The Experts below are selected from a list of 279 Experts worldwide ranked by ideXlab platform
Dror Harats - One of the best experts on this subject based on the ideXlab platform.
-
cellular and humoral immune responses to heat shock protein 65 are both involved in promoting Fatty Streak formation in ldl receptor deficient mice
Journal of the American College of Cardiology, 2001Co-Authors: Jacob George, Arnon Afek, Boris Gilburd, Yehuda Shoenfeld, Dror HaratsAbstract:OBJECTIVES This study was designed to determine the role of cellular and humoral immune responses to heat shock protein 65 (HSP65) in murine atherosclerosis. BACKGROUND Inflammatory processes appear to influence the progression of atherosclerosis. Immunization with HSP65 was previously shown to induce arteriosclerosis in rabbits and to enhance Fatty-Streak formation in mice. However, it has not been demonstrated directly whether HSP65-reactive antibodies and lymphocytes are separately capable of influencing lesion formation. METHODS Low density lipoprotein-receptor deficient (LDL-RD) mice were immunized with HSP65 or control bovine serum albumin (BSA). Lymph-node cells, splenocytes and immunoglobulin G (IgG) were obtained from the immunized mice and transferred separately to six groups of syngenic LDL-RD mice. RESULTS Adoptive transfer of HSP65-reactive lymph node cells increased Fatty-Streak formation in comparison with mice treated with BSA-primed cells. Similarly, transfer of splenocytes reactive with HSP65 led to enhanced Fatty-Streak generation compared with mice injected with BSA-sensitized splenocytes. Repeated intraperitoneal administration of IgG from serum of HSP65-immunized mice (every 10 days) enhanced Fatty-Streak formation in mice in comparison with their anti-BSA-IgG injected littermates. CONCLUSIONS Antibodies and lymphocytes reactive to HSP65 promote Fatty-Streak formation in mice, providing direct evidence for the proatherogenic properties of cellular and humoral immunity to HSP65.
-
interleukin il 4 deficiency does not influence Fatty Streak formation in c57bl 6 mice
Atherosclerosis, 2000Co-Authors: Jacob George, Aviv Shaish, Mary Mulkins, Sharon Casey, Randall C Schatzman, Elliott Sigal, Dror HaratsAbstract:Abundant data is present to implicate oxidatively modified low-density lipoprotein (oxLDL) in enhanced atherogenesis. Among the factors involved in LDL oxidation, an important role has been attributed to human 15-lipoxygenase (LO) and its murine analog 12-LO. The expression of these peroxidizing enzymes is under the control of cytokines, the principal of which is IL-4. In the present study we tested the hypothesis that knocking out the IL-4 gene from C57BL/6 mice would result in suppression of Fatty Streaks. For this purpose, we have fed 45 female IL-4 transgenic knockout (IL-4T KO) and 45 wild-type (WT) mice an atherogenic diet for 15 weeks. Consecutive determinations of the lipid profile from both study groups were performed at monthly intervals, and Fatty Streak formation was assessed at the aortic sinus level, upon sacrifice. The two study groups did not differ significantly with respect to the lipid profile or the uptake and degradation of iodinated oxLDL by their peritoneal macrophages. We found that the endogenous deficiency of IL-4 did not confer protection from early atherosclerosis in the IL-4T KO as compared to their WT littermates (determined at the aortic sinus). Immunohistochemical studies, Western blots and 12/15-LO activity assays revealed the presence and activity of 12/15-LO in macrophages of WT mice as well as in IL-4T KO mice. Both did not differ significantly between the study groups. The data from this study imply that deficiency in IL-4 does not affect early atherosclerosis in C57BL/6 mice fed a high-cholesterol diet.
