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Effect of a long-term treatment with a low-dose granulocyte colony-stimulating factor on post-infarction process in the heart.

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Although beneficial effects of granulocyte colony-stimulating factor (G-CSF) have been demonstrated on post-myocardia infarction (MI) process, the mechanisms and feasibility are not fully agreed yet. We investigated effects of a long-term treatment with a low-dose G-CSF started 1 day after the onset

Sesquiterpene lactone parthenolide, an inhibitor of IkappaB kinase complex and nuclear factor-kappaB, exerts beneficial effects in myocardial reperfusion injury.

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Sesquiterpene lactones are extracts of common medicinal Asteracae plants used in folk medicine for their anti-inflammatory activity. Recently, in vitro studies have shown that these compounds may interfere with pro-inflammatory gene regulation. This study examines the effects of parthenolide, a

Delayed anesthetic preconditioning protects against myocardial infarction via activation of nuclear factor-κB and upregulation of autophagy.

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OBJECTIVE Delayed volatile anesthetic preconditioning (APC) can protect against myocardial ischemia/reperfusion (I/R) injury; the delayed phase is called the second window of protection (SWOP), but the underlying mechanism is unclear. Nuclear factor-κB (NF-κB) is involved in the myocardial

Parthenolide-Induced Cytotoxicity in H9c2 Cardiomyoblasts Involves Oxidative Stress.

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BACKGROUND Cardiac cellular injury as a consequence of ischemia and reperfusion involves nuclear factor-κB (NF-κ B), amongst other factors, and NF-κ B inhibitors could substantially reduce myocardial infarct size. Parthenolide, a sesquiterpene lactone compound which could inhibit NF-κ B, has been

Parthenolide is neuroprotective in rat experimental stroke model: downregulating NF-κB, phospho-p38MAPK, and caspase-1 and ameliorating BBB permeability.

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Inflammatory damage plays an important role in cerebral ischemic pathogenesis and may represent a target for treatment. Parthenolide (PN) has been proved to elicit a wide range of biological activities through its anti-inflammatory action in the treatment of migraine, arthritis, and atherosclerosis.

Role of nuclear factor-κB in volatile anaesthetic preconditioning with sevoflurane during myocardial ischaemia/reperfusion.

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OBJECTIVE Anaesthetic preconditioning (APC) protects against myocardial ischaemia/reperfusion injury. Nuclear factor-kappaB (NF-kappaB) has been implicated in APC-induced myocardial protection in vitro. Our study tested the hypothesis that in-vivo APC with sevoflurane is triggered by NF-kappaB

Nuclear factor-[kappa]B inhibition provides additional protection against ischaemia/reperfusion injury in delayed sevoflurane preconditioning.

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OBJECTIVE Sevoflurane anaesthetic preconditioning (SPC) has been shown to limit nuclear factor-[kappa]B (NF-[kappa]B) activation and the production of inflammatory cytokines during myocardial ischaemia/reperfusion (I/R). Similarly, pharmacological inhibition of NF-[kappa]B using parthenolide is

High glucose induces plasminogen activator inhibitor-1 expression through Rho/Rho-kinase-mediated NF-kappaB activation in bovine aortic endothelial cells.

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Recently, it has become evident that elevated levels of plasminogen activator inhibitor-1 (PAI-1) are associated with myocardial infarction and stroke, especially in patients with diabetes. The molecular mechanisms involved in hyperglycemia-induced PAI-1 expression in bovine aortic endothelial cells

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Herbal & Natural Medicine

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