GCH1 3’-UTR C+243T by a TaqMan SNP Genotyping assay. Subsequent vascular events and death were de- termined over a 5-year follow-up period. The frequency of GCH1 3’-UTR +243 C/T or T/T genotype was significantly increased in patients with endpoint events as compared with those without events (74% vs 57.8%, P=0.06). Cox regression survival analysis indicated that an increased probability of death or new vascular events was found in patients with GCH1 3’-UTR +243 C/T or T/T genotype com- pared with those with GCH1 3’-UTR C/C genotype (40.6% vs 25.5%), GCH1 3’-UTR +243 C/T or T/T genotype relative to GCH1 3’-UTR C/C genotype was associated with the increased risk of death or vascular events even after adjustment for other risk factors (OR=2.171, 95% CI: 1.066-4.424, P=0.033). It was concluded that GCH1 3’-UTR C+243T variant was an independent predictor of worsening long-term outcomes in patients with first-onset ischemic stroke.

关键词： GTP cyclohydrolase 1 ischemic stoke outcome gene polymorphism

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Polystyrene nanoplastics induce glycolipid metabolism disorder via NF-κB and MAPK signaling pathway in mice

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Journal of Environmental Sciences 2024年第3期137卷 553-566页

作者： Xingpei Fan Xiaoyan Li Jiaxin Li Yuxia Zhang Xiangjuan Wei Hailong Hu Boya Zhang Haining Du Meimei Zhao Ruijiao Zhu Daqian Yang Yuri Oh Ning Gu School of Life Science and Technology Harbin Institute of TechnologyHarbin 150001China State Key Laboratory of Urban Water Resource and Environment Harbin Institute of TechnologyHarbin 150006China Department of Medicine Renal Electrolyte and Hypertension DivisionDepartment of GeneticsPerelman School of MedicineUniversity of PennsylvaniaPhiladelphia 19104USA Faculty of Education Wakayama UniversityWakayama 640-8441Japan

Nanoplastics-induced developmental and reproductive toxicity,neurotoxicity and immunotoxicity are a focus of widespread attention.However,the effects of nanoplastics(NPs)on glycolipid metabolism and the precise underlying mechanisms are unclear at present.Here,we showed that oral administration of polystyrene nanoparticles(PS-NPs)disrupts glycolipid metabolism,with reactive oxygen species(ROS)identified as a potential key signaling molecule.After PS-NPs treatment,excessive production of ROS induced the infammatory response and activated the antioxidant pathway through nuclear factor-erythroid factor 2-related factor 2.The activation of nuclear factor-κB(NFκB)signaling pathway induced the phosphorylation of the mitogen-activated protein kinases(MAPK)signaling pathway,which induced the activation of extracellular regulated kinases(ERK)and p38.Constitutive activation of the MAPK signaling proteins induced high continued phosphorylation of insulin receptor substrate-1,in turn,leading to decreased protein kinase B(Akt)activity,which weakened the sensitivity of liver cells to insulin signals and induced insulin resistance.In parallel,phosphorylation of Akt led to loss of control of Fo XO1,a key gene of gluconeogenesis,activating transcription of glucose-6-phosphatase(G6PC)and phosphoenolpyruvate carboxykinase(PEPCK)in a manner dependent on PGC1α.Moreover,the activated ERK promoted lipid accumulation through ERK-PPARγcascades.Therefore,sterol regulatory element-binding protein-1 and levels of its downstream lipogenic enzymes,ACC-1,were up-regulated.Upon treatment with the antioxidant resveratrol,PS-NPs-induced glucose and lipid metabolic disorders were improved by inhibiting ROS-induced activation of NFκB and MAPK signaling pathway in mice.Based on above,PS-NPs exposure disrupts glycolipid metabolism in mice,with ROS identified as a potential key signaling molecule.