-
Interleukin (IL)-4 deficiency does not influence Fatty Streak formation in C57BL/6 mice
Atherosclerosis, 2000Co-Authors: Jacob George, Aviv Shaish, Mary Mulkins, Sharon Casey, Randall C Schatzman, Elliott Sigal, Dror HaratsAbstract:Abundant data is present to implicate oxidatively modified low-density lipoprotein (oxLDL) in enhanced atherogenesis. Among the factors involved in LDL oxidation, an important role has been attributed to human 15-lipoxygenase (LO) and its murine analog 12-LO. The expression of these peroxidizing enzymes is under the control of cytokines, the principal of which is IL-4. In the present study we tested the hypothesis that knocking out the IL-4 gene from C57BL/6 mice would result in suppression of Fatty Streaks. For this purpose, we have fed 45 female IL-4 transgenic knockout (IL-4T KO) and 45 wild-type (WT) mice an atherogenic diet for 15 weeks. Consecutive determinations of the lipid profile from both study groups were performed at monthly intervals, and Fatty Streak formation was assessed at the aortic sinus level, upon sacrifice. The two study groups did not differ significantly with respect to the lipid profile or the uptake and degradation of iodinated oxLDL by their peritoneal macrophages. We found that the endogenous deficiency of IL-4 did not confer protection from early atherosclerosis in the IL-4T KO as compared to their WT littermates (determined at the aortic sinus). Immunohistochemical studies, Western blots and 12/15-LO activity assays revealed the presence and activity of 12/15-LO in macrophages of WT mice as well as in IL-4T KO mice. Both did not differ significantly between the study groups. The data from this study imply that deficiency in IL-4 does not affect early atherosclerosis in C57BL/6 mice fed a high-cholesterol diet.
-
enhanced Fatty Streak formation in c57bl 6j mice by immunization with heat shock protein 65
Arteriosclerosis Thrombosis and Vascular Biology, 1999Co-Authors: Jacob George, Arnon Afek, Boris Gilburd, Yehuda Shoenfeld, Pnina Keren, Aviv Shaish, Juri Kopolovic, Georg Wick, Dror HaratsAbstract:Abstract—Recent data suggest that the immune system is involved in atherogenesis. Thus, interest has been raised as to the possible antigens that could serve as the initiators of the immune reaction. In the current work, we studied the effects of immunization with recombinant heat shock protein-65 (HSP-65) and HSP-65–rich Mycobacterium tuberculosis (MT) on early atherogenesis in C57BL/6J mice fed either a normal chow diet or a high-cholesterol diet (HCD). A rapid, cellular immune response to HSP-65 was evident in mice immunized with HSP-65 or with MT but not in the animals immunized with phosphate-buffered saline (PBS) alone. Early atherosclerosis was significantly enhanced in HCD-fed mice immunized with HSP-65 (n=10; mean aortic lesion size, 45 417±9258 μm2) or MT (n=15; 66 350±6850 μm2) compared with PBS-injected (n=10; 10 028±3599 μm2) or nonimmunized (n=10; 9500±2120 μm2) mice. No Fatty Streak lesions were observed in mice fed a chow diet regardless of the immunization protocol applied. Immunohistoche...
F Bayard - One of the best experts on this subject based on the ideXlab platform.
-
transforming growth factor activity is a key determinant for the effect of estradiol on Fatty Streak deposit in hypercholesterolemic mice
Arteriosclerosis Thrombosis and Vascular Biology, 2007Co-Authors: Pierre Gourdy, F Bayard, Alexia Schambourg, Cedric Filipe, Victorine Douinechinard, Barbara Garmysusini, Bertrand Calippe, Francois Terce, Jeanfrancois ArnalAbstract:OBJECTIVE: Whereas estradiol prevents Fatty Streak deposit in immunocompetent apoE-/- or LDLr-/- mice, it is totally ineffective in immunodeficient mice, underlining the key role of immunoinflammation in this effect. In the present work, the role of several major pro- and antiinflammatory cytokines involved in the atheromatous process was evaluated in the effect of estradiol on Fatty Streak constitution. METHODS AND RESULTS: The preventive effect of estradiol was fully maintained in LDLr-/- mice grafted with bone marrow from either IFN-gamma or interleukin (IL)-12-deficient mice, showing that this beneficial effect was not mediated through a specific decrease in the production of these 2 proinflammatory cytokines. Furthermore, IL-10-/- apoE-/- mice remained protected by estradiol, excluding a significant contribution of this antiinflammatory cytokine. In contrast, the protective effect of estradiol was (1) associated with enhanced aortic expression of TGF-beta1 in apoE-/- mice during early steps of atherogenesis; (2) abolished and even reversed in apoE-/- mice administered with a neutralizing anti-TGF-beta antibody; (3) abolished in LDLr-/- mice grafted with bone marrow from Smad3-deficient mice. CONCLUSIONS: The status of the TGF-beta pathway crucially determines the antiatherogenic effect of estradiol in hypercholesterolemic mice, whereas neither IFN-gamma, IL-12, nor IL-10 are specifically involved in this protection.
