The effects of rosiglitazone on aortic atherosclerosis of cholesterol-fed rabbits

Song, Zhao; Zhang, Chunfang; Yang, Lin; Yang, Pengliang; Yu, Qi; Chu, Yangyang; Yang, Penghui; Fan, Jianglin; Liu, Enqi

doi:10.1016/j.thromres.2008.04.011

Cited by 20 publications

(18 citation statements)

References 34 publications

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“…This may be explained by low levels of systemic oxidative stress in WKY. Our results in SHR are in line with previous studies demonstrating actions of TZDs to oppose oxidative stress in the vasculature of animal models with atherosclerosis or other cardiovascular diseases (46,51,76).…”

Section: Rosiglitazone Therapy Reduces Oxidative Stress In Vasculatursupporting

confidence: 93%

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Treatment of spontaneously hypertensive rats with rosiglitazone ameliorates cardiovascular pathophysiology via antioxidant mechanisms in the vasculature

Potenza¹,

Gagliardi²,

Benedictis³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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Oxidative stress contributes to cardiovascular complications of diabetes, in part, by reducing the bioavailability of nitric oxide (NO). We investigated the mechanisms whereby the insulin sensitizer rosiglitazone may ameliorate oxidative stress in the vasculature of spontaneously hypertensive rats (SHR). Nine-week-old SHR were treated by gavage for 7 wk with rosiglitazone (5 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ) or vehicle control. Treatment of SHR with rosiglitazone lowered systolic blood pressure, reduced fasting plasma insulin and asymmetrical dimethylarginine, and increased insulin sensitivity (when compared with vehicle treatment). In vessel homogenates and serum from rosiglitazone-treated SHR, SOD activity was enhanced, while 8-iso-PGF2␣ (lipid peroxidation product) was reduced (when compared with samples from vehicle-treated SHR). Moreover, expression of p22phox (catalytic subunit of NADPH oxidase) as well as nitrotyrosine and superoxide content were all reduced in the aortas of rosiglitazone-treated SHR. In mesenteric vascular beds (MVB) isolated ex vivo from rosiglitazone-treated SHR, NO-dependent vasodilator actions of insulin were improved when compared with MVB from vehicle-treated SHR. Acute pretreatment of MVB from vehicle-treated SHR with apocynin (NADPH oxidase inhibitor) enhanced vasodilator actions of insulin (results comparable to those in MVB from rosiglitazone-treated SHR). In Langendorff heart preparations from rosiglitazone-treated SHR, ischemia/reperfusion injury caused infarcts 40% smaller than in hearts from vehicle-treated SHR. Acute pretreatment of hearts from vehicletreated SHR with apocynin produced similar results. Finally, rosiglitazone treatment of endothelial cells in primary culture reduced superoxide induced by insulin-resistant conditions. We conclude that rosiglitazone therapy in SHR increases SOD activity and decreases p22phox expression in the vasculature to reduce oxidant stress leading to an improved cardiovascular phenotype. oxidative stress RECIPROCAL RELATIONSHIPS between endothelial dysfunction and insulin resistance help explain the clustering of cardiovascular diseases including hypertension, coronary heart disease, and atherosclerosis with diabetes, obesity, and other insulin-resistant conditions (34,50). Endothelial dysfunction, characterized by reduced bioavailability of nitric oxide (NO), contributes to cardiovascular complications of diabetes (59). NO bioavailability is reduced when NO reacts with superoxide anion (O 2 Ϫ

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Section: Rosiglitazone Therapy Reduces Oxidative Stress In Vasculatursupporting

confidence: 93%

“…In addition, TZDs have anti-inflammatory actions in macrophages and vascular endothelium that may oppose atherosclerosis (35,48,76). This is reflected in the ability of TZD treatment to reduce serum C-reactive protein (63) and carotid intima-media thickness (45).…”

mentioning

confidence: 99%

Treatment of spontaneously hypertensive rats with rosiglitazone ameliorates cardiovascular pathophysiology via antioxidant mechanisms in the vasculature

