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浙江大学学报（医学版） 2016年第5期45卷 469-476页

作者：林先刚陈业农刘竹青安徽中医药大学针灸骨伤临床学院

目的：探讨姜黄素对慢性阻塞性肺疾病（COPD）模型大鼠肺动脉平滑肌细胞的作用及其分子生物学机制。方法：将75只雄性Wistar大鼠随机分为正常对照组，模型对照组，姜黄素小剂量组、中剂量组和大剂量组，采用HE染色法观察肺动脉管组织学... 详细信息

目的：探讨姜黄素对慢性阻塞性肺疾病（COPD）模型大鼠肺动脉平滑肌细胞的作用及其分子生物学机制。方法：将75只雄性Wistar大鼠随机分为正常对照组，模型对照组，姜黄素小剂量组、中剂量组和大剂量组，采用HE染色法观察肺动脉管组织学形态，免疫组织化学染色检测增殖细胞核抗原（PCNA）、凋亡相关蛋白Bcl-2、Bax，TUNEL法检测姜黄素对平滑肌细胞凋亡的影响，蛋白质印迹法检测肺组织SOCS-3／JAK2／STAT通路相关蛋白表达情况。结果：模型对照组右心室收缩压（RVSP）、右心室肥大指数（RVMI）均高于正常对照组（均P〈0．05），姜黄素大剂量组和中剂量组RVSP、RVMI均低于模型对照组（均P〈0．05）；模型对照组肺动脉管增厚、平滑肌细胞数量显著增多，而姜黄素中剂量组和大剂量组肺动脉管变薄、平滑肌细胞固缩、变形；模型对照组PCNA、Bcl-2相对表达量高于正常对照组（均P〈0．05），Bax相对表达量低于正常对照组（P〈0．05）；姜黄素中剂量组和大剂量组PCNA相对表达量低于模型对照组（均P〈0．05），Bax相对表达量高于模型对照组（均P〈0．05）；模型对照组SOCS-3蛋白减少、而磷酸化JAK2、STAT1、STA13增多，姜黄素中剂量组和大剂量纽SOCS．3蛋白增多，磷酸化JAK2、RVMISTAT3减少。结论：姜黄素可促进COPD大鼠平滑肌细胞凋亡，改善平均肺动脉压以及RVMI，这一作用可能与刺激SOCS-3／JAK2／STAT信号途径有关。

关键词：姜黄素/投药和剂量姜黄素/药理学肺疾病慢性阻塞性/药物疗法肺疾病慢性阻塞性/病理生理学肺动脉/细胞学肌平滑血管/药物作用疾病模型,动物

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哌替啶的舒血管作用及其机制

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浙江大学学报（医学版） 2004年第2期33卷 166-169页

作者：张雄柴灵莺童晓嵋陆源夏强浙江大学医学院基础医学部浙江杭州310031 浙江大学医学院

目的 :探讨哌替啶扩张血管导致低血压的机制。方法 :制备大鼠离体主动脉环 ,记录血管环张力 ,观察哌替啶对高钾和苯肾上腺素 (Ph E)预收缩血管的作用。结果 :哌替啶不影响血管的静止张力 ,但可对高钾和 Ph E诱导的收缩产生非内皮依赖的... 详细信息

目的 :探讨哌替啶扩张血管导致低血压的机制。方法 :制备大鼠离体主动脉环 ,记录血管环张力 ,观察哌替啶对高钾和苯肾上腺素 (Ph E)预收缩血管的作用。结果 :哌替啶不影响血管的静止张力 ,但可对高钾和 Ph E诱导的收缩产生非内皮依赖的舒张作用 ,并呈剂量 -反应关系。哌替啶既不影响咖啡因诱导的血管收缩 ,也不改变钌红作用后对高钾诱导收缩的抑制作用。在无钙条件下 ,哌替啶仍能抑制 Ph E的收缩 ,也抑制后续加入钙后引发的收缩。结论 :哌替啶对高钾和 Ph E诱导的血管收缩有舒张作用 ,机制可能与其阻断细胞膜钙通道和抑制 IP3敏感钙池的钙释放有关。

关键词：哌替啶/药理学血管/药物作用 IP3受体 Ryanodine受体主动脉

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丝裂素活化蛋白激酶在AngⅡ上调培养的血管平滑肌细胞转化生长因子-β受体表达中的作用

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陕西医学杂志 2008年第9期37卷 1128-1129,1173页

