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中国生理学会第23届全国会员代表大会暨生理学学术大会

作者： Wen-Jie CAI~1,Ming-Jie WANG~2,Yi-Chun ZHU~2 1 Department of Basic medicine,University of Shanghai for Science and Technology,Shanghai 200093,China 2 Department of Physiology and Pathophysiology,Fudan University Shanghai Medical College,Shanghai 200032,China

Introduction:Hydrogen sulfide(HS),the toxic gas,has been shown to play an important role in regulating physiological functions.Our previous study has shown that HS enhances angiogenesis in vitro and in vivo.But whether hydrogen sulfide influences cytoskeleton rearrangement so as to promote cell migration? And furthermore,does endogenous HS participate in the VEGF or bFGF effect on cytoskeleton? The answer is still unclear.Methods:Rhesus monkey choroid retinal Endothelial cells(RF/6A) were used.Rhodamine phalloidin was used to stain the cellular F-actin to show actin polymerization.cells were exposed to different concentrations of NaHS(1-200μmol/L) for 20 min.K channel blocker Glibenclamide(10μmol/L) or CSE inhibitor DL-propargylglycine (PAG,10 mmol/L) was given 1 h prior.Cultures were then washed and fixed for 20 min in PBS containing 40 g/L paraformaldehyde,permeabilized,and incubated with Rhodamine-conjugated phalloidin for 40 min.Following washing,cells were imaged with a Leica TCS SP2 confocal laser microscope.Scanning and transmission electron microscopy were done to observe the ultrastructural changes of the cell skeleton.Results: Relatively low concentrations of NaHS(1 and 10μmol/L) enhanced endothelial cell skeleton reorganization and stress fiber formation.Actin microfilament became thickened,tense and distributed with parallel manner.Furthermore, we observed that Glibenclamide partially prevented endothelial cell actin polymerization induced by 10μmol/L NaHS,while the Glibenclamide alone has little effects.10μmol/L NaHS treatment can turn the RF/6A Endothelial cells into elongated shape and increased pseudopodia formation.VEGF(20 ng/mL) and bFGF(10 ng/mL) can both boost the stress fiber formation.PAG abolished VEGF induced but not bFGF induced cell skeleton reorganization. Conclusion:The present study provides the first evidence that HS enhance endothelial cell actin polymerization, partially via the mediation of K channel opening.Endogenous HS is crucial to VEGF-induced cytoskeleton rearrangement.

关键词： hydrogen sulfide Endothelial cells migration actin polymerization

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Effects of ginsenosides on vascular reactivity in rat cerebral and renal arteries

Effects of ginsenosides on vascular reactivity in rat cerebr...

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两岸三地药理学与临床药理学术会议

作者： WONG Wing-tak LEUNG Fung-ping YUNG Lai-hang WONG Ricky Ngok Shun Department of Physiology Chinese University of Hong Kong Department of Biology Hong Kong Baptist University

Objective To investigate possible mechanisms underlying the antioxidant property(1)and the in vitro vasodilator effects(2)of the two ginsenosides,Rb1 and Rg1,in isolated rat renal and cerebral arter- ies.Methods Arterial rings were mounted in a multi-channel myograph for recording of isometric tension.To examine the antioxidant activity,some rings were exposed to a free radical-generating reaction(hypoxan- thine and xanthine oxidase)with and without pre-treatment with ginsenosides.The calcium antagonistic ef- fects were tested on rings contracted by membrane depolarization in elevated extracellular potassium ions,a condition that promoted Cainflux in vascular smooth muscle cells.Results Ginsenosides protected en- dothelial function(endothelial nitric oxide-dependent relaxation)against oxidative stress;(2)ginsenoside Rbl reduced the high K+-induced contractions of both renal and cerebral arteries while ginsenoside Rgl re- laxed the rat cerebral artery but not the renal artery.Conclusions Ginsenosides are vaso-protective via(1) the antioxidant activity which protects endothelial cell function and(2)the inhibition of Ca2+influx through voltage-sensitive Cachannels in vascular smooth muscle.The vasodilator effects may suggest the potential preventive or therapeutic values of ginsenosides against stroke and renal hypertension.

关键词： ginsenosides Endothelial cells relaxation

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Regulation of proliferation by KCa3.1 channels is independent of channel electrophysiological function

Regulation of proliferation by KCa3.1 channels is independen...

