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  • Ovid Technologies (Wolters Kluwer Health)  (36)
  • Li, Jian-Mei  (36)
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  • Ovid Technologies (Wolters Kluwer Health)  (36)
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  • 1
    Online Resource
    Online Resource
    Inhibitory Effects of AT 1 Receptor Blocker, Olmesartan, and Estrogen on Atherosclerosis Via Anti-Oxidative Stress
    Ovid Technologies (Wolters Kluwer Health) ; 2005
    In:  Hypertension Vol. 45, No. 4 ( 2005-04), p. 545-551
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 45, No. 4 ( 2005-04), p. 545-551
    Abstract: Abstracts— The present study explored the possibility that estrogen enhances the inhibitory effect of an angiotensin II type-1 (AT 1 ) receptor blocker (ARB), olmesartan, on atherosclerosis, focusing on oxidative stress using apolipoprotein E knockout mice (ApoEKO). After 6 weeks on a high-cholesterol diet, marked atherosclerotic lesion formation with an increase in oxidative stress, such as superoxide production, NAD(P)H oxidase activity and expression of p47 phox mRNA and rac-1 mRNA, were observed in the proximal aorta in both male and female ApoEKO mice, whereas these changes were less marked in female mice. Ovariectomy enhanced these parameters, the changes of which were reversed by 17β-estradiol (80 μg/kg per day) replacement. Treatment with olmesartan (3 mg/kg per day) significantly inhibited oxidative stress and atherosclerosis, whereas its inhibitory effects were more marked in female than in male or ovariectomized mice. Smaller doses of olmesartan (0.5 mg/kg per day) or 17β-estradiol (20 μg/kg per day) did not influence atherosclerosis and oxidative stress in ovariectomized mice, whereas co-administration of olmesartan and 17β-estradiol at these doses attenuated these parameters. An angiotensin-converting enzyme (ACE) inhibitor, temocapril, also inhibited atherosclerotic changes similarly to olmesartan. Moreover, angiotensin II–mediated activation of NAD(P)H oxidase in cultured vascular smooth muscle cells was attenuated by 17β-estradiol. These results indicate that estrogen and an ARB synergistically attenuate atherosclerosis at least partly via inhibition of oxidative stress.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.0000157409.88971.fc
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2005
    detail.hit.zdb_id: 2094210-2
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  • 2
    Online Resource
    Online Resource
    Angiotensin II Type-1 Receptor Blocker Valsartan Enhances Insulin Sensitivity in Skeletal Muscles of Diabetic Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Hypertension Vol. 43, No. 5 ( 2004-05), p. 1003-1010
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 43, No. 5 ( 2004-05), p. 1003-1010
    Abstract: Angiotensin II has been shown to contribute to the pathogenesis of insulin resistance; however, the mechanism is not well understood. The present study was undertaken to investigate the potential effect of an angiotensin II type-1 (AT 1 ) receptor blocker, valsartan, to improve insulin resistance and to explore the signaling basis of cross-talk of the AT 1 receptor- and insulin-mediated signaling in type 2 diabetic KK-Ay mice. Treatment of KK-Ay mice with valsartan at a dose of 1 mg/kg per day, which did not influence systolic blood pressure, significantly increased insulin-mediated 2-[ 3 H]deoxy- d -glucose (2-[ 3 H]DG) uptake into skeletal muscle and attenuated the increase in plasma glucose concentration after a glucose load and plasma concentrations of glucose and insulin. In contrast, insulin-mediated 2-[ 3 H]DG uptake into skeletal muscle was not influenced in AT 2 receptor null mice, and an AT 2 receptor blocker, PD123319, did not affect 2-[ 3 H]DG uptake and superoxide production in skeletal muscle of KK-Ay mice. Moreover, we observed that valsartan treatment exaggerated the insulin-induced phosphorylation of IRS-1, the association of IRS-1 with the p85 regulatory subunit of phosphoinositide 3 kinase (PI 3-K), PI 3-K activity, and translocation of GLUT4 to the plasma membrane. It also reduced tumor necrosis factor-α (TNF-α) expression and superoxide production in skeletal muscle of KK-Ay mice. Specific AT 1 receptor blockade increases insulin sensitivity and glucose uptake in skeletal muscle of KK-Ay mice via stimulating the insulin signaling cascade and consequent enhancement of GLUT4 translocation to the plasma membrane.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.0000125142.41703.64
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
    detail.hit.zdb_id: 2094210-2
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  • 3
    Online Resource
    Online Resource
    Effect of combination of calcium antagonist, azelnidipine, and AT1 receptor blocker, olmesartan, on atherosclerosis in apolipoprotein E-deficient mice
    Ovid Technologies (Wolters Kluwer Health) ; 2005
    In:  Journal of Hypertension Vol. 23, No. 7 ( 2005-07), p. 1383-1389
    Details
    In: Journal of Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 23, No. 7 ( 2005-07), p. 1383-1389
    Type of Medium: Online Resource
    ISSN: 0263-6352
    URL: Article
    DOI: 10.1097/01.hjh.0000173521.91104.5f
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2005