作者：孙银平张大伟王省王晓冰黄丽君新乡医学院病理生理教研室新乡453003 新乡医学院解剖学教研室

目的:探讨丝裂素活化蛋白激酶在血管紧张素Ⅱ(AngⅡ)诱导血管平滑肌细胞(VSMC)转化生长因子-β受体(TGF-βR1)上调中的作用。方法:培养大鼠主动脉VSMC,以10-7mol/L AngⅡ刺激作为AngⅡ组,AngⅡ刺激前分别应用10-5mol/L氯沙坦(Losartan)... 详细信息

目的:探讨丝裂素活化蛋白激酶在血管紧张素Ⅱ(AngⅡ)诱导血管平滑肌细胞(VSMC)转化生长因子-β受体(TGF-βR1)上调中的作用。方法:培养大鼠主动脉VSMC,以10-7mol/L AngⅡ刺激作为AngⅡ组,AngⅡ刺激前分别应用10-5mol/L氯沙坦(Losartan)、PD98059预处理,以正常的VSMC为对照组,细胞免疫化学法测定培养12h时VSMC TGF-βR1的含量。结果:与对照组相比,AngⅡ刺激培养12h的VSMC TGF-βR1表达上调(P<0.01);AngⅡ受体AT1型拮抗剂Losartan使TGF-βR1表达显著降低(P<0.01),丝裂素活化蛋白激酶抑制剂PD98059能显著降低TGF-βR1表达(P<0.05)。结论:AngⅡ通过AT1上调TGF-βR1的表达,丝裂原活化蛋白激酶参与AngⅡ的胞内信号转导。

关键词：肌平滑血管/药物作用血管紧张素Ⅱ 转化生长因子-β/代谢

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Expression of phosphodiesterase 4D (PDE4D) is regulated by both the cyclic AMP-dependent protein kinase and mitogen-activated protein kinase signaling pathways -: A potential mechanism allowing for the coordinated regulation of PDE4D activity and expression in cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第34期275卷 26615-26624页

作者： Liu, HG Palmer, D Jimmo, SL Tilley, DG Dunkerley, HA Pang, SC Maurice, DH Queens Univ Dept Pathol Kingston ON K7L 3N6 Canada Queens Univ Dept Pharmacol & Toxicol Kingston ON K7L 3N6 Canada Queens Univ Dept Anat & Cell Biol Kingston ON K7L 3N6 Canada

Multiple families of cyclic nucleotide phosphodiesterases (PDE) have been described, and the regulated expression of these genes in cells is complex. Although cAMP is known to control the expression of certain PDE in cells, presumably reflecting a system of feedback on cAMP signaling, relatively little is known about the influence of non-cAMP signaling systems on PDE expression. In this study, we describe a novel mechanism by which activators of the protein kinase C (PKC)-Raf-MEK-ERK cascade regulate phosphodiesterase 4D (PDE4D) expression in vascular smooth muscle cells (VSMC) and assess the functional consequences of this effect. Whereas a prolonged elevation of cAMP in VSMC resulted in a protein kinase A (PHA)-dependent induction of expression of two PDE4D variants (PDE4D1 and PDE4D2), simultaneous activation of both the cAMP/-PKA and PRC-Raf-MER-ERK signaling cascades blunted this cAMP-mediated increase in PDE4D expression. By using biochemical, molecular biological, and pharmacological approaches, we demonstrate that this PDE4D-selective effect of activators of the PKC-Raf-MEK-ERK cascade was mediated through a mechanism involving altered PDE4D mRNA stability and markedly attenuated the cAMP-mediated desensitization that results from prolonged activation of the cAMP signaling system in cells. The data are presented in the context of activators of the PKC-Raf-MEK-ERK cascade having both short and long term effects on PDE4D activity and expression in cells that may influence cAMP signaling.