-
involvement of interleukin 6 in atherosclerosis but not in the prevention of Fatty Streak formation by 17β estradiol in apolipoprotein e deficient mice
Atherosclerosis, 2001Co-Authors: R Elhage, J F Arnal, Simone Clamens, S Besnard, Ziad Mallat, Alain Tedgui, Arlette Maret, F BayardAbstract:Abstract Interleukin-6 (IL-6) gene expressed in bone marrow-derived stromal cells and osteoblasts contributes to the state of mineralization and its control by estradiol may be involved in the development of post-menopausal osteoporosis. Since IL-6 is also expressed in the different cell populations of the arterial wall, the purpose of this study was to gain more insight into its involvement in the atherosclerotic process and the atheroprotective effect of estradiol by studying double deficient mice at the apolipoprotein E and IL-6 loci (IL-6 −/− /E −/− ). At 1 year of age, IL-6 −/− /E −/− mice showed similar hypercholesterolemia to IL-6 +/+ /E −/− mice but presented significantly larger and more calcified lesions. In younger mice (sixteen weeks of age), no significant difference in Fatty Streaks could be detected in IL-6 +/+ /E −/− , IL-6 +/− /E −/− and IL-6 −/− /E −/− mice on a normal chow diet. Estrogen supplementation at this age induced a decrease of Fatty Streak formation in all three genotypes. The combined data indicate that IL-6 expression is involved at the fibrous plaque stage of the atherosclerotic process but does not constitute a direct target for estradiol to prevent Fatty Streak formation.
-
omapatrilat a dual angiotensin converting enzyme and neutral endopeptidase inhibitor prevents Fatty Streak deposit in apolipoprotein e deficient mice
Atherosclerosis, 2001Co-Authors: J F Arnal, C Castano, E Maupas, A Mugniot, Benoit Darblade, Pierre Gourdy, Jeanbaptiste Michel, F BayardAbstract:Abstract Angiotensin-converting enzyme (ACE) is mainly responsible for converting angiotensin I (AI) to angiotensin II (AII), and ACE inhibitors prevent atherosclerosis in animal models. Neutral endopeptidase 24.11 (NEP) degrades substance P, kinins and atrial natriuretic peptide (ANP), and aortic wall NEP activity was found to be increased in atherosclerosis. In the present study, we have evaluated the effect of candoxatril, a NEP inhibitor, and of omapatrilat, a dual ACE and NEP inhibitor, on the development of Fatty Streak in apolipoprotein E (apoE)-deficient mice. Groups of ten male apoE-deficient mice were given either placebo, candoxatril 50 mg/kg per day, or omapatrilat 10, or 100 mg/kg per day for 4 months. None of the treatments influenced body weight, serum total or HDL-cholesterol. Compared with the placebo, candoxatril did not protect the mice from Fatty Streak deposit. In contrast, omapatrilat dose dependently inhibited the constitution of Fatty Streak in apoE-deficient mice. The precise advantages of the dual ACE and NEP inhibition versus the inhibition of only ACE should now be considered in the prevention of atherosclerosis as well as in the occurrence of its complications.
