glycyrrhetinic acid/hypoxia

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Protective effect of gap junction uncouplers given during hypoxia against reoxygenation injury in isolated rat hearts.

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It has been shown that cell-to-cell chemical coupling may persist during severe myocardial hypoxia or ischemia. We aimed to analyze the effects of different, chemically unrelated gap junction uncouplers on the progression of ischemic injury in hypoxic myocardium. First, we analyzed the effects of

Protective effects of Glycyrrhizae radix extract and its compounds in a renal hypoxia (ischemia)-reoxygenation (reperfusion) model.

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Glycyrrhizae radix water extract (GRWE) and its two major constituents glycyrrhizin and 3-glycyrrhetinic monodesmoside, significantly suppressed LDH leakage and MDA release, whereas glycyrrhetinic acid had no effect. On the other hand, in rats subjected to ischemia-reperfusion, the activities of

[Inhibition of gap junctional intercellular communication protects astrocytes from hypoxia/reoxygenation injury].

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OBJECTIVE To investigate the effects of inhibiting gap junctional intercellular communication on hypoxia/reoxygenation injury in astrocytes. METHODS Primary cultured cerebral cortical astrocytes of neonate rats were divided into normal control group, hypoxia reoxygenation injury group and

[Acute hypoxia increases outward current and decreases gap junction of VSMCs in guinea-pig anterior inferior cerebellar artery].

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The aim of the present study was to investigate the effects of acute hypoxia on the electrophysiological properties of vascular smooth muscle cells (VSMCs) in arteriole. Guinea-pig anterior inferior cerebellar artery (AICA) segments were isolated, and outer layer connective tissue was removed by

[Effects of acute hypoxia on the electrophysiological properties of vascular smooth muscle cells of mesenteric artery in guinea pig].

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OBJECTIVE To observe the effects of acute hypoxia on the electrophysiological properties of vascular smooth muscle cells (VSMCs) of mesenteric artery in guinea pig. METHODS A segment of mesenteric artery (MA) (outer diameter < 100 µm) of guinea pig was digested with collagenase A and its adventitial

Hypoxia and reoxygenation-induced oxidant production increase in microvascular endothelial cells depends on connexin40.

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Connexins (Cx) are recognized as structural constituents of gap-junctional intercellular communication (GJIC). However, their function may extend beyond facilitating the exchange of metabolites and electrical signals between cells. In this study we asked if increased production of reactive oxygen

Administration of glycyrrhetinic acid reinforces therapeutic effects of mesenchymal stem cell-derived exosome against acute liver ischemia-reperfusion injury

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Recent studies have shown that mesenchymal stem cell-derived exosome could attenuate ischaemia-reperfusion (I/R) injury by suppressing inflammatory response in the liver. Glycyrrhetinic acid was also shown to be capable of repressing the TLR4 signalling pathway. However, it remains to be explored as

ATP release from vascular endothelia occurs across Cx43 hemichannels and is attenuated during hypoxia.

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BACKGROUND Extracellular ATP is an important signaling molecule for vascular adaptation to limited oxygen availability (hypoxia). Here, we pursued the contribution of vascular endothelia to extracellular ATP release under hypoxic conditions. UNASSIGNED We gained first insight from studying ATP

Involvement of gap junctions between smooth muscle cells in sustained hypoxic pulmonary vasoconstriction development: a potential role for 15-HETE and 20-HETE.

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In response to hypoxia, the pulmonary artery normally constricts to maintain optimal ventilation-perfusion matching in the lung, but chronic hypoxia leads to the development of pulmonary hypertension. The mechanisms of sustained hypoxic pulmonary vasoconstriction (HPV) remain unclear. The aim of

Gap junctions support the sustained phase of hypoxic pulmonary vasoconstriction by facilitating calcium sensitization.

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OBJECTIVE To determine the role of gap junctions (GJs) in hypoxic pulmonary vasoconstriction (HPV). RESULTS Studies were performed in rat isolated intrapulmonary arteries (IPAs) mounted on a myograph and in anaesthetized rats. Hypoxia induced a biphasic HPV response in IPAs preconstricted with

A heterotypic bystander effect for tumor cell killing after adeno-associated virus/phage-mediated, vascular-targeted suicide gene transfer.

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Suicide gene transfer is the most commonly used cytotoxic approach in cancer gene therapy; however, a successful suicide gene therapy depends on the generation of efficient targeted systemic gene delivery vectors. We recently reported that selective systemic delivery of suicide genes such as herpes

EDHF-mediated vasodilation involves different mechanisms in normotensive and hypertensive rat lungs.

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The role of endothelium-derived hyperpolarizing factor (EDHF) in regulating the pulmonary circulation and the participation of cytochrome P-450 (CYP450) activity and gap junction intercellular communication in EDHF-mediated pulmonary vasodilation are unclear. We tested whether tonic EDHF activity

Neuroprotective effects of roasted licorice, not raw form, on neuronal injury in gerbil hippocampus after transient forebrain ischemia.

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OBJECTIVE To observe neuroprotective effects of raw and roasted licorice against hypoxia and ischemic damage. METHODS When elucidating the protective effects of raw and roasted licorice, we analyzed the lactate dehydrogenase (LDH) release using PC12 cells after hypoxia in an in vitro study and after

ATP release by cardiac myocytes in a simulated ischaemia model: inhibition by a connexin mimetic and enhancement by an antiarrhythmic peptide.

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We studied the role of connexin hemichannels in the release of ATP by neonatal cardiac myocytes subject to ischaemic stress. Mechanical, osmotic and oxidative stress and changes in extracellular or intracellular Ca(2+) levels induce connexin hemichannels located in the plasma membrane to open and

Mechanisms of endothelium-dependent vasodilation in male and female, young and aged offspring born growth restricted.

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Numerous epidemiological studies have shown that cardiovascular dysfunction in adult life may be programmed by compromised growth in utero. Aging is a risk factor for vascular endothelial-dependent dysfunction. After birth, the impact of intrauterine growth restriction (IUGR) on normal aging

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