Real-time monitoring of nitric oxide and blood flow during ischemia-reperfusion in the rat testis

Kono, Tomoharu; Saito, Motoaki; Kinoshita, Yukako; Satoh, Itaru; Shinbori, Chiko; Satoh, Keisuke

doi:10.1007/s11010-005-9105-3

Cited by 33 publications

(32 citation statements)

References 13 publications

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“…Total NO and superoxide anion production measurement. After the organ bath study, total NO production (nitrite and nitrate) by aortic rings was determined using a modified Griess reaction method, as described previously (11,13). Briefly, after ACh (10 Ϫ5 M) was added, 100 l of K-H solution were taken from the organ bath and mixed with an equal volume of modified Griess reagent (1% sulfanilamide, 0.1% naphthylethylenediamine dihydrochloride, and 2% phosphoric acid).…”

Section: Methodsmentioning

confidence: 99%

Irisin improves endothelial function in obese mice through the AMPK-eNOS pathway

Han

Zhang

Hou

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

109

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Sun X. Irisin improves endothelial function in obese mice through the AMPK-eNOS pathway. Am J Physiol Heart Circ Physiol 309: H1501-H1508, 2015. First published September 14, 2015 doi:10.1152/ajpheart.00443.2015.-Irisin is a novel hormone secreted by myocytes. Lower levels of irisin are independently associated with endothelial dysfunction in obese subjects. The objective of this study was to explore whether irisin exerts a direct vascular protective effect on endothelial function in high-fat-diet-induced obese mice. Male C57BL/6 mice were given chow or a high-fat diet with or without treatment with irisin. Aortic endothelial function was determined by measuring endothelium-dependent vasodilatation (EDV). Nitric oxide (NO) in the aorta was determined. The effect of irisin on the levels of AMP-activated protein kinase (AMPK), Akt, and endothelial NO synthase (eNOS) phosphorylation in endothelial cells was determined. Human umbilical vein endothelial cells were used to study the role of irisin in the AMPK-eNOS pathway. Acetylcholine-stimulated EDV was significantly lower in obese mice compared with control mice. Treatment of obese mice with irisin significantly enhanced EDV and improved endothelial function. This beneficial effect of irisin was partly attenuated in the presence of inhibitors of AMPK, Akt, and eNOS. Treatment of obese mice with irisin enhanced NO production and phosphorylation of AMPK, Akt, and eNOS in endothelial cells. These factors were also enhanced by irisin in human umbilical vein endothelial cells in vitro. Suppression of AMPK expression by small interfering RNA blocked irisin-induced eNOS and Akt phosphorylation and NO production. We have provided the first evidence that irisin improves endothelial function in aortas of high-fat-diet-induced obese mice. The mechanism for this protective effect is related to the activation of the AMPK-eNOS signaling pathway. irisin; endothelial function; nitric oxide; obesity NEW & NOTEWORTHYIrisin improved endothelial function in aortas of high-fat-dietinduced obese mice. The mechanism for the protective effect of irisin is related to activation of the AMP-activated protein kinase-endothelial nitric oxide synthase signaling pathway.

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Section: Methodsmentioning

confidence: 99%

Irisin improves endothelial function in obese mice through the AMPK-eNOS pathway

Han

Zhang

Hou

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

109

View full text Add to dashboard Cite

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“…Following the determination of endothelial function, total NO production (nitrite and nitrate) by the aortic rings was determined via a modified Griess reaction method as described previously [22,23]. Briefly, after the ACh (10 -4 M) was added, 100 μL of K-H solution was taken from the organ bath and mixed with an equal volume of modified Griess reagent.…”

Section: Methodsmentioning

confidence: 99%

Induction of Haemeoxygenase-1 Improves FFA-Induced Endothelial Dysfunction in Rat Aorta

