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Medicinas Complementárias
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1.
Sci Rep ; 11(1): 22469, 2021 11 17.
Artículo en Inglés | MEDLINE | ID: mdl-34789834

RESUMEN

Atherosclerosis is a chronic inflammatory disease that may lead to the development of serious cardiovascular diseases. Aged garlic extract (AGE) has been reported to ameliorate atherosclerosis, although its mode of action remains unclear. We found that AGE increased the mRNA or protein levels of arginase1 (Arg1), interleukin-10 (IL-10), CD206 and hypoxia-inducible factor 2α (HIF2α) and decreased that of CD68, HIF1α and inducible nitric oxide synthase in the aorta and spleen of apolipoprotein E knockout mice. We also found that S-1-propenylcysteine (S1PC), a characteristic sulfur compound in AGE, increased the level of IL-10-induced Arg1 mRNA and the extent of M2c-like macrophage polarization in vitro. In addition, S1PC increased the population of M2c-like macrophages, resulting in suppressed the population of M1-like macrophages and decreased lipopolysaccharide-induced production of pro-inflammatory cytokines. These effects were accompanied by prolonged phosphorylation of the IL-10 receptor α (IL-10Rα) and signal transducer and activator of transcription 3 (STAT3) that inhibited the interaction between IL-10Rα and Src homology-2-containing inositol 5'-phosphatase 1 (SHIP1). In addition, administration of S1PC elevated the M2c/M1 macrophage ratio in senescence-accelerated mice. These findings suggest that S1PC may help improve atherosclerosis due to its anti-inflammatory effect to promote IL-10-induced M2c macrophage polarization.


Asunto(s)
Polaridad Celular/efectos de los fármacos , Cisteína/análogos & derivados , Ajo/química , Interleucina-10/farmacología , Macrófagos/metabolismo , Extractos Vegetales/administración & dosificación , Receptores de Interleucina-10/metabolismo , Factor de Transcripción STAT3/metabolismo , Transducción de Señal/efectos de los fármacos , Animales , Aterosclerosis/prevención & control , Células Cultivadas , Cisteína/administración & dosificación , Modelos Animales de Enfermedad , Activación de Macrófagos/efectos de los fármacos , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados para ApoE , Fosforilación/efectos de los fármacos , Fitoterapia/métodos , Placa Aterosclerótica/prevención & control , Proteínas Recombinantes/farmacología , Resultado del Tratamiento
2.
Mol Nutr Food Res ; 61(10)2017 10.
Artículo en Inglés | MEDLINE | ID: mdl-28726277

RESUMEN

SCOPE: Chronic inflammation plays a major role in the formation and progression of atherosclerotic plaques. To clarify the mode of action of aged garlic extract (AGE) to retard atherosclerosis, we investigated whether AGE suppresses the inflammation in apolipoprotein E-knockout (ApoE-KO) mice. METHODS AND RESULTS: ApoE-KO mice were fed standard diet with or without 3% AGE for 12 wk. AGE feeding inhibited the progression of atherosclerotic lesion by 27% and reduced the level of C-reactive protein (CRP) and thromboxane B2 (TXB2 ), a marker of platelet activation, in serum by 39 and 33%, respectively, compared to ApoE-KO mice without AGE treatment. AGE treatment also decreased the level of tumor necrosis factor alpha (TNF-α), a major stimulus inducing CRP production, in the liver by 35%. AGE decreased the level of interleukin-1 receptor-associated kinase 4 (IRAK4) by 60% and almost doubled the level of phospho-AMP-activated protein kinase (p-AMPK) in the liver. CONCLUSION: The anti-atherosclerotic effect of AGE involves the suppression of inflammation by reducing the serum level of CRP and TXB2 , and the protein level of TNF-α and IRAK4, and increasing AMPK activity in liver.