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2008北京国际生理科学学术大会

作者： MILLERSHIP Joanne BRUCE Jason I E DEVOR Daniel C FEARON Ian M Life Sciences the University of ManchesterManchester M13 9NTUK Department of Cell Biology and Physiology School of MedicineUniversity of PittsburghPittsburghPA 15261USA

Potassium channels regulate proliferation of a number of cell types.Of the potassium channel family, K3.1(IK1/SK4),is involved in the proliferation of Endothelial cells(EC),T lymphocytes and several cancer cell lines.With respect to Endothelial cells,these cells express a wide variety of ion channel types and subtypes,and the patterns of expression differ due to differences in vascular beds from which cells were isolated,passage number and culture conditions.For this reason,it is difficult to dissect,and examine in isolation,the functional role of a specific potassium channel in EC proliferation.Thus,to investigate the mechanisms underlying the role of K3.1 in cell proliferation in isolation,we performed proliferation assays in HEK293 cells expressing recombinant hK3.1 channels.In cells stably expressing this channel,selective inhibition of hK3.1 with 10μmol/L TRAM-34 reduced proliferation,while transient expression of hK3.1 in WT HEK293 cells increased proliferation.The mechanism by which hK3.1 stimulates cell proliferation is thought to be mediated by cell hyperpolarisation(via K efflux),which increases[Ca] by driving Ca influx through non-selective cation channels.However,when WT HEK293 cells were transiently transfected with a mutant(GYG/AAA)hK3.1 channel,which neither conducts K ions nor promotes Ca entry,proliferation was increased relative to control(mock-transfected)cells.Furthermore,when WT HEK293 cells were transiently transfected with a trafficking mutant(L18A/L25A)hK3.1 channel,which is not expressed at the cell surface,proliferation was also increased relative to control cells.Thus,both K efflux and Ca influx are not necessary for hK 3.1-induced proliferation in HEK293 cells,and nor does hK 3.1 need to be expressed at the cell surface.We propose that hK 3.1-induced cell proliferation is independent of electrophysiological function and arises potentially due to direct regulation of intracellular signalling pathways.In support of this hypothesis,in cells expressing hK3.1 pharmacological inhibition of E

关键词： KCa3.1 Endothelial cells proliferation MAP kinase

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Design,synthesis and the mechanism of anti-atherosclerosis of The novel Tetramethylpyrazine derivatives

Design,synthesis and the mechanism of anti-atherosclerosis o...

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华东六省一市生物化学与分子生物学会2008年学术交流会

作者： Cui Lei~(1)) Ding Qian~(1)) Wang Shou-xun~(1)) Liu Xin yong~(2)*) (~(1))Weifang Medical College,Weifang 261053,~(2))School of Pharmaceutical Sciences, Shandong University Ji-nan 25000)

Tetramethylpyrazine(TMP),the active ingredients of Chinese traditional medicine Chuanxiong with effect promoting blood flow,has been widely used in clinical for treatment of atherosclerosis.However,pharmacokinetics study show that TMP has low bioavailability,rapid metabolism and short half-life(T=2.89 h).The accumulated toxicity often appeared in the patients for keep an effective plasma concentration by the frequent administration. Structure-activity relationship studies indicated that pyrazine ring in the molecule of TMP might largely be the determinant of its pharmacodynamies,while the 4 substituted groups might primarily govern its pharmaookinetics and toxicity.Therefore,it is significance to design and synthesize the new TMP derivatives with high potency and high bioavailability. The Endothelial cells injury is not only the initiating factor of atherosclerosis,but also has an important role in the development of atherosclerosis-related diseases.So the protection of vascular Endothelial cells injury is a necessary means for the treatment of atherosclerosis.It’s generally believed that the free radicals production and calcium overload of Endothelial cells is positively related to the cell injury.In order to obtain the agents which have the effects on eliminating free radicals and reducing intraoellular calcium load,we designed,synthesized some TMP derivatives such as double esters,Sehiff bases,lactam,in which active groups and pharmacophores were introduced to the methyl groups of TMP.Anti-atherosclerotic activities and mechanisms of these new compounds were further studied and found some compounds exhibit better pharmacological activities than TMP by the tests of eliminating free radicals and reducing intracellular calcium load.The results provide good information for further investigation and development of the new generation of TMP drugs.

