Abstract:Abstract. The aim of the present study was to explore the effects of continuous and intermittent exercise on the thoracic aortic vasoreactivity and free radical metabolism in rats fed with a high-fat diet (HD). Sprague-Dawley (SD) rats were randomly divided into four groups (n=8, each group): Conventional diet (CD), HD, HD with continuous exercise (HCE) and HD with intermittent exercise (HIE). HCE rats swam once/day for 90 min; HIE rats performed swimming exercises 3 times/day, 30 min each time with an interva… Show more
“…Under normal physiological conditions, JAK2 mediates the signal transduction of a variety of cytokines, including erythropoietin, thrombopoietin, granulocyte-macrophage colony stimulating factor and IL-3, thus regulating and promoting cell proliferation (40). The present study showed that naringin also inhibited JAK2 protein expression in AS rat.…”
Section: A B a Bsupporting
confidence: 50%
“…5). However, treatment with naringin (20,40 and 80 mg/kg) mitigated this increased expression of STAT3 protein in AS mouse (Fig. 5).…”
Section: Effect Of Naringin On Stat3 Protein Expression In As Mousementioning
Abstract. Naringin is an abundant flavanone in pomelo, grapefruit as well as lime and its variants, has been shown to exhibit certain antioxidative, anti-inflammatory, anti-cancer and hypoglycemic effects. The aim of the current study was to evaluate the protective effects of naringin against ankylosing spondylitis (AS) and to elucidate the potential underlying mechanism. Firstly, a mouse model of ankylosing spondylitis (AS) was established. Next, osteocalcin (OC), alkaline phosphatase (ALP) and triglyceride (TG) activity values, inflammatory factor and oxidative stress were evaluated in the AS mice. Then, the Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) protein expression levels in the AS mice were investigated using western blot analysis. The results showed that naringin increased OC, ALP and TG activity values in the AS mouse model. Furthermore, inflammatory factor and oxidative stress levels in the AS mice were restrained by treatment with naringin. Furthermore, JAK2 and STAT3 protein expression levels were reduced by treatment with naringin. In conclusion, the present results indicated that the protective effects of naringin against AS are exerted via the induction of ossification, suppression of inflammation and oxidative stress and the downregulation of JAK2/STAT3 in mice.
“…Under normal physiological conditions, JAK2 mediates the signal transduction of a variety of cytokines, including erythropoietin, thrombopoietin, granulocyte-macrophage colony stimulating factor and IL-3, thus regulating and promoting cell proliferation (40). The present study showed that naringin also inhibited JAK2 protein expression in AS rat.…”
Section: A B a Bsupporting
confidence: 50%
“…5). However, treatment with naringin (20,40 and 80 mg/kg) mitigated this increased expression of STAT3 protein in AS mouse (Fig. 5).…”
Section: Effect Of Naringin On Stat3 Protein Expression In As Mousementioning
Abstract. Naringin is an abundant flavanone in pomelo, grapefruit as well as lime and its variants, has been shown to exhibit certain antioxidative, anti-inflammatory, anti-cancer and hypoglycemic effects. The aim of the current study was to evaluate the protective effects of naringin against ankylosing spondylitis (AS) and to elucidate the potential underlying mechanism. Firstly, a mouse model of ankylosing spondylitis (AS) was established. Next, osteocalcin (OC), alkaline phosphatase (ALP) and triglyceride (TG) activity values, inflammatory factor and oxidative stress were evaluated in the AS mice. Then, the Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) protein expression levels in the AS mice were investigated using western blot analysis. The results showed that naringin increased OC, ALP and TG activity values in the AS mouse model. Furthermore, inflammatory factor and oxidative stress levels in the AS mice were restrained by treatment with naringin. Furthermore, JAK2 and STAT3 protein expression levels were reduced by treatment with naringin. In conclusion, the present results indicated that the protective effects of naringin against AS are exerted via the induction of ossification, suppression of inflammation and oxidative stress and the downregulation of JAK2/STAT3 in mice.
“…HF‐induced obese mice also exhibit enhanced agonist‐induced contraction in rat aorta (Liu et al . ), rat basilar artery (Lima et al . ) and mouse aorta (Mundy et al .…”
Metabolic syndrome is a critically important precursor to the onset of many diseases, such as cardiovascular disease, and cardiovascular disease is the leading cause of death worldwide. The primary risk factors of metabolic syndrome include hyperglycaemia, abdominal obesity, dyslipidaemia, and high blood pressure. It has been well documented that metabolic syndrome alters vascular endothelial and smooth muscle cell functions in the heart, brain, kidney and peripheral vessels. However, there is less information available regarding how metabolic syndrome can affect pulmonary vascular function and ultimately increase an individual's risk of developing various pulmonary vascular diseases, such as pulmonary hypertension. Here, we review in detail how metabolic syndrome affects pulmonary vascular function.
“…A disfunção vascular associada à obesidade tem sido amplamente discutida, sendo que o aumento na contração vascular pode ocorrer tanto pela ativação das vias de sinalização envolvidas na contração, quanto por prejuízos relacionados à ativação das vias de relaxamento. Indo ao encontro de trabalhos prévios (Naruse et al, 2006;Chinen et al, 2007;Liu et al, 2015), que mostram os prejuízos no sistema vascular causado pela obesidade, em nosso estudo observamos que a obesidade potencializa a contração vascular, e que tal resposta independe da presença do endotélio, indicando uma possível disfunção no MLV.…”
Section: Discussionunclassified
“…Para avaliação do perfil lipídico, foram determinados os níveis séricos de colesterol total, triglicerídeos e HDL (Lipoproteínas de alta densidade -High density lipoproteins), por métodos enzimáticos(Liu et al, 2015), em amostras de soros obtidas conforme descrito acima. A partir da concentração sérica de triglicerídeos, foram calculadas as concentrações de VLDL (Lipoproteínas de muito baixa densidade -Very low density lipoproteins), utilizando o seguinte cálculo: VLDL (mg/dL)= Triglicerídeos (mg/dL)/5.…”
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