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Systemic zinc protoporphyrin administration reduces intracerebral hemorrhage-induced brain injury.

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Hemoglobin degradation products result in brain injury after intracerebral hemorrhage (ICH). Recent studies found that intracerebral infusion of heme oxygenase inhibitors reduces hemoglobin- and ICH-induced brain edema in rats and pigs. The present study examined whether systemic use of zinc

Zinc Protoporphyrin Attenuates White Matter Injury after Intracerebral Hemorrhage.

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Intracerebral hemorrhage (ICH)-induced white matter injury has not been well studied. The objective of this study was to examine the effect of zinc protoporphyrin (ZnPP) on white matter injury induced by ICH. This study was divided into two parts. In the first part, rats received either a needle

Zinc protoporphyrin aggravates cerebral ischemic injury following experimental subarachnoid hemorrhage.

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This study was aimed to evaluate the influence of an antagonist of heme oxygenase, zinc protoporphyrin IX (ZnPPIX), on the production of endogenous carbon monoxide (CO) and the secondary cerebral injury after subarachnoid hemorrhage (SAH). Wistar rats were divided into non-SAH, SAH, and ZnPPIX

The effect of intracisternal Zn (II) protoporphyrin IX on vasospasm process in the experimental subarachnoid hemorrhage model.

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BACKGROUND although there has been much work on it for years, cerebral vasospasm as a complication of subarachnoid bleeding is still an important cause of mortality and morbidity. The presented study was designed to examine the effects of heme oxygenase inhibitor, Zn (II) protoporphyrin IX, on

Mechanism of hepatoprotection in proestrus female rats following trauma-hemorrhage: heme oxygenase-1-derived normalization of hepatic inflammatory responses.

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Hepatic damage occurs in males and ovariectomized (OVX), not in proestrus (PE), females following trauma-hemorrhage (T-H). The mechanism responsible for hepatoprotection remains unknown. We hypothesized protection in PE is a result of enhanced heme oxygenase-1 (HO-1)-derived down-regulation of liver

Transient increase of free iron in rat livers following hemorrhagic-traumatic shock and reperfusion is independent of heme oxygenase 1 upregulation.

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Hemorrhagic-traumatic shock (HTS) followed by reperfusion induces heme oxygenase (HO) 1. Free iron (Fe2+) may cause oxidative stress, if not adequately sequestered. We aimed to characterize HO-1-mediated effects on Fe2+ levels in liver and transferrin-bound iron (TFBI) in plasma following HTS,

Protective effects of bilirubin against cyclophosphamide induced hemorrhagic cystitis in rats.

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OBJECTIVE The end product of the heme oxygenase pathway, bilirubin, is the most abundant endogenous antioxidant in mammals. We report the heme oxygenase-1 mediated production of bilirubin and its cytoprotective roles in cyclophosphamide induced hemorrhagic cystitis in rats. METHODS Female

Tin-protoporphyrin prevents experimental superficial siderosis in rabbits.

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Superficial siderosis of the human central nervous system is caused by small continuous or recurrent subarachnoid hemorrhages that lead to the destructive deposition of hemosiderin. The excessive tissue iron derives from heme that is oxidized in a rate-limiting step by the enzyme heme oxygenase

Induction of heme-oxygenase-1 prevents the systemic responses to hemorrhagic shock.

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Oxidant-mediated reperfusion injury of the gut is a major contributor of the systemic inflammatory response in hemorrhagic shock. Recent studies have suggested that heme-oxygenase-1 (HO-1) represents an endogenous protective mechanism against oxidant stress. We assessed whether HO-1 induction

Intestinal preconditioning prevents systemic inflammatory response in hemorrhagic shock. Role of HO-1.

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Intestinal ischemia-reperfusion has been implicated in the systemic inflammatory response and organ injury in hemorrhagic shock, but the exact role of the intestine has never been directly demonstrated. Preconditioning (PC) with brief periods of intermittent ischemia is a known potent anti-ischemic

Role of heme oxygenase in heme-mediated inhibition of rat brain Na+-K+-ATPase: protection by tin-protoporphyrin.

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Hemoglobin has been shown to inhibit brain Na+-K+-ATPase through an iron-dependent mechanism. Both hemoglobin and iron cause spontaneous peroxidation of brain lipids. Release of iron from the heme molecule in animal tissues is dependent on the activity of heme oxygenase. We hypothesized that

Pharmacological preconditioning with vitamin C attenuates intestinal injury via the induction of heme oxygenase-1 after hemorrhagic shock in rats.

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Pre-induction of heme oxygenase (HO)-1, which is regarded as an effective method of "organ preconditioning", exerts beneficial effects during hemorrhagic shock (HS). However, the available HO-1 inducers exhibit disadvantages such as toxicity or complex technical requirements. Therefore, a safe and

Heme-oxygenase-1 mRNA expression affects hemorrhagic shock-induced leukocyte adherence.

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BACKGROUND Hemorrhagic shock-related leukocyte adherence to endothelial cells is a key step in microvascular injury-related organ damage. Heme-oxygenase-1 (HO-1) metabolizes heme, a potent cytotoxic agent, to carbon monoxide and biliverdin. We hypothesized that changing HO-1 expression would change

Protective effects of a heme oxygenase-1-secreting Lactococcus lactis on mucosal injury induced by hemorrhagic shock in rats.

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OBJECTIVE To investigate the protective effects of a heme oxygenase-1 (HO-1)-secreting Lactococcus lactis (LL-HO-1) on mucosal injury induced by hemorrhagic shock in rats. METHODS The ability of recombinant LL-HO-1 to secrete biological active HO-1 in the rat intestine was determined in situ after 3

Vitamin C treatment attenuates hemorrhagic shock related multi-organ injuries through the induction of heme oxygenase-1.

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BACKGROUND Vitamin C (VitC) has recently been shown to exert beneficial effects, including protecting organ function and inhibiting inflammation, in various critical care conditions, but the specific mechanism remains unclear. Induction of heme oxygenase (HO)-1, a heat shock protein, has been shown

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