    detail.hit.zdb_id: 2017684-3
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  • 4
    Online Resource
    Online Resource
    Nifedipine inhibited angiotensin II-induced monocyte chemoattractant protein 1 expression: involvement of inhibitor of nuclear factor kappa B kinase and nuclear factor kappa B-inducing kinase
    Ovid Technologies (Wolters Kluwer Health) ; 2006
    In:  Journal of Hypertension Vol. 24, No. 1 ( 2006-01), p. 123-130
    Details
    In: Journal of Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 24, No. 1 ( 2006-01), p. 123-130
    Type of Medium: Online Resource
    ISSN: 0263-6352
    URL: Article
    DOI: 10.1097/01.hjh.0000198031.30095.d1
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2006
    detail.hit.zdb_id: 2017684-3
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  • 5
    Online Resource
    Online Resource
    Temporary Pretreatment With the Angiotensin II Type 1 Receptor Blocker, Valsartan, Prevents Ischemic Brain Damage Through an Increase in Capillary Density
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Stroke Vol. 39, No. 7 ( 2008-07), p. 2029-2036
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 39, No. 7 ( 2008-07), p. 2029-2036
    Abstract: Background and Purpose— We investigated the effect of temporary treatment with a nonhypotensive dose of valsartan on ischemic brain damage in C57BL/6 mice. Methods— We separated the mice into 3 groups of valsartan treatment before middle cerebral artery (MCA) occlusion: (1) for 4 weeks: Val (2W, 2W) ; (2) for 2 weeks followed by its cessation for 2 weeks: Val (2W, -) ; and (3) no treatment for 4 weeks: Val (-, -) . Results— Ischemic volume, DNA damage, superoxide production, and mRNA levels of monocyte chemoattractant protein-1 and tumor necrosis factor-α on the ipsilateral side after 24 hours of MCA occlusion were significantly reduced in both Val (2W, 2W) and Val (2W, -) mice compared with those in Val (-, -) mice, whereas these parameters were larger in Val (2W, -) mice than in Val (2W, 2W) mice. Moreover, mice in both the Val (2W, 2W) and Val (2W, -) groups exhibited an increase in cerebral blood flow in the peripheral territory of the MCA 1 hour after MCA occlusion, with increases in endothelial nitric oxide synthase activation and nitric oxide production. Before MCA occlusion, treatment with valsartan did not influence superoxide production or mRNA levels of monocyte chemoattractant protein-1 and tumor necrosis factor-α in the brain. However, the capillary density in the brain in both Val (2W, 2W) and Val (2W, -) mice was increased before MCA occlusion. Conclusions— Our results suggest that temporary valsartan treatment could protect against ischemic brain damage even after its cessation, at least in part due to an increase in capillary density.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.107.503458
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
    detail.hit.zdb_id: 1467823-8
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  • 6
    Online Resource
    Online Resource
    Deletion of Angiotensin II Type 2 Receptor Attenuates Protective Effects of Bone Marrow Stromal Cell Treatment on Ischemia–Reperfusion Brain Injury in Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Stroke Vol. 39, No. 9 ( 2008-09), p. 2554-2559
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 39, No. 9 ( 2008-09), p. 2554-2559
    Abstract: Background and Purpose— Protective effects of bone marrow stromal cells (MSCs) on ischemic brain damage have been highlighted. We examined the possibility that deletion of AT 2 receptor could attenuate the cerebroprotective effects of MSC using AT 2 receptor-deficient mice ( Agtr2 − ) and the effect of selective AT 1 receptor blocker. Methods— Wild-type mice ( Agtr2 + ) were subjected to 3 hours of focal brain ischemia followed by reperfusion (ischemia–reperfusion injury). Simultaneously, Agtr2 + -MSC, Agtr2 − -MSC, or saline was injected through the tail vein. Results— Survival rates at 6 days after ischemia–reperfusion injury were as follows: approximately 50% in saline-injected mice, 80% in Agtr2 + -MSC-injected mice, and 20% in Agtr2 − -MSC-injected mice. Neurological deficit after ischemia–reperfusion injury was improved in Agtr2 + -MSC-injected mice, but not in Agtr2 − -MSC-injected mice. After 48 hours of ischemia–reperfusion injury, brain infarct size was reduced in Agtr2 + -MSC-injected mice, but not in Agtr2 − -MSC-injected mice. Moreover, brain edema was significantly ameliorated in Agtr2 + -MSC-treated mice but not in Agtr2 − -MSC-treated mice. Furthermore, the increase in mRNA expression of tumor necrosis factor-α and monocyte chemoattractant protein-1 in the ischemic brain was less in Agtr2 + -MSC-treated mice in the ipsilateral site, but was similar in the contralateral hemisphere. Tumor necrosis factor-α level was increased in both the contralateral hemisphere and ipsilateral hemisphere of Agtr2 − -MSC-treated mice. In contrast, monocyte chemoattractant protein-1 levels tended to increase Agtr2 − -MSC-treated mice without a significant difference. Treatment of MSC with an AT 1 receptor blocker, valsartan, significantly improved survival rates in Agtr2 − -MSC-injected mice. Conclusions— These results suggest that AT 2 receptor signaling in MSC attenuated brain damage and neurological deficit (deleted).