Han

Hui²,

Zhang³

et al. 2015

Cell Physiol Biochem

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Background: The induction of haemeoxygenase-1 (HO-1) exerts beneficial effects in the setting of endothelial dysfunction in obesity. High free fatty acid (FFA) levels are a common feature of obesity and are the primary cause of endothelial dysfunction. The objective of our study was to explore the effects of HO-1 induction on FFA-induced endothelial dysfunction in rats. Methods: Rats received FFA treatment with either cobalt protoporphyrin (CoPP) to induce HO-1 or stannous protoporphyrin (SnPP) to inhibit HO-1. Endothelial function was determined by measuring endothelium-dependent vasodilatation (EDV). Nitric oxide (NO) production, superoxide production and nuclear factor (NF)-κB expression in the aorta were each determined. The levels of adenosine monophosphate (AMP)-activated kinase (AMPK) and endothelial nitric oxide synthase (eNOS) expression in endothelial cells were determined via Western blotting. Results: Induction of HO-1 by CoPP decreased circulating FFA, high-sensitivity C-reactive protein and malondialdehyde levels and increased serum adiponectin and glutathione levels compared with the FFA group (P<0.05). High FFA levels resulted in EDV impairment, which was improved by HO-1 induction (P<0.05). Induction of HO-1 increased NO levels and reduced aortic superoxide production and NF-κB expression compared with the FFA group. The FFA group exhibited decreased AMPK expression and eNOS phosphorylation, both of which were enhanced via HO-1 induction (P<0.05). The beneficial effects of CoPP on EDV were partially attenuated in vitro in the presence of inhibitors of AMPK, phosphatidylinositol 3-kinase (PI3K), and eNOS. Conclusions: HO-1 induction with CoPP improves FFA-induced endothelial dysfunction in the rat aorta. The protective mechanism appears to be related to the activation of the AMPK-PI3K-eNOS pathway as a result of increased adiponectin levels as well as decreased inflammation and oxidative stress.

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“…The above responses to NO are important for long term regulation of VSMC during vascular remodeling, but a more important acute physiologically role of NO in these cells is to regulate vascular smooth muscle tone to control blood flow [82][83][84][85]. On a molecular level, VSMC contracture involves interactions between myosin and the actin cytoskeleton.…”

Section: Inhibition Of Nitric Oxide Signaling By Thrombospondin-1mentioning

confidence: 99%

Thrombospondins: from structure to therapeutics

Isenberg

Frazier

Roberts

2008

Cell. Mol. Life Sci.

118

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Thrombospondin-1 is secreted protein that modulates vascular cell behavior via several cell surface receptors. In vitro, nanomolar concentrations of thrombospondin-1 are required to alter endothelial and vascular smooth muscle cell adhesion, proliferation, motility, and survival. Yet, much lower levels of thrombospondin-1 are clearly functional in vivo. This discrepancy was explained with the discovery that the potency of thrombospondin-1 increases more than 100-fold in the presence of physiological levels of NO. Thrombospondin-1 binding to CD47 inhibits NO signaling by preventing cGMP synthesis and activation of its target cGMP-dependent protein kinase. This potent antagonism of NO signaling allows thrombospondin-1 to acutely constrict blood vessels, accelerate platelet aggregation and, if sustained, inhibit angiogenic responses. Acute antagonism of NO signaling by thrombospondin-1 is important for hemostasis but becomes detrimental for tissue survival of ischemic injuries. New therapeutic approaches targeting thrombospondin-1 or CD47 can improve recovery from ischemic injuries and overcome a deficit in NO-responsiveness in aging.

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Real-time monitoring of nitric oxide and blood flow during ischemia-reperfusion in the rat testis

Cited by 33 publications

References 13 publications

Irisin improves endothelial function in obese mice through the AMPK-eNOS pathway

Irisin improves endothelial function in obese mice through the AMPK-eNOS pathway

Induction of Haemeoxygenase-1 Improves FFA-Induced Endothelial Dysfunction in Rat Aorta

Thrombospondins: from structure to therapeutics

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