hemin/infarction

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

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

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

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,

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

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

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

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,

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

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

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

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

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

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