关键词： 8-溴环腺苷一磷酸/药理学血管紧张素Ⅱ/药理学细胞培养的环AMP/代谢环AMP依赖性蛋白激酶类/生理学放线菌酮/药理学更生霉素/药理学酶抑制剂/药理学福司柯林/药理学异喹啉类/药理学丝裂原激活蛋白激酶激酶类/代谢丝裂原激活蛋白激酶类/生理学肌平滑血管/药物作用肌平滑血管/酶学蛋白激酶C/代谢蛋白质合成抑制药/药理学原癌基因蛋白质c-raf/代谢 RNA 信使/代谢信号传导磺胺类十四酰佛波乙酯/药理学动物大鼠

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Effects of eicosapentaenoic acid and docosahexaenoic acid on plasma membrane fluidity of aortic endothelial cells

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LIPIDS 1999年第12期34卷 1297-1304页

作者： Hashimoto, M Hossain, MS Yamasaki, H Yazawa, K Masumura, S Shimane Med Univ Dept Physiol Izumo Shimane 6938501 Japan Sagami Chem Res Ctr Sagamihara Kanagawa 229 Japan

We investigated the relative effects of n-3 eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n-3) on the plasma membrane fluidity of endothelial cells (EC) cultured from the thoracic aorta by determining fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene (DPH) and its cationic derivative trimethylamino-DPH (TMA-DPH). Fluidity assessed by TMA-DPH demonstrated no significant differences in plasma membranes of vehicle (dimethyl sulfoxide;DMSO)-, EPA-, and DHA-treated EC. Plasma membrane fluidity assessed by DPH polarization, however, was significantly higher in the order of DHA > EPA > DMSO. Total cholesterol content decreased significantly by 28.4 and 15.9% in the plasma membranes of DHA- and EPA-treated cells, respectively. Total phospholipid content remained unaltered in the plasma membranes of the three groups of cells;however, the molar ratio of total cholesterol to phospholipid decreased significantly only in the membranes of DHA-treated EC. The unsaturation index in the plasma membranes of EPA- and DHA-treated cells increased by 35.7 and 64.3%, respectively, compared with that in the plasma membranes of control cells. The activities of catalase and glutathione peroxidase in the whole-cell homogenates, and levels of lipid peroxides in either the whole-cell homogenates or in plasma membrane fractions were not altered in EPA- or DHA-treated EC. These results indicate that the influence of DHA is greater than that of EPA in increasing plasma membrane fluidity of vascular EC. We speculate that the greater effect of DHA compared to EPA is due to its greater ability to decrease membrane cholesterol content or the cholesterol/phospholipid molar ratio, or both, and also to its greater ability in elevating the unsaturation index in the plasma membranes of EC.

关键词：主动脉/代谢过氧化氢酶/代谢细胞膜/药物作用细胞培养的胆固醇/代谢二苯己三烯/类似物和衍生物二十二碳六烯酸类/药理学二十碳五烯酸/药理学内皮血管/药物作用脂肪酸类/代谢荧光染料谷胱甘肽过氧化酶/代谢过氧化脂质类/代谢膜流动性/药物作用磷脂类/代谢大鼠 Wistar 动物女(雌)性大鼠

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Activation of mitogen-activated protein kinase pathways by cyclic GMP and cyclic GMP-dependent protein kinase in contractile vascular smooth muscle cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第48期274卷 34301-34309页

作者： Komalavilas, P Shah, PK Jo, HJ Lincoln, TM Univ Alabama Birmingham Div Mol & Cellular Pathol Dept Pathol Birmingham AL 35294 USA

Vascular smooth muscle cells (VSMC) exist in either a contractile or a synthetic phenotype in vitro and in vivo. The molecular mechanisms regulating phenotypic modulation are unknown. Previous studies have suggested that the serine/threonine protein kinase mediator of nitric oxide (NO) and cyclic GMP (cGMP) signaling, the cGMP-dependent protein kinase (PKG) promotes modulation to the contractile phenotype in cultured rat aortic smooth muscle cells (RASMC). Because of the potential importance of the mitogen-activated protein kinase (MAP kinase) pathways in VSMC proliferation and phenotypic modulation, the effects of PKG expression in PKG-deficient and PKG-expressing adult RASMC on MAP kinases were examined. In PKG-expressing adult RASMC, 8-para-chlorophenylthio-cGMP activated extracellular signal- regulated kinases (ERK1/2) and c-Jun N-terminal kinase (JNK). The major effect of PKG activation was increased activation by MAP kinase kinase (MEK). The cAMP analog, 8-Br-cAMP inhibited ERK1/2 activation in PKG-deficient and PKG-expressing RASMC but had no effect on JNK activity. The effects of PKG on ERK and JNK activity were additive with those of platelet-derived growth factor (PDGF), suggesting that PKG activates MEK through a pathway not used by PDGF. The stimulatory effects of cGMP on ERK and JNK activation mere also observed in low-passaged, contractile RASMC still expressing endogenous PKG, suggesting that the effects of PKG expression were not artifacts of cell transfections. These results suggest that in contractile adult RASMC, NO-cGMP signaling increases MAP kinase activity. Increased activation of these MAP kinase pathways may be one mechanism by which cGMP and PKG activation mediate c-fos induction and increased proliferation of contractile adult RASMC.