关键词： Nanoplastics Resveratrol Hyperglycemia Lipid metabolism Infammatory response Reactive oxygen species(ROS)

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Comprehensive effects of traditional Chinese medicine treatment on heart failure and changes in B-type natriuretic peptide levels: A meta-analysis

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World Journal of Clinical Cases 2024年第4期12卷 766-776页

作者： Li-Li Xia Shu-Yun Yang Jun-Yao Xu Han-Qing Chen Zhu-Yuan Fang hypertension Research institute Affiliated Hospital of Nanjing University of Chinese MedicineNanjing 210004Jiangsu ProvinceChina Department of General Practice Southeast University Affiliated Zhongda HospitalNanjing 210009Jiangsu ProvinceChina

BACKGROUND Heart failure(HF),a common cardiovascular condition,is characterized by significant morbidity and mortality.While traditional Chinese medicine(TCM)is often used as a complementary approach in HF management,systematic evalua-tions of its impact on clinical outcomes,TCM syndrome scores,and B-type natriuretic peptide(BNP)levels are lacking.This study fills this gap through a comprehensive analysis of randomized controlled trials(RCTs)focusing on TCM for HF treatment.It encompasses an assessment of methodological quality,a meta-analysis,and an evaluation of evidence quality based on established standards.The results offer crucial insights into the potential advantages and constraints of TCM in HF management.RCTs on TCM for HF treatment published since the establishment of the database were searched in four Chinese and English databases,including China National Knowledge Infrastructure,Wanfang,VIP Information Chinese Science and Technology Journal,and PubMed.Methodological quality was assessed for the included studies with the Cochrane risk-of-bias assessment tool,and the meta-analysis and publication bias assessment was performed with the RevMan5.3 software.Finally,the quality of evidence was rated according to the GRADE criteria.RESULTS A total of 1098 RCTs were initially retrieved.After screening,16 RCTs were finally included in our study,which were published between 2020 and 2023.These RCTs involved 1660 HF patients,including 832 in the TCM group[TCM combined with conventional Western medicine(CMW)treatment]and 828 in the CWM group(CWM treatment).The course of treatments varied from 1 wk to 3 months.TCM syndrome differentiation was analyzed in 11 of the included RCTs.In all included RCTs,outcome indicators included comprehensive clinical outcomes,TCM syndrome scores,and BNP levels.The meta-analysis results showed significant differences between the TCM and CWM groups in terms of comprehensive clinical outcomes[risk ratio=-0.54;95%confidence interval(CI)=-0.61,-0.47;P<0.00001],TCM syndrome scores[weighte

关键词： Traditional Chinese medicine Heart failure Comprehensive clinical outcomes Traditional Chinese medicine syndrome score B-type natriuretic peptide level Meta-analysis©The Author(s)2024.Published by Baishideng Publishing Group Inc.

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Simvastatin Increases the Activity of Endothelial Nitric Oxide Synthase via Enhancing Phosphorylation

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2009年第3期29卷 286-290页

作者：李小霞汪培华徐西振王勇夏永汪道文 The institute of hypertension and Department of Internal Medicine Tongji Hospital Tongji Medical College Huazhong University of Science Davis Heart & Lung Research institute the Ohio State University Medical Center

3-hydroxy-3-methylgulutaryl-coenzyme A （HMG-CoA） reductase inhibitors or statins are a kind of lipid-lowering agents and have been used for the prevention and treatment of Cardiovascular diseases. Recent studies suggested that statins, besides lowering cholesterol, may protect vessels by enhancing the activity of endothelial nitric oxide synthase （eNOS）. In the present study, we investigated if simvastatin increases eNOS activity through its phosphorylation in 293 cells （293-eNOS） with stable expression of eNOS. The results showed that incubation of 293-eNOS cells with simvastatin （10 μm/L） for 2 h significantly increased in the activity of eNOS as shown by the conversion of L-arginine to L-citrulline （2889.70±201.51 versus 5630.18＋218.75 pmol/min . mg proteins）（P〈0.01）. Western blotting revealed that simvastatin increased phosphorylation of eNOS at 1177 （ser） and also 495 （thr） but did not affect the overall expression of eNOS or inducible NOS. Further study found that simvastatin raised phosphorylation levels of Akt and AMPK, and such effect could be antagonized by Akt inhibitor or AMPK inhibitor. These results suggest that simvastatin could stimulate,the activity of eNOS via its phosphorylation by Akt and AMPK, which provides a new mechanism, other than lipid-lowering effect, for the cardiovascular protection of statins.