Asunto(s)
Ajo/química , Inflamación/tratamiento farmacológico , Extractos Vegetales/farmacología , Proteínas Quinasas Activadas por AMP/sangre , Animales , Aterosclerosis/prevención & control , Biomarcadores/sangre , Proteína C-Reactiva/metabolismo , Dieta , Progresión de la Enfermedad , Inflamación/sangre , Quinasas Asociadas a Receptores de Interleucina-1/sangre , Hígado/efectos de los fármacos , Hígado/metabolismo , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados para ApoE , Extractos Vegetales/sangre , Tromboxano B2/sangre , Factor de Necrosis Tumoral alfa/sangre
3.
Molecules ; 22(4)2017 Mar 31.
Artículo en Inglés | MEDLINE | ID: mdl-28362335

RESUMEN

S-1-Propenyl-l-cysteine (S1PC) is a stereoisomer of S-1-Propenyl-l-cysteine (SAC), an important sulfur-containing amino acid that plays a role for the beneficial pharmacological effects of aged garlic extract (AGE). The existence of S1PC in garlic preparations has been known since the 1960's. However, there was no report regarding the biological and/or pharmacological activity of S1PC until 2016. Recently, we performed a series of studies to examine the chemical, biological, pharmacological and pharmacokinetic properties of S1PC, and obtained some interesting results. S1PC existed only in trace amounts in raw garlic, but its concentration increased almost up to the level similar of SAC through aging process of AGE. S1PC showed immunomodulatory effects in vitro and in vivo, and reduced blood pressure in a hypertensive animal model. A pharmacokinetic study revealed that S1PC was readily absorbed after oral administration in rats and dogs with bioavailability of 88-100%. Additionally, S1PC had little inhibitory influence on human cytochrome P450 activities, even at a concentration of 1 mM. Based on these findings, S1PC was suggested to be another important, pharmacologically active and safe component of AGE similar to SAC. In this review, we highlight some results from recent studies on S1PC and discuss the potential medicinal value of S1PC.


Asunto(s)
Cisteína/química , Cisteína/farmacología , Ajo/química , Extractos Vegetales/química , Extractos Vegetales/farmacología , Vías Biosintéticas , Cisteína/análogos & derivados , Cisteína/síntesis química , Cisteína/farmacocinética , Extractos Vegetales/farmacocinética , Azufre/química , Factores de Tiempo
4.
Mol Nutr Food Res ; 61(5)2017 05.
Artículo en Inglés | MEDLINE | ID: mdl-28074608

RESUMEN

SCOPE: In this study, we investigated the effect of aged garlic extract (AGE) on the high level of blood glucose in Tsumura Suzuki Obese-Diabetes (TSOD) mice. METHODS AND RESULTS: TSOD mice were fed standard diet with or without 2% AGE for 19 weeks. AGE treatment lowered the blood glucose level and significantly reduced the plasma level of glycated albumin in TSOD mice as compared with those without AGE treatment. In addition, AGE treatment increased the level of phosphorylated AMP-activated protein kinase (AMPK) in the adipose tissue, liver and muscle that played an important role in the maintenance of insulin sensitivity. Moreover, AGE treatment also suppressed the mRNA expression of fatty acid synthase, a known factor regulated by AMPK, and monocyte chemoattractant protein 1, one of the representative inflammatory chemokines, in the adipose tissue but not in the liver. CONCLUSION: AGE treatment suppresses the increase of plasma glycated albumin level in TSOD mice and this effect is accompanied by the activation of AMPK in adipose tissue, and suggests that AGE may play a potential role in the prevention and treatment of type 2 diabetes.


Asunto(s)
Proteínas Quinasas Activadas por AMP/metabolismo , Tejido Adiposo/efectos de los fármacos , Ajo/química , Extractos Vegetales/farmacología , Albúmina Sérica/metabolismo , Proteínas Quinasas Activadas por AMP/genética , Tejido Adiposo/metabolismo , Animales , Glucemia/metabolismo , Quimiocina CCL2/genética , Quimiocina CCL2/metabolismo , Diabetes Mellitus Tipo 2/tratamiento farmacológico , Dieta , Ácido Graso Sintasas/genética , Ácido Graso Sintasas/metabolismo , Manipulación de Alimentos , Productos Finales de Glicación Avanzada , Resistencia a la Insulina , Hígado/efectos de los fármacos , Hígado/metabolismo , Masculino , Ratones , Ratones Obesos , Músculo Esquelético/efectos de los fármacos , Músculo Esquelético/metabolismo , ARN Mensajero/genética , ARN Mensajero/metabolismo , Albúmina Sérica Glicada
5.
J Nutr ; 146(2): 460S-463S, 2016 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-26764329

