Biochemical and Biophysical Research Communications
Regular ArticleInduction of Heme Oxygenase-1 Can Act Protectively against Cardiac Ischemia/Reperfusion in Vivo
References (25)
- et al.
Beneficial role of bile pigments as an endogenous tissue protector: anti-complement effects of biliverdin and conjugated bilirubin
Biochim. Biophys. Acta
(1993) - et al.
Regional difference in induction of heme oxygenase-1 protein following rat transient forebrain ischemia
Neurosci. Lett.
(1996) - et al.
Induction of the haem oxygenase gene expression during the reperfusion of ischemic rat myocardium
J. Mol. Cell. Cardiol.
(1996) - et al.
Balloon injury does not induce heme oxygenase-1 expression, but administration of hemin inhibits neointimal formation in balloon-injured rat carotid artery
Biochem. Biophys. Res. Commun.
(1999) - et al.
Heme oxygenase and cardiac function in ischemic/reperfused rat hearts
Free Radic. Biol. Med.
(1999) - et al.
Direct measurement of free radical generation following reperfusion of ischemic myocardium
Proc. Natl. Acad. Sci. USA
(1987) - et al.
Generation of superoxide in cardiomyocytes during ischemia before reperfusion
Am. J. Physiol.
(1999) - et al.
Catalase-overexpressing transgenic mouse heart is resistant to ischemia- reperfusion injury
Am. J. Physiol.
(1997) - et al.
Recombinant adenovirus-mediated cardiac gene transfer of superoxide dismutase and catalase attenuates postischemic contractile dysfunction
Circulation
(1998) - et al.
Bilirubin is an antioxidant of possible physiological importance
Science
(1987)
Expression of HSP 70, immediate-early response and heme oxygenase genes in ischemic-reperfused rat liver
Lab. Invest.
Induction of kidney heme oxygenase-1 (HSP32) mRNA and protein by ischemia/reperfusion: Possible role of heme as both promotor of tissue damage and regulator of HSP32
J. Pharmacol. Exp. Ther.
Cited by (113)
The role of carbon monoxide and heme oxygenase-1 in COVID-19
2020, Toxicology ReportsModulation of the monocyte/macrophage system in heart failure by targeting heme oxygenase-1
2019, Vascular PharmacologyStudy on the detoxification mechanisms to 5,10,15,20-tetrakis (4-sulfonatophenyl) porphyrinato iron(III) chloride (FeTPPS), an efficient pro-oxidant of heme water-soluble analogue
2018, Journal of Inorganic BiochemistryCitation Excerpt :Upregulation of HO-1 represents one of the most critical cytoprotective mechanisms in maintaining antioxidant/oxidant homeostasis. Many studies even reported the upregulation of HO-1 induced by heme make heme as an indirect anti-oxidant at nontoxic concentrations and plays a key role in preventing injury caused by many diseases [34–45]. It suggests that the deleterious effects of heme exhibit only at high concentration when the protective ability of heme detoxification is overwhelmed.
Systemic hemin therapy attenuates blood-brain barrier disruption after intracerebral hemorrhage
2014, Neurobiology of DiseaseCitation Excerpt :Delaying the first hemin injection until 3 h after ICH induction did not significantly diminish this effect. Although a hemin dose approximating 26 mg/kg hemin has frequently been employed in animal studies (Attuwaybi et al., 2004; Belcher et al., 2006; Hangaishi et al., 2000; Takizawa et al., 1998), the dose of ferric heme that is currently approved for human use is 1–4 mg/kg administered daily for 3–14 days, with a recommended daily dose of 3–4 mg/kg (Anderson et al., 2005) and a maximum of 6 mg/kg/24 h. To further test the translational relevance of hemin therapy, additional experiments were conducted using a similar dose (4 mg/kg). Evans blue leakage into the striatal parenchyma in mice treated with this lower hemin dose was somewhat greater than at the higher dose but was about half of that observed in vehicle-treated mice (Fig. 3).
Histopathological and immunohistochemical alterations in rat heart after thyroidectomy and the role of hemin and ketoconazole in treatment
2012, Biomedicine and Pharmacotherapy
- 1
To whom correspondence should be addressed at Department of Cardiovascular Medicine, University of Tokyo, Graduate School of Medicine, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-8655, Japan. Fax: 81-3-3974-2236. E-mail: [email protected].