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Hemin-induced erythroid differentiation changes the sensitivity of K562 cells to tumor necrosis factor-alpha.
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Tumor necrosis factor-alpha (TNF) can inhibit the growth of erythroid progenitors (erythroid colony-forming units [CFU-E] and erythroid burst-forming units [BFU-E]) at picomolar concentrations, but only if added within the first 48 h of culture. These data suggested that cells undergoing erythroid
Protective effects of heme-oxygenase expression against endotoxic shock: inhibition of tumor necrosis factor-alpha and augmentation of interleukin-10.
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BACKGROUND
Heme-oxygenase (HO)-1 acts as an inducible defense against oxidative stress and could play an important role in inflammation models, providing protection against oxidative stress and systemic inflammatory response. The objective of this study was to improve the role of HO-1 on systemic
Upregulation of heme oxygenase-1 with hemin prevents D-galactosamine and lipopolysaccharide-induced acute hepatic injury in rats.
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Heme oxygenase-1 (HO-1), the rate-limiting enzyme in heme catabolism, has been shown to be induced during oxidative injury, and its induction acts as an important cellular defense mechanism against such injuries. In this study, we examined the functional roles of HO-1 induction in a rat model of
Hemin ameliorates indomethacin-induced small intestinal injury in mice through the induction of heme oxygenase-1.
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OBJECTIVE
Although non-steroidal anti-inflammatory drugs can induce intestinal injury, the mechanisms are not fully understood, and treatment has yet to be established. Heme oxygenase-1 (HO-1) has recently gained attention for anti-inflammatory and cytoprotective effects. This study aimed to
Protective effects of hemin in an experimental model of ventilator-induced lung injury.
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Mechanical ventilation is an indispensable life-support modality for critically ill patients with acute lung injury or acute respiratory distress syndrome. Unfortunately, mechanical ventilation even the protective ventilation strategies may evoke ventilator-induced lung injury. Heme oxygenase-1
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
Suppression of TNF-alpha gene expression by hemin: implications for the role of iron homeostasis in host inflammatory responses.
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Tumor necrosis factor alpha (TNF-alpha) has multiple effects on iron homeostasis and erythropoiesis and has been implicated in the pathogenesis of the anemia of inflammation. We postulated that intracellular iron in turn may regulate the expression of TNF-alpha. In the human monocytic leukemia cell
Therapeutic potential of hemin in acetaminophen nephrotoxicity in rats.
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The therapeutic potential of hemin, the heme oxygenase-1 inducer, was investigated against renal damage induced by acute acetaminophen overdose in rats. Nephrotoxicity was induced by a single oral dose of acetaminophen (2.5g/kg). Hemin was given as a single s.c. injection (40μmol/kg), 1h following
Hemin treatment abrogates monocrotaline-induced pulmonary hypertension.
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Treatment of rats with monocrotaline (MCT), a pyrrolizidine alkaloid plant toxin, is known to cause pulmonary hypertension (PH), and it has been used as a useful experimental model of PH. Recent findings suggested that pulmonary inflammation may play a significant role in the pathogenesis of
An upregulation of interleukin-2 receptor, transferrin receptor expression and cytokine production mediated by hemin in human peripheral blood mononuclear cells.
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BACKGROUND
We previously reported that hemin-induced mitogenicity in mouse splenocytes was potentiated up to two-fold by interleukin (IL)-2, and the combination of hemin and IL-2 was also effective in inducing cytotoxicity for NK-resistant target cells. The purpose of this study was to investigate
Protective effect of hemin against cadmium-induced testicular damage in rats.
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The protective effect of hemin, the heme oxygenase-1 inducer, was investigated in rats with cadmium induced-testicular injury, in which oxidative stress and inflammation play a major role. Testicular damage was induced by a single i.p. injection of cadmium chloride (2mg/kg). Hemin was given for
Hemin therapy suppresses inflammation and retroperitoneal adipocyte hypertrophy to improve glucose metabolism in obese rats co-morbid with insulin-resistant type-2 diabetes.
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OBJECTIVE
Visceral adiposity and impaired glucose metabolism are common patho-physiological features in patients co-morbid with obesity and type-2 diabetes. We investigated the effects of the heme-oxygenase (HO) inducer hemin and the HO blocker stannous-mesoporphyrin (SnMP) on glucose metabolism,
Eff ects of hemin, a heme oxygenase-1 inducer in L-arginine-induced acute pancreatitis and associated lung injury in adult male albino rats.
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OBJECTIVE
The aim of the current study was to assess the protective outcome of hemin, a heme oxygenase-1 (HO-1) inducer on L-arginine-induced acute pancreatitis in rats. Acute pancreatitis (AP) is considered to be a critical inflammatory disorder with a major impact on the patient health. Various
Effect of hemin on the physiology and virulence of Bacteroides gingivalis W50.
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Bacteroides gingivalis W50 was grown in a chemostat under steady-state conditions at pH 7.5 +/- 0.2 and a constant growth rate of 6.9 h for periods of up to 6 weeks (146 bacterial generations) in a complex medium. Hemin was capable of limiting the growth of cells up to a concentration of
Hemin augments growth and hemoglobinization of erythroid precursors from patients with diamond-blackfan anemia.
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Diamond-Blackfan anemia (DBA) is congenital pure red-cell anemia due to a differentiation block in erythroid precursors. The disease is commonly caused by mutations in genes for ribosomal proteins. Despite the identification of disease causal genes, the disease pathogenesis is not completely
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