关键词： 8-溴环腺苷一磷酸/药理学生物碱类/药理学主动脉卡唑类细胞培养的环GMP/类似物和衍生物环GMP/药理学环GMP依赖性蛋白激酶类/拮抗剂和抑制剂环GMP依赖性蛋白激酶类/遗传学环GMP依赖性蛋白激酶类/代谢酶激活/药物作用酶抑制剂/药理学基因表达吲哚类/药理学 JNK丝裂原活化蛋白激酶类 MAP激酶激酶4 MAP激酶激酶激酶类/代谢丝裂原活化蛋白激酶1/代谢丝裂原活化蛋白激酶3 丝裂原激活蛋白激酶激酶类/代谢丝裂原激活蛋白激酶类/代谢肌收缩/药物作用肌收缩/生理学肌平滑血管/细胞学肌平滑血管/药物作用肌平滑血管/酶学血小板源性生长因子/药理学蛋白质丝氨酸苏氨酸激酶吡咯类/药理学大鼠 Sprague-Dawley 重组融合蛋白质类/药物作用重组融合蛋白质类/遗传学重组融合蛋白质类/代谢硫代核苷酸类/药理学时间因素转染肿瘤坏死因子α/药理学 p38丝裂原活化蛋白激酶类动物大鼠

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Bacterial lipopolysaccharide activates NF-κB through Toll-like receptor 4 (TLR-4) in cultured human dermal endothelial cells -: Differential expression of TLR-4 and TLR-2 in endothelial cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第15期275卷 11058-11063页

作者： Faure, E Equils, O Sieling, PA Thomas, L Zhang, FX Kirschning, CJ Polentarutti, N Muzio, M Arditi, M Cedars Sinai Med Ctr Steven Spielberg Pediat Res Ctr Ahmanson Dept Pediat Div Pediat Infect Dis Los Angeles CA 90048 USA Univ Calif Los Angeles Sch Med Los Angeles CA 90048 USA Univ Calif Los Angeles Sch Med Dept Med Div Dermatol Los Angeles CA 90095 USA Tech Univ Munich Inst Med Microbiol & Immunol D-81675 Munich Germany Mario Negri Inst Pharmacol Res Dept Immunol & Cell Biol I-20157 Milan Italy

A missense mutation in the cytoplasmic domain of the Toll-like receptor-4 (TLR-4) has been identified as the defect responsible for lipopolysaccharide (LPS) hyporesponsiveness in C3H/HeJ mice, TLR-4 and TLR-2 have recently been implicated in LPS signaling in studies where these receptors were overexpressed in LPS nonresponsive 293 human embryonic kidney cells. However, the signaling role of TLR-4 or TLR-2 in human cells with natural LPS response remains largely undefined. Here we show that human dermal microvessel endothelial cells (HMEC) and human umbilical vein endothelial cells express predominantly TLR-4 but very weak TLR-2 and respond vigorously to LPS but not to Mycobacterium tuberculosis 19-kDa lipoprotein, Transient transfection of non-signaling mutant forms of TLR-4 and anti-TLR-4 monoclonal antibody inhibited LPS-induced NF-KB activation in HMEC, while a monoclonal antibody against TLR-2 was ineffective. In contrast to LPS responsiveness, the ability of HMEC to respond to 19-kDa lipoprotein correlated with the expression of TLR-2. Transfection of TLR-2 into HMEC conferred responsiveness to 19-kDa lipoprotein, These data indicate that TLR-4 is the LPS signaling receptor in HMEC and that human endothelial cells (EC) express predominantly TLR-4 and weak TLR-2, which may explain why they do not respond to 19-kDa lipoprotein. The differential expression of TLRs on human EC may have important implications in the participation of vascular EC in innate immune defense mechanisms against various infectious pathogens, which may use different TLRs to signal.

