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Targeting and modulating infarct macrophages with hemin formulated in designed lipid-based particles improves cardiac remodeling and function.
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Uncontrolled activation of pro-inflammatory macrophages after myocardial infarction (MI) accelerates adverse left ventricular (LV) remodeling and dysfunction. Hemin, an iron-containing porphyrin, activates heme oxygenase-1 (HO-1), an enzyme with anti-inflammatory and cytoprotective properties. We
Cardioprotective effect of hemin in isoprenaline-induced myocardial infarction. Role of ATP sensitive potassium channel and endothelial nitric oxide synthase.
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Ischemic heart disease is a common cardiac health problem. Despite the significant advances in prevention and treatment of this disorder, its incidences and complications are very serious. So, the search for more antioxidants and anti-inflammatory agents with cardioprotective effects is an urgent
Hyperglycemia in streptozotocin-induced diabetic rat increases infarct size associated with low levels of myocardial HO-1 during ischemia/reperfusion.
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This study investigated the role of heme oxygenase (HO)-1 in the cardiac tissue injury of acute ischemia/reperfusion (I/R) in diabetic streptozotocin (STZ)-induced hyperglycemic rats. The effects of 1) hemin, an inducer of HO expression and activity, and 2) zinc protoporphyrin IX (ZnPP-IX), an
[Protection effect and mechanism of hemin against ischemia/reperfusion injury in rat hearts].
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OBJECTIVE
To investigate whether the cardioprotective effect of hemin against ischemia/reperfusion (I/R) injury is through the inhibition of calpain activity, and to explore its underlying mechanism.
METHODS
Sixty-four SD rats were randomly divided into eight groups (n = 8): sham, I/R, MDL+ I/R,
Hemin, a heme oxygenase-1 inducer, restores the attenuated cardioprotective effect of ischemic preconditioning in isolated diabetic rat heart.
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BACKGROUND
Attenuated cardioprotective effect of ischemic preconditioning (IPC) by reduced nitric oxide (NO) is a hallmark during diabetes mellitus (DM). Recently, we reported that the formation of caveolin-endothelial nitric oxide synthase (eNOS) complex decreases the release of NO, which is
Hemin‑mediated neuroglobin induction exerts neuroprotection following ischemic brain injury through PI3K/Akt signaling.
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The aim of the present study was to uncover the mechanism underlying the neuroprotection of Hemin‑mediated neuroglobin (Ngb) in an in vivo model of brain injury. Sixty healthy male Sprague-Dawley rats were randomly divided into 5 groups (n=12, each group): sham surgery, ischemia, Hemin, LY294002
Joint protective effect of exogenous neuroglobin and hemin in rat focal ischemic brain tissues.
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OBJECTIVE
To investigate the joint protective effect of exogenous neuroglobin (Ngb) and hemin on ischemic brain tissue in rats and its possible mechanisms.
METHODS
Sprague Dawley rats (n = 175) were randomly divided into five groups (n = 35): sham, ischemia, hemin intervention, Ngb plasmid
Hemin offers neuroprotection through inducing exogenous neuroglobin in focal cerebral hypoxic-ischemia in rats.
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OBJECTIVE
To investigate the inducible effect of hemin on exogenous neuroglobin (Ngb) in focal cerebral hypoxic-ischemia in rats.
METHODS
125 healthy SD rats were randomly divided into five groups: sham-operation control group, operation group, hemin treatment group, exogenous Ngb treatment group,
[Cardioprotective effects of NOS and PKC under hemin induced ischemia/reperfusion injury in rat hearts].
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OBJECTIVE
Whether hemin, a heme oxygenase 1 (HO-1) inducer, reduces ischemia/reperfusion injury and whether NO synthase (NOS) and PKC are involved in the cardioprotective effects were investigated in the present study.
METHODS
The Langendorff model of isolated rat heart was used. The ventricular
[Involvement of potassium channel in hemin-induced cardioprotection in rat hearts].
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OBJECTIVE
To investigate the effects of heme oxygenase 1 inducer hemin on protection of ischemia-reperfusion injury in rats and its mechanisms.
METHODS
The Langendorff model of isolated rat heart was used; the left anterior descending coronary artery was occluded for 30 min and subsequently
Hemin-Bridged MOF Interface with Double Amplification of G-Quadruplex Payload and DNAzyme Catalysis: Ultrasensitive Lasting Chemiluminescence MicroRNA Imaging.
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Here we report a double-amplified sensing platform for ultrasensitive chemiluminescence (CL) miRNA detection in real patients' blood, in which a hemin-bridged metal-organic framework (MOF) is employed as a functional interface to boost the payload and catalysis of G-quadruplex (G4) DNAzymes. Hemin
Heme oxygenase-1 prevents heart against myocardial infarction by attenuating ischemic injury-induced cardiomyocytes senescence.
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Heme oxygenase-1 and the ischemia-reperfusion injury in the rat heart.
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Carbon monoxide (CO) is a signaling gas produced intracellularly by heme oxygenase (HO) enzymes using heme as a substrate. During heme breakdown, HO-1 and HO-2 release CO, biliverdin, and Fe(2+). In this study, we investigated the effects of manipulation of the HO-1 system in an in vivo model of
Induction of heme oxygenase-1 can act protectively against cardiac ischemia/reperfusion in vivo.
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Enhanced production of reactive oxygen species plays a role in myocardial injury following ischemia/reperfusion. Heme oxygenase-1 (HO-1) is a heme-catabolizing enzyme that is induced by and acts against oxidant-induced tissue injury. We examined whether HO-1 expression was regulated following
Heme oxygenase system and hypertension: a comprehensive insight.
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Hypertension is a complex interplay of interrelated etiologies, and the leading risk factor for many cardiovascular morbidity and mortality worldwide. Cardinal pathophysiological features of hypertension include enhanced vascular inflammation, vascular remodeling, vascular contractility and
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