Suppressive effects of cacao liquor polyphenols (CLP) on LDL oxidation and the development of atherosclerosis in Kurosawa and Kusanagi-hypercholesterolemic rabbits

Kurosawa, Tohru; Itoh, Fumi; Nozaki, Aiko; Nakano, Yoshihisa; Katsuda, Shin Ichiro; Osakabe, Naomi; Tsubone, Hirokazu; Kondo, Kazuo; Itakura, Hiroshige

doi:10.1016/j.atherosclerosis.2004.12.003

Cited by 74 publications

(50 citation statements)

References 41 publications

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“…ONOO Ϫ contributes to atherogenesis by promoting lipid peroxidation. 31 In contrast to hypercholesterolemic WT mice, JNK2 Ϫ/Ϫ mice were protected against lipid peroxidation, as determined by TBARS in aortic lysates.…”

Section: Discussionmentioning

confidence: 96%

c-Jun N-Terminal Kinase 2 Deficiency Protects Against Hypercholesterolemia-Induced Endothelial Dysfunction and Oxidative Stress

et al. 2008

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Background-Hypercholesterolemia-induced endothelial dysfunction due to excessive production of reactive oxygen species is a major trigger of atherogenesis. The c-Jun-N-terminal kinases (JNKs) are activated by oxidative stress and play a key role in atherogenesis and inflammation. We investigated whether JNK2 deletion protects from hypercholesterolemia-induced endothelial dysfunction and oxidative stress. Methods and Results-Male JNK2 knockout (JNK2 Ϫ/Ϫ ) and wild-type (WT) mice (8 weeks old) were fed either a high-cholesterol diet (HCD; 1.25% total cholesterol) or a normal diet for 14 weeks. Aortic lysates of WT mice fed a HCD showed an increase in JNK phosphorylation compared with WT mice fed a normal diet (PϽ0.05). Endothelium-dependent relaxations to acetylcholine were impaired in WT HCD mice (PϽ0.05 versus WT normal diet). In contrast, JNK2 Ϫ/Ϫ HCD mice did not exhibit endothelial dysfunction (96Ϯ5% maximal relaxation in response to acetylcholine; PϽ0.05 versus WT HCD). Endothelium-independent relaxations were identical in all groups. A hypercholesterolemia-induced decrease in nitric oxide (NO) release of endothelial cells was found in WT but not in JNK2 Ϫ/Ϫ mice. In parallel, endothelial NO synthase expression was upregulated only in JNK2 Ϫ/Ϫ HCD animals, whereas the expression of antioxidant defense systems such as extracellular superoxide dismutase and manganese superoxide dismutase was decreased in WT but not in JNK2 Ϫ/Ϫ HCD mice. In contrast to JNK2 Ϫ/Ϫ mice, WT HCD displayed an increase in O 2 Ϫ and ONOO Ϫ concentrations as well as nitrotyrosine staining and peroxidation. Conclusions-JNK2 plays a critical role as a mediator of hypercholesterolemia-induced endothelial dysfunction and oxidative stress. Thus, JNK2 may provide a novel target for prevention of vascular disease and atherosclerosis.

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Section: Discussionmentioning

confidence: 96%

c-Jun N-Terminal Kinase 2 Deficiency Protects Against Hypercholesterolemia-Induced Endothelial Dysfunction and Oxidative Stress

et al. 2008

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“…Although nitrotyrosine immunoreactivity was detected in both endothelial and smooth muscle cells of diabetic animals, aortas from diabetic WT mice exhibited markedly enhanced immunostaining compared with p66 ShcϪ/Ϫ mice. Because by promoting lipid peroxidation ONOO Ϫ contributes to atherogenesis (25), we also measured TBARS in aortic tissue as a marker of in vivo lipid peroxidation (26). p66…”

Section: Discussionmentioning

confidence: 99%

Genetic deletion of p66 ^Shc adaptor protein prevents hyperglycemia-induced endothelial dysfunction and oxidative stress