关键词：细胞培养的果蝇蛋白质类内皮血管/药物作用内皮血管/代谢脂多糖类/药理学膜糖蛋白类/生理学小鼠近交BALBC 小鼠近交C3H NF-κB/代谢受体细胞表面/生理学皮肤/细胞学 Toll样受体2 Toll样受体4 Toll样受体动物人类小鼠

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Vascular endothelial growth factor (VEGF)-driven actin-based motility is mediated by VEGFR2 and requires concerted activation of stress-activated protein kinase 2 (SAPK2/p38) and geldanamycin-sensitive phosphorylation of focal adhesion kinase

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第14期275卷 10661-10672页

作者： Rousseau, S Houle, F Kotanides, H Witte, L Waltenberger, J Landry, J Huot, J Univ Laval Hotel Dieu Quebec Ctr Rech Cancerol Quebec City PQ G1R 2J6 Canada Univ Ulm Med Ctr Dept Internal Med 2 D-89081 Ulm Germany ImClone Syst Inc Dept Mol & Cell Biol New York NY 10014 USA

In endothelial cells, vascular endothelial growth factor (VEGF) induces an accumulation of stress fibers associated with new actin polymerization and rapid formation of focal adhesions at the ventral surface of the cells. This cytoskeletal reorganization results in an intense motogenic activity. Using porcine endothelial cells expressing one or the other type of the VEGF receptors, VEGFR1 or VEGFR2, or human umbilical vein endothelial cells pretreated with a VEGFR2 neutralizing antibody, we show that VEGFR2 is responsible for VEGF-induced activation of the stress-activated protein kinase-2/p38 (SAPK2/p38), phosphorylation of focal adhesion kinase (FAK), and enhanced migratory activity. Activation of SAPK2/p38 triggered actin polymerization whereas FAX, which was phosphorylated independently of SAPK2/p38, initiated assembly of focal adhesions. Both processes contributed to the formation of stress fibers. Geldanamycin, an inhibitor of HSP90 blocked tyrosine phosphorylation of FAK, assembly of focal adhesions, actin reorganization, and cell, migration, all of which were reversed by overexpressing HSP90. We conclude that VEGFR2 mediates the physiological effect of VEGF on cell migration and that two independent pathways downstream of VEGFR2 regulate actin-based motility. One pathway involves SAPK2/p38 and leads to enhanced actin polymerization activity. The other involves HSP90 as a permissive signal transduction factor implicated in FAK phosphorylation and assembly of focal adhesions.

关键词：肌动蛋白类/生理学抗体/药理学苯醌类钙-钙调素依赖性蛋白激酶类/代谢细胞黏附细胞运动/药物作用细胞运动/生理学细胞培养的细胞支架蛋白质类/生理学内皮生长因子/药理学内皮血管/细胞学内皮血管/药物作用内皮血管/生理学酶激活黏着斑激酶1 黏着斑蛋白酪氨酸激酶类 HSP90热休克蛋白质类/拮抗剂和抑制剂 HSP90热休克蛋白质类/遗传学 HSP90热休克蛋白质类/生理学内酰胺类大环淋巴因子/药理学丝裂原激活蛋白激酶类桩蛋白磷蛋白类/生理学磷酰化蛋白酪氨酸激酶类/拮抗剂和抑制剂蛋白酪氨酸激酶类/代谢原癌基因蛋白质类/生理学醌类/药理学受体蛋白质酪氨酸激酶类/免疫学受体蛋白质酪氨酸激酶类/生理学受体生长因子/免疫学受体生长因子/生理学受体血管内皮生长因子脐静脉血管内皮生长因子A 血管内皮生长因子受体1 血管内皮生长因子类纽蛋白/生理学 p38丝裂原活化蛋白激酶类人类

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A phosphatidylinositol 3-kinase/Akt pathway, activated by tumor necrosis factor or interleukin-1, inhibits apoptosis but does not activate NFκB in human endothelial cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第20期275卷 15458-15465页

作者： Madge, LA Pober, JS Yale Univ Sch Med Boyer Ctr Mol Med Interdepartmental Program Vasc Biol & Transplanta New Haven CT 06536 USA