-
differential effects of interleukin 1 receptor antagonist and tumor necrosis factor binding protein on Fatty Streak formation in apolipoprotein e deficient mice
Circulation, 1998Co-Authors: R Elhage, Jeanfrancois Arnal, Arlette Maret, Marietherese Pieraggi, J C Thiers, F BayardAbstract:Background—The cytokines interleukin 1 (IL-1) and tumor necrosis factor (TNF) are secreted by the different cell populations of the vascular wall and have been suggested to promote atherosclerosis. Methods and Results—Their respective roles in Fatty-Streak formation in apolipoprotein E–deficient mice were investigated by use of IL-1 receptor antagonist and TNF binding protein. Estradiol-17β was used as a positive control. Blocking TNF seemed to be active in female animals but not in males. IL-1 receptor antagonist was as effective as or more effective than estradiol in both sexes. Conclusions—IL-1 plays a crucial role in the initial step of the atherosclerotic process in this animal model, and blocking the activity of this cytokine should be considered as a therapeutic possibility.
-
prevention of Fatty Streak formation of 17β estradiol is not mediated by the production of nitric oxide in apolipoprotein e deficient mice
Circulation, 1997Co-Authors: R Elhage, F Bayard, V Richard, P Holvoet, N Duverger, Catherine Fievet, Jeanfrancois ArnalAbstract:Background Estrogens have atheroprotective properties, the mechanisms of which remain obscure. Estrogens have recently been reported to increase endothelial NO synthase expression in castrated animals and to prevent the degradation of NO by decreasing superoxide anion production in cultured endothelial cells. In both cases, increased NO bioavailability would promote vasodilation, inhibit proliferation of the adjacent vascular smooth muscle, reduce platelet aggregation, and inhibit monocyte adhesion to the endothelium and the inflammatory reaction induced by cytokines, all key contributors in the development of atherosclerosis. Methods and Results In the present work, the respective roles of 17β-estradiol and NO in the development of the atherosclerotic process were investigated in castrated apolipoprotein E–deficient (apo E KO) mice, which spontaneously develop Fatty Streak lesions within 3 months. N ω -Nitro-l-arginine methyl ester (L-NAME), an NO synthase inhibitor, 50 mg · kg −1 · d −1 , increased arterial blood pressure and decreased cerebellum cGMP content, demonstrating the blockade of NO production, but did not influence the atherogenic process in castrated apo E KO mice. Conclusions 17β-Estradiol decreased the size of the aortic lesions approximately threefold, and the magnitude of this vasculoprotective effect was not altered by L-NAME. Moreover, L-NAME increased circulating malonyldialdehyde (MDA)-modified LDL, which was not altered by 17β-estradiol, leading to a complete dissociation between circulating MDA-modified LDL and parietal lesions.
Jacob George - One of the best experts on this subject based on the ideXlab platform.
-
cellular and humoral immune responses to heat shock protein 65 are both involved in promoting Fatty Streak formation in ldl receptor deficient mice
Journal of the American College of Cardiology, 2001Co-Authors: Jacob George, Arnon Afek, Boris Gilburd, Yehuda Shoenfeld, Dror HaratsAbstract:OBJECTIVES This study was designed to determine the role of cellular and humoral immune responses to heat shock protein 65 (HSP65) in murine atherosclerosis. BACKGROUND Inflammatory processes appear to influence the progression of atherosclerosis. Immunization with HSP65 was previously shown to induce arteriosclerosis in rabbits and to enhance Fatty-Streak formation in mice. However, it has not been demonstrated directly whether HSP65-reactive antibodies and lymphocytes are separately capable of influencing lesion formation. METHODS Low density lipoprotein-receptor deficient (LDL-RD) mice were immunized with HSP65 or control bovine serum albumin (BSA). Lymph-node cells, splenocytes and immunoglobulin G (IgG) were obtained from the immunized mice and transferred separately to six groups of syngenic LDL-RD mice. RESULTS Adoptive transfer of HSP65-reactive lymph node cells increased Fatty-Streak formation in comparison with mice treated with BSA-primed cells. Similarly, transfer of splenocytes reactive with HSP65 led to enhanced Fatty-Streak generation compared with mice injected with BSA-sensitized splenocytes. Repeated intraperitoneal administration of IgG from serum of HSP65-immunized mice (every 10 days) enhanced Fatty-Streak formation in mice in comparison with their anti-BSA-IgG injected littermates. CONCLUSIONS Antibodies and lymphocytes reactive to HSP65 promote Fatty-Streak formation in mice, providing direct evidence for the proatherogenic properties of cellular and humoral immunity to HSP65.