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.107.513275
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
    detail.hit.zdb_id: 1467823-8
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  • 7
    Online Resource
    Online Resource
    Diabetes-Associated Cognitive Impairment Is Improved by a Calcium Channel Blocker, Nifedipine
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Hypertension Vol. 51, No. 2 ( 2008-02), p. 528-533
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 51, No. 2 ( 2008-02), p. 528-533
    Abstract: Nifedipine, a calcium channel blocker, has been reported to exert pleiotropic effects on atherosclerosis, mainly through its antioxidative properties. However, the effect of the calcium channel blocker on cognitive impairment associated with type 2 diabetes mellitus is not well known. Here, we examined the possibility that a calcium channel blocker could improve cognitive function in a type 2 diabetic mouse model, KK-A y . KK-A y mice subjected to 20 trials of a passive avoidance task every week from 7 weeks of age exhibited impairment of the increase in avoidance rate and, moreover, exaggeration of its age-dependent decline, especially after 12 weeks of age. Oral administration of nifedipine at a nonhypotensive dose (0.001% in laboratory chow) to KK-A y mice from 10 weeks of age improved cognitive function. Nifedipine treatment decreased serum insulin level to one fifth of that in KK-A y mice without nifedipine. Moreover, nifedipine treatment significantly reduced superoxide anion production in the brain. Furthermore, treatment with nifedipine markedly reduced the mRNA level of Id-1, inhibitor of neural differentiation, in the brain hippocampus. We also observed the increase in blood flow in the brain in KK-A y mice with nifedipine treatment compared with nontreated mice. Taken together, our findings suggest that nifedipine ameliorates impaired cognitive function in type 2 diabetic mice, at least because of attenuation of hyperinsulinemia and superoxide production in the brain and possible upregulation of the neural differentiation-controlling gene, Id-1.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.107.101634
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
    detail.hit.zdb_id: 2094210-2
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  • 8
    Online Resource
    Online Resource
    Aldosterone and Angiotensin II Synergistically Induce Mitogenic Response in Vascular Smooth Muscle Cells
    Ovid Technologies (Wolters Kluwer Health) ; 2005
    In:  Circulation Research Vol. 97, No. 5 ( 2005-09-02), p. 434-442
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 97, No. 5 ( 2005-09-02), p. 434-442
    Abstract: Interaction between aldosterone (Aldo) and angiotensin II (Ang II) in the cardiovascular system has been highlighted; however, its detailed signaling mechanism is poorly understood. Here, we examined the cross-talk of growth-promoting signaling between Aldo and Ang II in vascular smooth muscle cells (VSMC). Treatment with a lower dose of Aldo (10 −12 mol/L) and with a lower dose of Ang II (10 −10 mol/L) significantly enhanced DNA synthesis, whereas Aldo or Ang II alone at these doses did not affect VSMC proliferation. This effect of a combination of Aldo and Ang II was markedly inhibited by a selective AT 1 receptor blocker, olmesartan, a mineralocorticoid receptor antagonist, spironolactone, an MEK inhibitor, PD98059, or an EGF receptor tyrosine kinase inhibitor, AG1478. Treatment with Aldo together with Ang II, even at noneffective doses, respectively, synergistically increased extracellular signal-regulated kinase (ERK) activation, reaching 2 peaks at 10 to 15 minutes and 2 to 4 hours. The early ERK peak was effectively blocked by olmesartan or an EGF receptor kinase inhibitor, AG1478, but not by spironolactone, whereas the late ERK peak was completely inhibited by not only olmesartan, but also spironolactone. Combined treatment with Aldo and Ang II attenuated mitogen-activated protein kinase phosphatase-1 (MKP-1) expression and increased Ki-ras2A expression. The late ERK peak was not observed in VSMC treated with Ki-ras2A-siRNA. Interestingly, the decrease in MKP-1 expression and the increase in Ki-ras2A expression were restored by PD98059 or AG1478. These results suggest that Aldo exerts a synergistic mitogenic effect with Ang II and support the notion that blockade of both Aldo and Ang II could be more effective to prevent vascular remodeling.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.0000180753.63183.95
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2005
    detail.hit.zdb_id: 1467838-X
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  • 9
    Online Resource
    Online Resource