Tumor necrosis factor (TNF) and interleukin-1 (IL-1) activate the transcription of both anti-apoptotic and pro-inflammatory gene products in human endothelial cells (EC) via NF kappa B. Here we report that both TNF and IL-1 activate the anti-apoptotic protein kinase Akt in growth factor and serum-deprived EC, assessed by Western blotting for phospho-Akt, Phosphorylation of Akt is blocked by LY294002 or wortmannin, inhibitors of phosphatidylinositol 3-kinase (PIS-kinase), Consistent with these biochemical observations, TNF and IL-1 reduce apoptosis caused by growth factor and serum deprivation, and this action is also blocked by LY294002. Although Akt has been reported to activate NF kappa B, LY294002 does not prevent TNF- or IL-1-induced degradation of I kappa B alpha, beta, or epsilon, transcription of NF kappa B-dependent E-selectin or ICAM-1 promoter-reporter genes, or surface expression of E-selectin or ICAM-1 in human EC, LY294002 potentiates the activation of mitogen-activated protein kinases and stress-activated protein kinases by TNF and IL-1, suggesting Akt inhibits these responses. We conclude that TNF and IL-1 activate a PI 3-kinase/Akt anti-apoptotic pathway and that the anti-apoptotic effects of Akt are independent of NF kappa B. Moreover, the PI 3-kinase/Akt pathway does not play a major role in the pro-inflammatory responses of EC to TNF or IL-1.

关键词：雄二烯类/药理学细胞凋亡/药物作用细胞凋亡/生理学细胞培养的色酮类/药理学培养基无血清内皮血管/细胞学内皮血管/药物作用内皮血管/生理学酶激活酶抑制剂/药理学白细胞介素1/药理学动力学吗啉类/药理学 NF-κB/代谢蛋白质丝氨酸苏氨酸激酶蛋白酪氨酸激酶类/代谢原癌基因蛋白质类/代谢原癌基因蛋白质c-akt 重组蛋白质类/药理学肿瘤坏死因子α/药理学脐静脉人类

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Regulation of prostaglandin H₂ synthase activity by nitrogen oxides

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BIOCHEMISTRY 1999年第38期38卷 12505-12513页

作者： Upmacis, RK Deeb, RS Hajjar, DP Cornell Univ Joan & Sanford I Weill Med Coll Dept Biochem New York NY 10021 USA Cornell Univ Joan & Sanford I Weill Med Coll Ctr Vasc Biol New York NY 10021 USA

Nitric oxide and its derivatives have been shown to both activate and inhibit prostaglandin H-2 synthase 1 (PGHS-1), We set out to determine the mechanisms by which different nitrogen oxide derivatives modulate PGHS-1 activity. To this end, we show that 3-morpholinosydnonimine hydrochloride (SIN-1), a compound capable of generating peroxynitrite, activates purified PGHS-1 and also stimulates PGE(2) production in arterial smooth muscle cells in the presence of exogenous arachidonic acid. The effect of SIN-1 in smooth muscle cells was abrogated by superoxide and peroxynitrite inhibitors, which supports the hypothesis that peroxynitrite is an activating species of PGHS-1. Indeed, authentic peroxynitrite also induced PGE(2) production in arachidonic acid-stimulated cells. In contrast, when cells were exposed to the nitric oxide-releasing compound 1-hydroxy-2-oxo-3-[(methylamino)propyl]-3-methyl-1-triazene (NOC-7), PGHS-1 enzyme activity was inhibited in the presence of exogenous arachidonic acid. Finally, in lipid-loaded smooth muscle cells, we demonstrate that SIN-1 stimulates arachidonic acid-induced PGE(2) production;albeit, the extent of activation is reduced compared to that under normal conditions. These results indicate that formation of peroxynitrite is a key intermediary step in PGHS-1 activation. However, other forms of NOx inhibit PGHS-1. These results may have implications in the regulation of vascular function and tone in normal and atherosclerotic arteries.

关键词：主动脉胸动脉硬化/酶学动脉硬化/代谢细胞培养的环氧化酶1 酶激活/药物作用酶抑制剂/代谢自由基清除剂/代谢肼类/代谢同工酶类/分离和提纯同工酶类/代谢膜蛋白质类吗多明/类似物和衍生物吗多明/拮抗剂和抑制剂吗多明/代谢肌平滑血管/药物作用肌平滑血管/酶学硝酸盐类/代谢一氧化氮/代谢一氧化氮供体/代谢氧化氮类/代谢青霉胺/类似物和衍生物青霉胺/代谢过氧化物/代谢前列腺素拮抗药/代谢前列腺素内过氧化物合酶类/分离和提纯前列腺素内过氧化物合酶类/代谢 S-亚硝基-N-乙酰基青霉胺绵羊超氧化物类/代谢动物男(雄)性大鼠

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