-
interleukin il 4 deficiency does not influence Fatty Streak formation in c57bl 6 mice
Atherosclerosis, 2000Co-Authors: Jacob George, Aviv Shaish, Mary Mulkins, Sharon Casey, Randall C Schatzman, Elliott Sigal, Dror HaratsAbstract:Abundant data is present to implicate oxidatively modified low-density lipoprotein (oxLDL) in enhanced atherogenesis. Among the factors involved in LDL oxidation, an important role has been attributed to human 15-lipoxygenase (LO) and its murine analog 12-LO. The expression of these peroxidizing enzymes is under the control of cytokines, the principal of which is IL-4. In the present study we tested the hypothesis that knocking out the IL-4 gene from C57BL/6 mice would result in suppression of Fatty Streaks. For this purpose, we have fed 45 female IL-4 transgenic knockout (IL-4T KO) and 45 wild-type (WT) mice an atherogenic diet for 15 weeks. Consecutive determinations of the lipid profile from both study groups were performed at monthly intervals, and Fatty Streak formation was assessed at the aortic sinus level, upon sacrifice. The two study groups did not differ significantly with respect to the lipid profile or the uptake and degradation of iodinated oxLDL by their peritoneal macrophages. We found that the endogenous deficiency of IL-4 did not confer protection from early atherosclerosis in the IL-4T KO as compared to their WT littermates (determined at the aortic sinus). Immunohistochemical studies, Western blots and 12/15-LO activity assays revealed the presence and activity of 12/15-LO in macrophages of WT mice as well as in IL-4T KO mice. Both did not differ significantly between the study groups. The data from this study imply that deficiency in IL-4 does not affect early atherosclerosis in C57BL/6 mice fed a high-cholesterol diet.
-
Interleukin (IL)-4 deficiency does not influence Fatty Streak formation in C57BL/6 mice
Atherosclerosis, 2000Co-Authors: Jacob George, Aviv Shaish, Mary Mulkins, Sharon Casey, Randall C Schatzman, Elliott Sigal, Dror HaratsAbstract:Abundant data is present to implicate oxidatively modified low-density lipoprotein (oxLDL) in enhanced atherogenesis. Among the factors involved in LDL oxidation, an important role has been attributed to human 15-lipoxygenase (LO) and its murine analog 12-LO. The expression of these peroxidizing enzymes is under the control of cytokines, the principal of which is IL-4. In the present study we tested the hypothesis that knocking out the IL-4 gene from C57BL/6 mice would result in suppression of Fatty Streaks. For this purpose, we have fed 45 female IL-4 transgenic knockout (IL-4T KO) and 45 wild-type (WT) mice an atherogenic diet for 15 weeks. Consecutive determinations of the lipid profile from both study groups were performed at monthly intervals, and Fatty Streak formation was assessed at the aortic sinus level, upon sacrifice. The two study groups did not differ significantly with respect to the lipid profile or the uptake and degradation of iodinated oxLDL by their peritoneal macrophages. We found that the endogenous deficiency of IL-4 did not confer protection from early atherosclerosis in the IL-4T KO as compared to their WT littermates (determined at the aortic sinus). Immunohistochemical studies, Western blots and 12/15-LO activity assays revealed the presence and activity of 12/15-LO in macrophages of WT mice as well as in IL-4T KO mice. Both did not differ significantly between the study groups. The data from this study imply that deficiency in IL-4 does not affect early atherosclerosis in C57BL/6 mice fed a high-cholesterol diet.