关键词： simvastatin nitric oxide synthase phosphorylation endothelial cells

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Therapeutic neovascularization by autologous transplantation with expanded endothelial progenitor cells from peripheral blood into ischemic hind limbs

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Acta Pharmacologica Sinica 2005年第9期26卷 1069-1075页

作者： Chun-ling FAN Ping-jin GAO Zai-qian CHE Jian-jun LIU Jian WEI Ding-liang ZHU~2 Shanghai Key Laboratory Of Vascular Biology,Shanghai institute of hypertension,Ruijin Hospital,Shanghai Second Medical University and National Key Laboratory for Medical Genomics,Health Science Center,Shanghai institute for Biological Sciences,Chinese Academy of Sciences,Shanghai 200025,China Shanghai Key Laboratory of Vascular Biology Shanghai Institute of Hypertension Ruijin Hospital Shanghai Second Medical University and National Key Laboratory for Medical Genomics Health Science Center Shanghai Institute for Biological Sciences Chinese Academy of Sciences Shanghai China

Aim:To investigate the hypothesis that transplantation with expanded autolo-gous endothelial progenitor cells(EPC)could enhance neovascularization.Methods:Peripheral blood mononuclear cells(PB-MNC)isolated from New ZealandWhite rabbits were cultured in vitro.At d 7,the adherent cells were collected forautologous transplantation.Rabbits with severe unilateral hind limb ischemiawere randomly assigned to receive phosphate-buffered saline or expanded EPC inphosphate-buffered saline,administered by intramuscular injection in 6 sites ofthe ischemic thigh at postoperative d 7.Neovascularization was monitored byusing the calf blood pressure ratio to indicate tissue perfusion,digital subtractionangiography to identify collateral vessel development and histological analysisof capillary density in the ischemic limb at d 35 after surgery.Results:Autolo-gous EPC transplantation produced significant amelioration in ischemic hind limbs,as indicated by a greater calf blood pressure ratio(0.52±0.04 vs 0.42±0.05,P<0.01),angiographic score(1.44±0.06 vs 0.98±0.08,P<0.01)and capillary density in muscle(195.2±5.4/mm~2 vs 169.4±6.4/mm~2,P<0.05),than controls.Conclusion:Transplan-tation of autologous expanded EPC can promote neovascularization in ischemichindlimbs.

关键词： vascular endothelium hindlimb ischemia physiologic neovascularization stem cell transplantation

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Intramuscular delivery of rAAV-mediated kallikrein gene reduces hypertension and prevents cardiovascular injuries in model rats

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Acta Pharmacologica Sinica 2007年第12期28卷 1898-1906页

作者： Yao WANG~(2,3),Ling-bo HOU~(2,3),Zhen-jun LIU~2,Yan WANG~2,Chun-lian CHEN~2,Xiao XIAO~(2,4),Dao-wen WANG~(2,5)~2 institute of hypertension and Department of Internal Medicine,Tongji Hospital,Tongji Medical College,Huazhong University of Science andTechnology,Wuhan 430030,China ~4 Departments of Molecular Genetics and Biochentistry and Gene Therapy Center University of Pittsburgh,Pittsburgh,PA 15261,USA institute of hypertension and Department of Internal Medicine Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China Departments of Molecular Genetics and Biochemistry and Gene Therapy Center University of Pittsburgh Pittsburgh USA

Aim:The overexpression of the human tissue kallikrein （HK） gene can reduceblood pressure and ameliorate the secondary syndromes associated with hyper-tension in animal models.The current study was designed to investigate hy-potensive effect of intramuscular delivery of HK gene.Methods:We generatedan recombinant adeno-associated virus （rAAV） vector expressing human tissuekallikrein under the control of a cytomegalovirus promoter and administered therAAV-HK vector to a spontaneously hypertensive rat model at a dose of 1×1010virons/rat through intramuscular injection.Results:A persistent,high-level ex-pression of HK post-gene delivery was confirmed by ELISA.The systolic bloodpressure in the rats receiving rAAV-LacZ and saline increased from 171.3 mmHg to182.3 mmHg 28 weeks' post injection.In contrast,the delivery of the HK gene byAAV vectors attenuated the increase of the systolic blood pressure in the treatedgroup.The systolic blood pressure was only slightly lowered （from a level of 174mmHg to 170.5 mmHg） post-vector administration.The difference in blood pres-sure between the treated group and the control groups is statistically significantat 12.6 mmHg.The hypotensive effect of rAAV-HK persisted until the end of thetesting period.In addition,a significant amelioration of cardiovascularhypertrophy,renal injury,and collagen depositions in the rAAV-HK-treated ani-mals were also observed.Conclusion:All the effects are comparable with thoseof intravenous delivery.Therefore,the intramuscular administration of rAAV-HKmay be used in gene therapy for hypertension.