关键词： Tetramethylpyrazine（TMP） TMP derivatives atherosclerosis Endothelial cells oxyradical calcium overload

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Soft Substrate Induces endothelial Cell Inflammation and Disrupts Endothelium Integrity

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Journal of Biosciences and Medicines 2021年第2期9卷 92-102页

作者： Yiling Tan Xiuli Mao Huanli Wang School of Biomedical Engineering Shanghai Jiao Tong University Shanghai China

Atherosclerosis (AS) is the main cause of death and disability all over the world. A lot of efforts have been devoted to treat AS, among which tissue engineering blood vessel materials, including artificial blood vessels, stents and vascular patches, have brought hope to ameliorate the symptoms in AS patients. However, there remains a large percentage of implantation failure due to the incompatibility of the material with the body. AS is a multi-factor related disease, and chronic inflammation is a major event that involves with its pathogenesis and development. Since previous studies suggested that the stiffness of the blood vessel might affect the inflammatory conditions, in this paper, we investigate the mechanism of how substrate stiffness could affect the inflammation response of the Endothelial cells (ECs). Polyacrylamide (PA) based hydrogels at different concentrations were used as the culture substrate for ECs. The mRNA expression level of VCAM-1 and ICAM-1 was determined by qRT-PCR. EC chemotactic effect was evaluated by the number of THP-1 adhered to EC monolayer. The protein levels of IκBα and NF-κB were determined by western blotting analysis. The expression and localization of the major adherens junctions (AJs) proteins, VE-cadherin and β-catenin, were evaluated by western blotting and immunofluorescence staining. Our results showed that ECs cultured on soft substrate (1 kPa) demonstrated more chemotactic effect and the amount of the monocytes adhered to them was higher than that on harder substrate (20 kPa, p endothelial monolayer changed with the substrate stiffness. Compared with ECs on normal substrate (20 kPa), the protein expression level of β-catenin decreased (p < 0.05), and immunofluorescence staining of VE-cadherin and β-caten

关键词： Substrate Stiffness Endothelial cells Inflammation Adherens Junction

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An experimentalstudy ofinferior vena cavalstentin canine

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Chinese Medical Journal 1999年第9期 48-53页

作者：张小明汪忠镐郭建军

Objective To investigate the feasibility of our self made inferior vena cave (IVC) stent Methods Self expanding, stainless steel, Z shaped stents were deployed in the IVC of 14 dogs They were randomly divided into four groups, four dogs in the first three groups, and 2 in the fourth group. IVC specimens were taken at 2, 4, 8 and 16 weeks following stent deployment No anticoagulant or antiplatelet therapy was given Results All stents were widely stretched out and so was the vessel lumen No thrombus was present and the patency was 100% in all groups The stents were completely covered by neointima 2 weeks after stent deployment The neointimal thickness varied significantly: the thinnest at 2 weeks, the thickest at 4 weeks and becoming thinner at 8 weeks and stable until 16 weeks The inflammatory reaction was gradually reduced Under scanning electronic microscopy, the neointima was covered by a layer of Endothelial cells 2 weeks following stenting, which were irregularly shaped and aligned The cells became slender,spindle shaped and aligned parallel to the direction of bolld flow 4 weeks afterwards Conclusion Experimental study indicated that our self expanding IVC stent was feasible for clinical application

关键词： Endothelial cells Stent Inferior vena cava

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Expression and effects of union exchangers （AEs） on HUVECs apoptosis induced by hyperglucose

Expression and effects of union exchangers （AEs） on HUVECs...

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第十五届国际药理学大会

作者： Li Qing Huang Qiren Peng Weijie He Ming Department of Pharmacology Nanchang University School of Pharmaceutical Science Nanchang 330006 P R.China

＜正＞ Dysregulation of Endothelial cells （ECs） is an initial step of angiopathy resulted inby diabetes mellitus （DM）. Anion exchangers （AEs） are likely to play an important role in angiopathy. The study is to examine the expression of AEs in humanumbilical vein cells （HUVECs） and investigate if AEs participate in HUVECsapoptosis induced by high glucose. HUVECs were treated with DMEM containingglucose （5.5, 27.8, 40.0, 55.6 mmol·L-1, respectively）for72 h. Apoptosiswas detected by TUNNL assays and AEs mRNA levels were examined by RT-PCR The results showed that glucose exposed for 72 h resulted in expression up-regulation of AE2 mRNA and apoptosis rate enhancement in a concentration - de-pendent manner, while corresponding Ph and osmotic pressure did not affect thesechanges. In additional, expression of AE1 and AE3 mRNA failed to detect incase of hyperglucose. The results suggest that hyperglucose may up - regulateAE2 expression and AE2 may play a critical role in ECs apoptosis induced by hyperglycemia.