-
enhanced Fatty Streak formation in c57bl 6j mice by immunization with heat shock protein 65
Arteriosclerosis Thrombosis and Vascular Biology, 1999Co-Authors: Jacob George, Arnon Afek, Boris Gilburd, Yehuda Shoenfeld, Pnina Keren, Aviv Shaish, Juri Kopolovic, Georg Wick, Dror HaratsAbstract:Abstract—Recent data suggest that the immune system is involved in atherogenesis. Thus, interest has been raised as to the possible antigens that could serve as the initiators of the immune reaction. In the current work, we studied the effects of immunization with recombinant heat shock protein-65 (HSP-65) and HSP-65–rich Mycobacterium tuberculosis (MT) on early atherogenesis in C57BL/6J mice fed either a normal chow diet or a high-cholesterol diet (HCD). A rapid, cellular immune response to HSP-65 was evident in mice immunized with HSP-65 or with MT but not in the animals immunized with phosphate-buffered saline (PBS) alone. Early atherosclerosis was significantly enhanced in HCD-fed mice immunized with HSP-65 (n=10; mean aortic lesion size, 45 417±9258 μm2) or MT (n=15; 66 350±6850 μm2) compared with PBS-injected (n=10; 10 028±3599 μm2) or nonimmunized (n=10; 9500±2120 μm2) mice. No Fatty Streak lesions were observed in mice fed a chow diet regardless of the immunization protocol applied. Immunohistoche...
Russell Ross - One of the best experts on this subject based on the ideXlab platform.
-
atherogenesis during low level hypercholesterolemia in the nonhuman primate i Fatty Streak formation
Arteriosclerosis Thrombosis and Vascular Biology, 1990Co-Authors: J Masuda, Russell RossAbstract:Although a large body of data is available concerning atherogenesis in animals maintained at high levels of hypercholesterolemia, little data are available for animals maintained at lower levels of hypercholesterolemia for longer periods of time, closer to those observed in humans. The chronologic sequence of cellular events and interactions that occur during the formation of the lesions of atherosclerosis was investigated during relatively low level hypercholesterolemia (200 to 400 mg/dl) in a series of nonhuman primates (Macaca nemestrina). The arterial tree of each animal was examined by light microscopy and scanning and transmission electron microscopy. Immunohistochemical staining with monoclonal antibodies specific for smooth muscle cells, monocyte-macrophages, and T-lymphocytes was performed to analyze the cellular composition of the lesions. After 6 months of low level hypercholesterolemia, the surface of the aorta contained large numbers of adherent leukocytes, many of which were in the process of entering the artery. This resulted in irregularly shaped nodular elevations, or Fatty Streaks, preferentially located at branch sites and bifurcations. The Fatty Streaks consisted of intimal accumulations of numerous lipid-laden macrophages together with relatively small numbers of T-lymphocytes. With lesion progression, the thickness of the Fatty Streaks increased, and their surfaces became irregular and frequently showed disruptions of covering endothelial cells resulting in exposure of subendothelial macrophages. Platelet microthrombi were observed over some of the exposed macrophages at some branches or bifurcations in every animal studied. These observations made during the early phases of atherosclerosis lesion formation are virtually identical to those described in our previous reports in high level hypercholesterolemic nonhuman primates (600 to 1000 mg/dl) with the exception that the changes occurred more slowly in the lower levels of hypercholesterolemia.