Camici

Schiavoni

Francia

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

230

166

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Increased production of reactive oxygen species (ROS) and loss of endothelial NO bioavailability are key features of vascular disease in diabetes mellitus. The p66 Shc adaptor protein controls cellular responses to oxidative stress. Mice lacking p66 Shc (p66 Shc؊/؊ ) have increased resistance to ROS and prolonged life span. The present work was designed to investigate hyperglycemia-associated changes in endothelial function in a model of insulin-dependent diabetes mellitus p66 Shc؊/؊ mouse. p66 Shc؊/؊ and wild-type (WT) mice were injected with citrate buffer (control) or made diabetic by an i.p. injection of 200 mg of streptozotocin per kg of body weight. Streptozotocin-treated p66 Shc؊/؊ and WT mice showed a similar increase in blood glucose. However, significant differences arose with respect to endothelial dysfunction and oxidative stress. WT diabetic mice displayed marked impairment of endotheliumdependent relaxations, increased peroxynitrite (ONOO ؊ ) generation, nitrotyrosine expression, and lipid peroxidation as measured in the aortic tissue. In contrast, p66 Shc؊/؊ diabetic mice did not develop these high-glucose-mediated abnormalities. Furthermore, protein expression of the antioxidant enzyme heme oxygenase 1 and endothelial NO synthase were up-regulated in p66 Shc؊/؊ but not in WT mice. We report that p66 Shc؊/؊ mice are resistant to hyperglycemia-induced, ROS-dependent endothelial dysfunction. These data suggest that p66 Shc adaptor protein is part of a signal transduction pathway relevant to hyperglycemia vascular damage and, hence, may represent a novel therapeutic target against diabetic vascular complications.

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“…In this experiment, 0.47% cholesterol load to the animals could generate hypercholesterolemia. Studies in both animals and humans have demonstrated that prolonged high cholesterol concentration in the circulating blood positively correlates with developing atherosclerosis (Pratico, 2001;Kurosawa et al, 2005). These changes are associated with the phenomenon that excessive load of cholesterol to the liver, above the acceptable level of its normal physiological limit, causes the liver to be unable in metabolizing the lipids, thus resulting in high cholesterol return in the circulating blood (Kushi et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Chemical composition and effect of an essential oil of Salix aegyptiaca L., Salicaceae, (musk willow) in hypercholesterolemic rabbit model

Karimi¹,

Hayatgheybi²,

Shamspur³

et al. 2011

Rev. bras. farmacogn.

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Abstract:The essential oils (EO) of Salix aegyptiaca L., Salicaceae (SA), leaves were extracted using the hydrodistillation method and their chemical composition was further determined by GC-MS. 1,4-Dimethoxybenzene was the main isolated compound. Other major isolated constitutes were phenylethyl alcohol, carvone, citronellol, methyleugenol, eugenol, n-tetradecane and 4´-methoxyacetophenone. Twenty rabbits were equally divided into four groups: Normal control (NC) which fed a standard diet and three cholesterol-fed groups: HC, HC+1.0% SA and HC+3.0% SA groups which received 0.0, 1.0 and 3.0% EO, respectively for four weeks. The serum lipid and lipoprotein profiles and atherogenic index (AI) were measured weekly. The high cholesterol diet significantly raised the TC, LDL-C, VLDL-C, HDL-C, TG and AI level compared with NC group. HC+1.0% SA and HC+3.0% SA groups showed similar results compared with HC group. It can be concluded that the EO of SA leaves could not prevent dyslipidemia that occurred in rabbits following inclusion of cholesterol in diet in both dose-and time-dependent manners.

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Suppressive effects of cacao liquor polyphenols (CLP) on LDL oxidation and the development of atherosclerosis in Kurosawa and Kusanagi-hypercholesterolemic rabbits

Cited by 74 publications

References 41 publications

c-Jun N-Terminal Kinase 2 Deficiency Protects Against Hypercholesterolemia-Induced Endothelial Dysfunction and Oxidative Stress

c-Jun N-Terminal Kinase 2 Deficiency Protects Against Hypercholesterolemia-Induced Endothelial Dysfunction and Oxidative Stress

Genetic deletion of p66 ^Shc adaptor protein prevents hyperglycemia-induced endothelial dysfunction and oxidative stress

Chemical composition and effect of an essential oil of Salix aegyptiaca L., Salicaceae, (musk willow) in hypercholesterolemic rabbit model

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Suppressive effects of cacao liquor polyphenols (CLP) on LDL oxidation and the development of atherosclerosis in Kurosawa and Kusanagi-hypercholesterolemic rabbits

Cited by 74 publications

References 41 publications

c-Jun N-Terminal Kinase 2 Deficiency Protects Against Hypercholesterolemia-Induced Endothelial Dysfunction and Oxidative Stress

c-Jun N-Terminal Kinase 2 Deficiency Protects Against Hypercholesterolemia-Induced Endothelial Dysfunction and Oxidative Stress

Genetic deletion of p66 Shc adaptor protein prevents hyperglycemia-induced endothelial dysfunction and oxidative stress

Chemical composition and effect of an essential oil of Salix aegyptiaca L., Salicaceae, (musk willow) in hypercholesterolemic rabbit model

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Genetic deletion of p66 ^Shc adaptor protein prevents hyperglycemia-induced endothelial dysfunction and oxidative stress