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Andrographolide stimulates p38 mitogen-activated protein kinase-nuclear factor erythroid-2-related factor 2-heme oxygenase 1 signaling in primary cerebral endothelial cells for definite protection against ischemic stroke in rats.

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Stroke pathogenesis involves complex oxidative stress-related pathways. The nuclear factor erythroid-2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) pathways have been considered molecular targets in pharmacologic intervention for ischemic diseases. Andrographolide, a labdane diterpene, has

Rosmarinic acid elicits neuroprotection in ischemic stroke via Nrf2 and heme oxygenase 1 signaling.

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Rosmarinic acid (RA) can elicit a neuroprotective effect against ischemic stroke, but the precise molecular mechanism remains poorly understood. In this study, an experimental ischemic stroke model was established in CD-1 mice (Beijing Vital River Laboratory Animal Technology, Beijing, China) by

Up-regulation of heme oxygenase-1 protects against cold injury-induced brain damage: a laboratory-based study.

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Heme oxygenase-1 (HO-1), a kind of stress protein, is critical for the protection against ischemic stroke and cerebrovascular endothelium damage. However, the effects of HO-1 on trauma-induced brain injury are still unknown. Hence, we attempted to use a cold injury-induced brain trauma (CIBT) model

Heme oxygenase-1 aggravates heat stress-induced neuronal injury and decreases autophagy in cerebellar Purkinje cells of rats.

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We previously reported that heat stroke induces autophagy as a protection mechanism against neurodegeneration in the brain. Heme oxygenase (HO)-1 is a stress protein and can be induced by heat stress (HS). Cerebellar Purkinje cells are selectively vulnerable to heat-induced injury. In this study, we

Paradoxical protection from atherosclerosis and thrombosis in a mouse model of sickle cell disease.

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Sickle cell disease (SCD) is associated with vascular complications including premature stroke. The role of atherothrombosis in these vascular complications is unclear. To determine the effect of SCD on atherosclerosis and thrombosis, mice with SCD along with controls were generated by

Epileptic seizures increase circulating endothelial cells in peripheral blood as early indicators of cerebral vascular damage.

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Circulating endothelial cells (CECs) are nonhematopoetic mononuclear cells in peripheral blood that are dislodged from injured vessels during cardiovascular disease, systemic vascular disease, and inflammation. Their occurrence during cerebrovascular insults has not been previously described.

Modulatory effect of interleukin-1beta on rat isolated basilar artery contraction.

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An increased level of cytokine interleukin-1 (IL-1) has been detected around the site of stroke. However, the effect of IL-1beta on the basilar artery has received little attention. We evaluated the effects of IL-1beta on the contractile response of rat isolated basilar artery by measuring isometric

[Risk of cadrdiovascular diseases in lead-exposed workers of crystal glassworks. Part I. Effect of lead on blood pressure and lipid metabolism].

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BACKGROUND Chronic occupational or environmental exposure to small doses of lead results in cardiovascular disorders: arterial hypertension, lipid metabolism disturbances and exacerbation of free radical processes. Each of these changes determines an independent cardiovascular risk factor. The aim

Up-regulation of astroglial heme oxygenase-1 by a synthetic (S)-verbenone derivative LMT-335 ameliorates oxygen-glucose deprivation-evoked injury in cortical neurons.

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Excessive generation of free radicals is regarded as a major detrimental factor in cerebral ischemic insults. Neurons are particularly vulnerable to oxidative stress due to their limited anti-oxidant capacity. As an important source of antioxidants in the brain, astroglia are now thought to be

The role of haem oxygenase in renal vascular reactivity in normotensive and hypertensive rats.

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OBJECTIVE To evaluate the contribution of the haem oxygenase-carbon monoxide (CO) system to renal vascular tone in normotensive Wistar rats and in the stroke-prone spontaneously hypertensive rats (SHR-SPs). METHODS An isolated perfused rat kidney preparation was used in which perfusion

Roles of heme oxygenase/carbon monoxide system in genetically hypertensive rats.

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Although carbon monoxide (CO) has been suggested to be involved in the regulation of cardiovascular function through activation of soluble guanylyl cyclase, the pathophysiological significance in hypertension remains unknown. We therefore examined the effects of heme oxygenase (HO) inhibitor zinc

Hemopexin promotes angiogenesis via up-regulating HO-1 in rats after cerebral ischemia-reperfusion injury.

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Ischemia-reperfusion (I/R) is a critical pathophysiological change of ischemic stroke. Heme-oxygenase-1 (HO-1) is a rate-limiting enzyme of eliminating excessive free heme by combining with hemopexin (HPX), a plasma protein contributing to alleviating infarct size due to ischemia stroke. This study

Pharmacological induction of heme oxygenase-1 by a triterpenoid protects neurons against ischemic injury.

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OBJECTIVE Heme oxygenase-1 (HO-1) is an inducible Phase 2 enzyme that degrades toxic heme; its role in cerebral ischemia is not fully understood. We hypothesize that chemically induced HO-1 upregulation with the novel triterpenoid CDDO-Im (2-cyano-3,12 dioxooleana-1,9 dien-28-oyl imidazoline), a

Hemopexin alleviates cognitive dysfunction after focal cerebral ischemia-reperfusion injury in rats.

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Ischemia-reperfusion (I/R) is a critical pathophysiological basis of cognitive dysfunction caused by ischemia stroke. Heme-oxygenase-1 (HO-1) is the rate-limiting enzyme for the elimination of excessive free heme by combining with hemopexin (HPX), a plasma protein that contributes to

Modulation of thrombin-induced neuroinflammation in BV-2 microglia by carbon monoxide-releasing molecule 3.

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Carbon monoxide-releasing molecules are emerging as a new class of pharmacological agents that regulate important cellular function by liberating CO in biological systems. Here, we examined the role of carbon monoxide-releasing molecule 3 (CORM-3) in modulating neuroinflammatory responses in BV-2

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