-
atherogenesis during low level hypercholesterolemia in the nonhuman primate ii Fatty Streak conversion to fibrous plaque
Arteriosclerosis Thrombosis and Vascular Biology, 1990Co-Authors: J Masuda, Russell RossAbstract:This study focuses on the formation of lesions of atherosclerosis in the aortas and iliac arteries of nonhuman primates (Macaca nemestrina) maintained on a low level hypercholesterolemic diet (plasma cholesterol 200 to 400 mg/dl) for 2, 3, or 3.5 years. Advanced lesions, or fibrous plaques, were found in all of the animals. The extent and severity of the lesions were closely related to the level and duration of hypercholesterolemia. The presence of monocyte-macrophages, T-lymphocytes, and smooth muscle cells, and the interactions of those cells that precede fibrous plaque formation in these long-term, relatively low level hypercholesterolemic monkeys were similar to those observed in previously published studies of high level hypercholesterolemia in nonhuman primates, with one principal difference: the fibrous plaques in the longer-term, low level hypercholesterolemic animals contained increased amounts of fibrous connective tissue, more smooth muscle cells, and fewer macrophages. As in the studies with high levels of hypercholesterolemia, fibrous plaques were more frequently observed in the abdominal aorta and iliac arteries than in the thoracic aorta and aortic arch. Fibrous plaques were preferentially located at the branches and bifurcations of the arteries. These anatomic sites were consistent with those that contained Fatty Streaks and fibroFatty lesions in the animals fed the diet for shorter periods of time. These data are compatible with the proposal that many of the Fatty Streaks are converted to fibroFatty lesions, some of which ultimately become converted to fibrous plaques.
Cesar L Ramireztortosa - One of the best experts on this subject based on the ideXlab platform.
-
curcuma longa extract supplementation reduces oxidative stress and attenuates aortic Fatty Streak development in rabbits
Clínica e Investigación en Arteriosclerosis, 2003Co-Authors: Jose L Quiles, Cesar L Ramireztortosa, Concepcion M Aguilera, Maurizio Battino, Maria D Mesa, M C Ramireztortosa, M AlegretAbstract:Objetivo En este estudio se evalua el efecto de un extracto de Curcuma longa sobre el desarrollo de aterosclerosis experimental (estrias grasas) en conejos, y su interaccion con otros antioxidantes plasmaticos. Metodos y resultados Dos grupos de conejos macho New Zealand White, un grupo control y un grupo que recibio extracto de curcuma (CU), fueron alimentados con dieta aterogenica. El grupo CU fue tratado adicionalmente con un extracto hidroalcoholico de curcuma por via oral. Seis animales de cada grupo se sacrificaron a los 10, 20 y 30 dias. En comparacion con el grupo CU, el grupo control presento concentraciones plasmaticas de peroxidos lipidicos significativamente superiores en todos los tiempos ensayados (10, 20 y 30 dias) y valores de d-tocoferol y coenzima Q significativamente menores a los 20 y 30 dias. El analisis histologico de las estrias grasas revelo que la lesion en la aorta toracica abdominal fue significativamente menor en el grupo CU que en el grupo control a los 30 dias. Conclusiones Los suplementos de Curcuma longa reducen el estres oxidativo y atenuan el desarrollo de estrias grasas en conejos alimentados con una dieta rica en colesterol.
-
curcuma longa extract supplementation reduces oxidative stress and attenuates aortic Fatty Streak development in rabbits
Arteriosclerosis Thrombosis and Vascular Biology, 2002Co-Authors: Jose L Quiles, Dolores M Mesa, Cesar L Ramireztortosa, Concepcion M Aguilera, Maurizio BattinoAbstract:Objective— This study evaluates the effect of a Curcuma longa extract on the development of experimental atherosclerosis (Fatty Streak) in rabbits and its interaction with other plasmatic antioxidants. Methods and Results— Two experimental groups of male New Zealand White rabbits, a control group and a curcuma-extract (CU) group, were fed an atherogenic diet. Additionally, the CU group received an oral curcuma hydroalcoholic extract. Six animals from each experimental group were killed after 10, 20, and 30 days. Compared with the CU group, the control group showed significantly higher plasma lipid peroxide at all experimental times (10, 20, and 30 days) and significantly lower α-tocopherol and coenzyme Q levels at 20 and 30 days. Histological results for the Fatty Streak lesions revealed damage in the thoracic and abdominal aorta that was significantly lower in the CU group than in the control group at 30 days. Conclusions— Supplementation with Curcuma longa reduces oxidative stress and attenuates the dev...