RESUMEN

BACKGROUND: Aged garlic extract (AGE) has been shown to retard the progression of coronary calcification in patients with coronary artery disease. OBJECTIVE: To clarify the mechanism of AGE's action to retard atherosclerosis, we investigated whether AGE suppresses the formation and progression of atherosclerosis in Apolipoprotein E (Apoe)-knockout (ApoE-KO) mice. METHODS: Male C57BL/6J mice (control mice, 5 wk old) were fed a standard diet, whereas male ApoE-KO mice (5 wk old) were fed a standard diet with or without 3% AGE for 12 or 24 wk. After the treatment, blood samples, aortas, and spleens were collected from all mice. Concentrations of total cholesterol (TC), HDL cholesterol, and triglycerides (TGs) in serum were measured. The area of atherosclerotic lesion in the aorta was examined by Oil Red O staining. The relative abundances of monocytes plus macrophages (CD11b(+) cells) and interferon-γ-producing CD4(+) T cells in spleen were assessed by flow cytometric analysis. RESULTS: The atherosclerotic lesion areas in the aortas of ApoE-KO mice were 87 and 114 times as great (P < 0.01) as those in control mice at 12 and 24 wk, respectively. AGE feeding significantly inhibited the progression of atherosclerotic lesion area in ApoE-KO mice by 22% (P < 0.05) at 12 wk. In addition, serum concentrations of TC and TGs in ApoE-KO mice were significantly higher than those in control mice at 12 and 24 wk. Treatment with AGE significantly suppressed the increases in serum concentrations of TC and TGs in ApoE-KO mice by 21% (P < 0.05) and 19% (P < 0.05) at 24 wk, respectively, and reduced the relative abundance of CD11b(+) cells in ApoE-KO mice by 24% (P < 0.05) at 12 wk. CONCLUSION: These data suggest that the antiatherosclerotic activity of AGE is at least partly due to the suppression of inflammation and lipid deposition in the vessels during the early stage of atherosclerotic development in ApoE-KO mice.


Asunto(s)
Aterosclerosis/prevención & control , Colesterol/sangre , Ajo , Inflamación/prevención & control , Fitoterapia , Extractos Vegetales/uso terapéutico , Triglicéridos/sangre , Animales , Aorta/patología , Apolipoproteínas E/sangre , Aterosclerosis/sangre , Aterosclerosis/etiología , Aterosclerosis/patología , Antígenos CD11/metabolismo , Progresión de la Enfermedad , Inflamación/sangre , Inflamación/inmunología , Mediadores de Inflamación/sangre , Interferón gamma/metabolismo , Macrófagos/metabolismo , Masculino , Ratones Endogámicos C57BL , Ratones Noqueados , Extractos Vegetales/farmacología , Placa Aterosclerótica/sangre , Placa Aterosclerótica/etiología , Placa Aterosclerótica/prevención & control , Bazo/efectos de los fármacos , Linfocitos T/metabolismo
6.
J Virol ; 76(6): 3015-22, 2002 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-11861867

RESUMEN

An oligonucleotide with a dimeric hairpin guanosine quadruplex (basket type structure) (dG3T4G3-s), containing phosphorothioate groups, was able to inhibit human immunodeficiency virus type 1 (HIV-1)-induced syncytium formation and virus production (as measured by p24 core antigen expression) in peripheral blood mononuclear cells. This oligonucleotide lacks primary sequence homology with the complementary (antisense) sequences to the HIV-1 genome. Furthermore, this oligonucleotide may have increased nuclease resistance. The activity of this oligonucleotide was increased when the phosphodiester backbone was replaced with a phosphorothioate backbone. In vivo results showed that dG3T4G3-s was capable of blocking the interaction between gp120 and CD4. We also found that dG3T4G3-s specifically inhibits the entry of T-cell line-tropic HIV-1 into cells. This compound is a viable candidate for evaluation as a therapeutic agent against HIV-1 in humans.


Asunto(s)
VIH-1/efectos de los fármacos , Leucocitos Mononucleares/virología , Oligonucleótidos/química , Oligonucleótidos/farmacología , Células Gigantes/efectos de los fármacos , Guanosina/química , Proteína p24 del Núcleo del VIH/efectos de los fármacos , Infecciones por VIH/virología , VIH-1/fisiología , Humanos , Fosfatos/química , Timidina/química
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