    Abstract 362: Knockout of NADPH Oxidase 2 Improves Global Metabolism and Endothelial Function in Aging Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 37, No. suppl_1 ( 2017-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 37, No. suppl_1 ( 2017-05)
    Abstract: Oxidative stress attributable to the activation of a Nox2-containing NADPH oxidase has been suggested to play a crucial role in the development of aging-associated vascular diseases. However, the mechanism of endothelial Nox2 activation in normal aging process remains unclear. In this study, we investigated the therapeutic potential of targeting Nox2 in improving global metabolism and endothelial function at old age by using age-matched wild-type and Nox2 knockout mice at 3-4 months (young); 11-12 months (middle aged) and 21-22 months (aging). Compared to young mice, middle-aged and ageing wild-type mice had significantly higher blood pressure, hyperglycaemia, hyperinsulinaemia. These were accompanied by oxidative stress in multiple organs including the lung, the liver, the heart and the vessels. The vessel motor function was examined in an organ bath using aortas isolated from these mice. Endothelium-dependent vessel relaxation to acetylcholine was significantly impaired in aortas of wild-type aging mice, and this was accompanied by increased expressions of Nox2 and markers of inflammation, activation of MAPK and Akt and decreased insulin receptor expression and function. However, these aging-associated disorders in aortas were significantly reduced by knocking out Nox2 in mice. In response to high glucose plus high insulin challenge, coronary microvascular endothelial cells isolated from wild-type mice displayed significantly increased Nox2 expression, oxidative stress and cell senescence, e.g. increased p53 expression and β-galactosidase activity. However, these responses were absent or significantly reduced in the endothelial cells isolated from Nox2 knockout mice. In conclusion, metabolic disorders in particular hyperglycaemia and insulin resistance play an important role in mediating Nox2 activation and oxidative stress in multiple organs in aging. Nox2 is involved in normal aging process-associated vascular inflammation and oxidative damage of endothelial dysfunction.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.37.suppl_1.362
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 1494427-3
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  • 10
    Online Resource
    Online Resource
    Fluvastatin Enhances the Inhibitory Effects of a Selective Angiotensin II Type 1 Receptor Blocker, Valsartan, on Vascular Neointimal Formation
    Ovid Technologies (Wolters Kluwer Health) ; 2003
    In:  Circulation Vol. 107, No. 1 ( 2003-01-07), p. 106-112
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 107, No. 1 ( 2003-01-07), p. 106-112
    Abstract: Background— The present studies were undertaken to investigate the potential effect of a hydroxymethylglutaryl coenzyme A reductase inhibitor (statin) to enhance the inhibitory effect of an angiotensin (Ang) II type 1 (AT 1 ) receptor blocker (ARB) on vascular neointimal formation and to explore the cellular mechanism of cross-talk of the AT 1 receptor and statin in vascular smooth muscle cells (VSMCs). Methods and Results— Neointimal formation and the proliferation of VSMCs induced by cuff placement around the femoral artery were significantly inhibited by treatment with an ARB, valsartan, at a dose of 0.1 mg · kg −1 · d −1 and with fluvastatin at a dose of 1 mg · kg −1 · d −1 , which did not influence mean arterial blood pressure or plasma cholesterol level, whereas valsartan or fluvastatin alone at these doses did not affect neointimal formation or the proliferation of VSMCs. Pretreatment with fluvastatin (≈5 μmol/L) for 24 hours significantly inhibited Ang II (1 μmol/L)–mediated DNA synthesis and c-fos promoter activity in cultured VSMCs. Moreover, pretreatment of VSMCs with fluvastatin significantly inhibited Ang II–mediated extracellular signal-regulated kinase (ERK) activation and tyrosine- and serine-phosphorylation of signal transducer and activator of transcription (STAT)1 and STAT3. AT 1 receptor–mediated recruitment of Rac-1 to Janus kinase (Jak) family/STATs was also inhibited by fluvastatin. Consistent with these in vitro results, phosphorylation of ERK, STAT1, and STAT3 was attenuated by the coadministration of valsartan and fluvastatin even at low doses in vivo. Conclusion— These results suggest that the cholesterol-independent inhibition of AT 1 receptor–mediated VSMC proliferation by statins may contribute to the beneficial effects of statins combined with an ARB on vascular diseases.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.0000043244.13596.20
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2003
    detail.hit.zdb_id: 1466401-X
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