hemin/inflamación

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N-methyl-D-aspartic acid receptor 1 (NMDAR1) aggravates secondary inflammatory damage induced by hemin-NLRP3 pathway after intracerebral hemorrhage.

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OBJECTIVE Inflammation plays a critical role in secondary brain damage after intracerebral hemorrhage (ICH). However, the mechanisms of inflammatory injury following ICH are still unclear, particularly the involvement of NLRP3 inflammasome, which are crucial to sterile inflammatory responses. In

Hemin attenuated oxidative stress and inflammation to improve wound healing in diabetic rats.

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Oxidative stress and persistent inflammation play crucial role in the progression of diabetic wound complications. Hemeoxgenase-1 (HO-1) by degrading hemin has been shown to display anti-oxidant and anti-inflammatory effects. Further, hemin is a potent HO-1 inducer. Thus, the current study was aimed

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

Hemin impairs resolution of inflammation via microRNA-144-3p-dependent downregulation of ALX/FPR2.

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The pathomechanisms of complications due to blood transfusion are not fully understood. Elevated levels of heme derived from stored RBCs are thought to be associated with transfusion reactions, especially inflammatory responses. Recently, the proinflammatory effect of heme has been

Induction of heme oxygenase-1 with hemin reduces obesity-induced adipose tissue inflammation via adipose macrophage phenotype switching.

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Adipose macrophages with the anti-inflammatory M2 phenotype protect against obesity-induced inflammation and insulin resistance. Heme oxygenase-1 (HO-1), which elicits antioxidant and anti-inflammatory activity, modulates macrophage phenotypes and thus is implicated in various inflammatory diseases.

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,

Hemin arginate-induced heme oxygenase 1 expression improves liver microcirculation and mediates an anti-inflammatory cytokine response after hemorrhagic shock.

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Microvascular failure is a major determinant for the development of hepatocellular dysfunction after hemorrhagic shock. Induction of heme oxygenase (HO) 1 may confer hepatocellular protection. Hemin arginate (HAR) induces HO-1 and protects against shock-induced organ failure. The mechanisms are not

Cofilin signaling in hemin-induced microglial activation and inflammation.

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Intracerebral hemorrhage (ICH) is the most severe form of stroke and is further exacerbated by the secondary injury involving inflammatory response due to the activation of microglia. This secondary injury is partly due to the toxic effects of hemin, an endogenous breakdown product of hemoglobin.

Inhibitory effects of chlorophyllin, hemin and tetrakis(4-benzoic acid)porphyrin on oxidative DNA damage and mouse skin inflammation induced by 12-O-tetradecanoylphorbol-13-acetate as a possible anti-tumor promoting mechanism.

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Reactive oxygen species (ROS) from both endogenous and exogenous sources can cause oxidative DNA damage and dysregulated cell signaling, which are involved in the multistage process of carcinogenesis such as tumor initiation, promotion and progression. A number of structurally different

Hemin reduces inflammation associated with TNBS-induced colitis.

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UNASSIGNED Hemin is a heme-oxygenase inducer, which can confer anti-inflammatory, cytoprotective, and antiapoptotic effects. These properties are beneficial therapeutical effects to inflammatory bowel disease (IBD). IBD is a worldwide health problem characterized by chronic inflammation of

Anti-inflammatory and antihyperalgesic effects of the combination of ibuprofen and hemin in adjuvant-induced arthritis in the Wistar rat.

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OBJECTIVE Although, pharmacological activation of heme oxygenase (HO)-1 has shown to produce ameliorative effects in various experimental models of inflammation, but such beneficial effects have not been observed in adjuvant-induced arthritis. Further, the upregulated activity of HO-1 has been

The anti-inflammatory mechanism of heme oxygenase-1 induced by hemin in primary rat alveolar macrophages.

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Alveolar macrophages (AMs) can initiate lung inflammation by producing pro-inflammatory cytokines and chemokines, but they participate actively in the prevention of inflammation during acute lung injury (ALI). Heme oxygenase-1 (HO-1) is mainly expressed in AMs and has anti-inflammatory properties in

Pro-stimulatory role of methemoglobin in inflammation through hemin oxidation and polymerization.

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Inflammation or vascular occlusion by parasitized red blood cell contributes to the pathogenesis of cerebral malaria. The current study aimed to characterize the role of major pro-oxidant factor methemoglobin present in the malaria culture supernatant contributing in inflammation during malaria.

Abrogation of macrophage-mediated suppression of T-lymphocyte proliferation with hemoglobin and hemin is a function of iron content.

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Hemoglobin, hemin, and ferric ion (Fe) were shown to reverse peritoneal exudate cell (PEC)-mediated suppression of concanavalin A-elicited murine spleen cell activation. Titration of hemoglobin and hemin relative to Fe showed a direct relationship between Fe content and reversal of PEC suppression.

[Effect of hemin on severe acute pancreatitis-associated lung injury in rats and its mechanism].

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OBJECTIVE To investigate the effect of hemin on lung injury following severe acute pancreatitis (SAP) in rats and to explore its rudimentary mechanism. METHODS Thirty-six rats were randomly divided into 3 groups: a control group, a SAP model group, and a hemin-pretreated group. Rats were sacrificed

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