关键词： anion exchangers Endothelial cells apoptosis diabetes mellites

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ORIENTATION,DIVISION AND PROLIFERATION

ORIENTATION,DIVISION AND PROLIFERATION

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中国力学学会学术大会'2005

作者： Wang Hongbing Huang Qiping Deng Xiaoyan (Key Lab for Biomechanics & Tissue Engineering of Ministry oany ,chongqing 400044,China) (Department of Bioengineering, Beihang Universty,Beijing 100083,China)

The group behavior of vascular Endothelial cells (ECV-304) in response to cyclic stretching was studied by using a dot of EC cells cultured on a rectangle silicon rubber membrane. Differently from their response to flow-induced shear stress, under cyclic stretching, vascular Endothelial cells elongated and rearranged their orientation in the direction perpendicular to the stretching. Morphologically, the cyclic stretching changed the EC do from a circular shape into an oval, of which the long axis was along the direction perpendicular to the stretching. The elongation ratio (long axis:short axis) of the confluent oval dot of EC cells increased with time. There existed a polarization phenomenon in EC cell division and proliferation under cyclic stretching, i.e., cells proliferated advantageously in the direction perpendicular to the stretching over other directions. We therefore believe that the shape change of the EC dot was not a result from the orientation change of individual cells but from the difference in cell proliferation rate in different directions.

关键词： cyclic stretching Endothelial cells Cell proliferation orphology

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The antiarteriosclerosis mechanisnis of Scallop skirt-glycosaminoglycan

The antiarteriosclerosis mechanisnis of Scallop skirt-glycos...

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第十五届国际药理学大会

作者： Liu Sai Sun Fusheng Wang Shaojun Chu Xianghua Ju Chuanxia Department of Pharmacology Medical College Qingdao University Qingdao Shandong. 266021 China Qingdao Municipal Hospital. Qingdao. Shandong 266021 China

＜正＞ In order to investigate the antiarteriosclerosis mechanisms of scallop skirt-glycosaminoglycan（SS-GAG）, RT-PCR analysis, immunohistochemical staining, enzymatic method and flow cytometry so on were employed. SS-GAG can inhibit the formation of foam cells derived from macrophage（ U937） and vascular smooth muscles cells （ VSMCs）. and decrease the overexpression of some cytokines （TNFα, IL-6 and IL-8） and intracellular Ca2+ level. Furthermore, SS-GAG up-regulated the mRNA and protein expression of low density lipoprotein （LDL） receptors and scavenger receptor class B, type Ⅰ（SR-BI）, a well characterized high density lipoprotein （ HDL） receptor in macrophage （ RAW264.7） . It also down-regulated the overexpression of scavenger receptor CD36 induced by Ox-LDL lesion, restrained the oxidative modification of RAW264.7 to LDL.SS-GAG can modulate lipoprotein metabolic disorders and the expression of some lipoprotein receptors. At the same time. SS-GAG inhibited excessive proliferation of VSMCs and protected Endothelial cells from oxidation damage. The above is mavbe the antiarteriosclerosis mechanisms of SS-GAG.

关键词： SS-GAG. arteriosclerosis macrophage VSMCs Endothelial cells

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The progress of study for snake venom metalloproteinases

The progress of study for snake venom metalloproteinases

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第七届全国酶学学术讨论会

作者： Liu Wei, Li Yan-jun, Liu Juan, Liu Yan-yong, Dong Zhi-hai (Beijing Research Institute of Pharmaceutical chemistry,Beijing 102205)

The biochemical features Of metalloproteinases isolated from snake venoms arereviewed.together with their role in the pathogenesis of the local tissue damage aftersnake envenomations.Various venom metalloproteinases differ in their structure.Some enzymes are only composed of metalloproteinase domain,others have highcysteine domains and others have an additional lectin-like subunit.All Of them arezinc-dependent enzymes with highty similar zinc binding characterization.Some

关键词： snake venom hemorrhage metalloproteinases local tissue damage basement membrane Endothelial cells

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