关键词： recombinant adeno-associated virus vector human tissue kallikrein intramuscular administration hypertension gene therapy cardiovascular remodeling spontaneously hypertensive rat

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Association of DRD2 polymorphisms and chlorpromazine-induced extrapyramidal syndrome in Chinese schizophrenic patients

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Acta Pharmacologica Sinica 2006年第8期27卷 966-970页

作者： Sheng-nan WU~(2,3,5,6) Rui GAO~(2,3,6) Qing-he XING~(2,3,6) Hua-fang LI~4 Yi-feng SHEN~4 Niu-fan GU~4 Guo-yin FENG~4 Lin HE~(2,3,7)2 Bio-X Life Science Research Center,Shanghai Jiaotong University,Shanghai 200030,China 3 institute of Nutritional Sciences,SIBS,Chinese Academy of Sciences,Shanghai 200031,China 4 Shanghai institute of Mental Health,Shanghai 200030,China 5 Shanghai institute of hypertension,Ruijin Hospital,Medical School of Shanghai Jiaotong University,Shanghai 200025,China Bio-X Life Science Research Center Shanghai Jiaotong University Shanghai China institute of Nutritional Sciences SIBS Chinese Academy of Sciences Shanghai China Shanghai institute of hypertension Ruijin Hospital Medical School of Shanghai Jiaotong University Shanghai China Shanghai institute of Mental Health Shanghai China

Aim:Extrapyramidal syndrome (EPS) is most commonly affected by typical antip-sychotic drugs that have a high affinity with the D2 receptor.Recently,manyresearch groups have reported on the positive relationship between the geneticvariations in the DRD2 gene and the therapeutic response in schizophrenia pa-tients as a result of the role of variations in the receptor in modulating receptorexpression.In this study,we evaluate the role DRD2 plays in chlorpromazine-induced EPS in schizophrenic patients.Methods:We identified seven SNP(singlenucleotide polymorphism) (-141Cins>del,TaqIB,TaqID,Ser311Cys,rs6275,rs6277and TaqIA) in the DRD2 gene in 146 schizophrenic inpatients (59 with EPS and 87without EPS according to the Simpson-Angus Scale) treated with chlorpromazineafter 8 weeks.The alleles of all loci were determined by PCR (polymerase chainreaction).Results:Polymorphisms TaqlD,Ser311Cys and rs6277 were not poly-morphic in the population recruited in the present study.No statistical signifi-cance was found in the allele distribution of-141Cins>del,TaqIB,rs6275 andTaqIA or in the estimated haplotypes (constituted by TaqIB,rs6275 and TaqIA) inlinkage disequilibrium between the two groups.Conclusion:Our results did notlend strong support to the view that the genetic variation of the DRD2 gene playsa major role in the individually variable adverse effect induced by chlorpromazine,at least in Chinese patients with schizophrenia.Our results confirmed a previousstudy on the relationship between DRD2 and EPS in Caucasians.

关键词： dopamine receptors basal ganglia disease polymorphism chlorpromazine schizophrenia

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Identification of Common Variants within KCNK17 in Chinese Han Population

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2010年第1期30卷 13-17页

作者：唐洲平丁虎徐宇军徐沙贝 Department of Neurology Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology The institute of hypertension and Department of Internal Medicine Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology

KCNK17 is a member of the acid-sensitive subfamily of tandem pore K+ channels,which are open at all membrane potentials and contribute to cellular resting membrane potential.Recent genome-wide study(GWA)has shown that variants within KCNK17 confer genetic susceptibility for increasing ischemic stroke.In an effort to discover additional polymorphism(s),we scrutinized the genetic polymorphisms in the KCNK17.By direct DNA sequencing in 32 individuals,we identified nine sequence variants within the 16kb of whol...

关键词： polymorphism haplotypes KCNK17 ischemic stroke Chinese Han population

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