Potenza¹,

Gagliardi²,

Benedictis³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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“…17 ). However, a study on cholesterol-fed rabbits revealed that rosiglitazone significantly reduced aortic atherosclerosis without modifying the plasma levels of glucose, insulin or lipid profile 18 . It is believed that PPARs are involved during the angiogenesis process 7 .…”

Section: Discussionmentioning

confidence: 99%

Rosiglitazone enhances neovascularization in diabetic rat ischemic hindlimb model

Khazaei¹,

Salehi²

2012

BIOMED PAP

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Background. There is increasing evidence that peroxisome proliferator-activated receptors (PPARs) may be involved in the regulation of angiogenesis. In this study, we examined whether rosiglitazone, a PPARγ agonist, can restore angiogenesis in a rat hindlimb ischemia model of diabetes. Methods. Male wistar rats were divided into four groups (n=6 each): control, diabetic and control and diabetic rats who received rosiglitazone (8 mg/kg/day). Diabetes was induced by streptozotocin (55 mg/kg; ip). After 21 days, serum concentrations of nitric oxide (NO), vascular endothelial growth factor (VEGF) and soluble VEGF receptor-2 (VEGFR-2) were measured and neovascularization in ischemic legs was evaluated by immunohistochemistry. Results. Capillary density and capillary/fiber ratio in hindlimb ischemia of diabetic animals were significantly lower than the control group (P<0.05). Rosiglitazone significantly restored neovascularization in diabetic animals (P<0.05). Conclusions. rosiglitazone enhances neovascularization in diabetic ischemic skeletal muscle and could be considered for treatment of peripheral artery disease in diabetic subjects.

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“…Population studies consistently demonstrate a curvilinear relationship between systemic levels of either total cholesterol or LDL-C and cardiovascular risk [12]. Animal studies that involve dietary cholesterol feeding or impairment of LDL metabolism typically cause formation of atherosclerotic lesions within the artery wall [15,16]. This is further supported by pathologic observations that following entry into the vessel wall, LDL is rapidly oxidized, rendering it an avid target for uptake by macrophages to become foam cells [17].…”

Section: Ldl-c and Cardiovascular Diseasementioning

confidence: 96%

Statin Effects on Both Low-Density Lipoproteins and High-Density Lipoproteins: Is There a Dual Benefit?

Uno

Nicholls

2010

Curr Atheroscler Rep

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Considerable evidence has demonstrated that use of statins has a beneficial impact on both progression of atherosclerosis and cardiovascular events. Accordingly, statins have been increasingly used in preventive strategies to reduce cardiovascular risk. More recent reports have demonstrated an incremental benefit with use of higher doses of statins and when used early in the setting of acute ischemic syndromes. Although lowering levels of low-density lipoprotein cholesterol is likely to underscore the majority of the clinical benefit, emerging evidence suggests that additional properties may also be important. In particular, a number of reports have demonstrated that modest elevations in levels of high-density lipoprotein cholesterol are likely to contribute to the benefit of statins. As a result, a favorable influence on the ratio of atherogenic and protective lipid species is likely to have the most profound impact on cardiovascular risk in statin-treated individuals.

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The effects of rosiglitazone on aortic atherosclerosis of cholesterol-fed rabbits

Cited by 20 publications

References 34 publications

Treatment of spontaneously hypertensive rats with rosiglitazone ameliorates cardiovascular pathophysiology via antioxidant mechanisms in the vasculature

Treatment of spontaneously hypertensive rats with rosiglitazone ameliorates cardiovascular pathophysiology via antioxidant mechanisms in the vasculature

Rosiglitazone enhances neovascularization in diabetic rat ischemic hindlimb model

Statin Effects on Both Low-Density Lipoproteins and High-Density Lipoproteins: Is There a Dual Benefit?

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