Effect of the Heme Oxygenase Inducer Hemin on Blood Haemostasis Measured by High‐frequency Ultrasound

Rochefort, Gaël Y.; Libgot, R.; Desbuards, Nicolas; Schlecht, Deborah; Ossant, F.; Eder, Véronique; Antier, Daniel

doi:10.1111/j.1440-1681.2007.04720.x

Cited by 3 publications

(2 citation statements)

References 41 publications

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“…In the present study,w eexamined for the first time the in-vivo potential anti-thrombotic effect of the HO-1inducerhemin in a highlyr eproducibler at vasculart hrombosis model (26).W e showedthat chronic hemin treatment prevented electric-induced carotid thrombosis without provoking major perturbations of haemostasis and pressure.Wechoose to study the effect of hemin at the dose of 50 mg/kg/donthe basis of our previous work designed to studythe hemin effects on the coagulation process (29) and where hemin, administrated at the concentration of 50 mg/ kg/d,a ppears to cause disturbance in haemostasis as heparin does.…”

Section: Discussionmentioning

confidence: 99%

Heme oxygenase-1 inducer hemin prevents vascular thrombosis

Desbuards¹,

Rochefort²,

Schlecht³

et al. 2007

Thromb Haemost

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Hemin is a heme oxygenase-1 (HO-1) inducer which provides endogenous carbon monoxide known for playing roles in cell proliferation, inflammation or aggregation process. The objective of the current study was to examine the effect of prophylactic treatment with hemin in a thrombosis vascular model. Three groups of Wistar rats, control (n = 6), hemin (n = 6) and hemin + HO-1 inhibitor (n = 6), were used for this study. Hemin-treated animals received hemin (50 mg/kg/d; I.P.) for seven days and HO-1 inhibitor group received hemin at the same dose and SnPP IX (60 mg/kg/d; I.P.). All animals were exposed to electric stimulation of the left carotid according to Kawasaki's procedure to induce reproducible thrombus formation. The hemin treatment did not induce blood pressure disturbance. Effects of hemin on vascular thrombosis were quantified by histopathology and its influence on haemostasis was assessed by measuring prothrombin time (PT), activated partial thromboplastin time (APTT) and blood parameters at the end of treatment. The HO-1 mRNA and protein level variation were also checked out. Results showed that chronic treatment with hemin significantly (p < 0.01) reduced the vascular occlusion degree when compared to control and hemin SnPP groups with 7.2 +/- 4.6 vs. 71.1 +/- 14.7 and 74.0 +/- 8.8%, respectively. Moreover, we observed significant (p < 0.05) perturbations of blood parameters in hemin-treated and hemin-SnPP treated rats. Interestingly, hemin treatment did not significantly increase both PT and APTT. Finally, the HO-1 mRNA and protein levels were increased in hemin-treated carotid artery. In conclusion, hemin by inducing HO-1 expression may be a preventive agent against clinical disorders associated to an increased risk of thrombosis events and may limit haemorrhagic risks.

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Section: Discussionmentioning

confidence: 99%

Heme oxygenase-1 inducer hemin prevents vascular thrombosis

Desbuards¹,

Rochefort²,

Schlecht³

et al. 2007

Thromb Haemost

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“…chronic hemin treatment after subtotal nephrectomy prevented the progression of CKD and was more efficient than the AT-1 receptor antagonist losartan in protecting the renal function. We have chosen to study the effect of hemin at the dose of 50 mg/kg/twice per week on the basis of our previous work describing the effect of chronic hemin treatment on vascular thrombosis in normotensive rats [12, 33]. This choice was reinforced by published toxicity studies in rats with high doses of hemin (93,168 and 300 mg/kg per day) which did not lead to liver or renal dysfunction [34].…”

Section: Discussionmentioning

confidence: 99%

Heme Oxygenase-1 Inducer Hemin Attenuates the Progression of Remnant Kidney Model

Desbuards

Hyvelin²,

Machet³

et al. 2009

Nephron Exp Nephrol

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Backgrounds/Aims: Heme oxygenase-1 (HO-1) has been shown to protect against fibrotic proliferation and apoptosis in several models of renal damage. The purpose of this study was to evaluate the impact of a treatment with the HO-1 inducer hemin on the progression of chronic kidney disease in nephrectomized rats versus the AT1 receptor antagonist losartan. Methods: The rats underwent 5/6 renal ablation and after the procedure received either losartan (20 mg/kg/day; n = 9), hemin (50 mg/kg/twice a week; n = 8) or vehicle (n = 8) over a 12-week period. At week 12, blood pressure was measured, urine, blood and remnant kidney were collected for biochemical (proteinuria, urea, creatinine) and histopathological (degrees of glomerulosclerosis and tubular atrophy) analysis. The expressions of HO-1, bone morphogenic protein 7 (BMP-7) and TGF-β were assessed by immunochemistry, and the level of the apoptosis marker protein caspase-3 by Western blot, on the remnant kidney. Results: Hemin significantly reduced blood pressure, proteinuria, inhibited the expression of TGF-β and caspase-3 protein and increased BMP-7 expression protein. Hemin-treated rats had lower glomerulosclerosis and tubular atrophy indexes than controls. Conclusion: Hemin treatment attenuates the progression of chronic kidney disease and appears more efficient than losartan in our rat model hypothetically because of the impact of hemin on the renal expression of BMP-7.

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Linking Labile Heme with Thrombosis

Hopp

Imhof

2021

JCM

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Thrombosis is one of the leading causes of death worldwide. As such, it also occurs as one of the major complications in hemolytic diseases, like hemolytic uremic syndrome, hemorrhage and sickle cell disease. Under these conditions, red blood cell lysis finally leads to the release of large amounts of labile heme into the vascular compartment. This, in turn, can trigger oxidative stress and proinflammatory reactions. Moreover, the heme-induced activation of the blood coagulation system was suggested as a mechanism for the initiation of thrombotic events under hemolytic conditions. Studies of heme infusion and subsequent thrombotic reactions support this assumption. Furthermore, several direct effects of heme on different cellular and protein components of the blood coagulation system were reported. However, these effects are controversially discussed or not yet fully understood. This review summarizes the existing reports on heme and its interference in coagulation processes, emphasizing the relevance of considering heme in the context of the treatment of thrombosis in patients with hemolytic disorders.

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Effect of the Heme Oxygenase Inducer Hemin on Blood Haemostasis Measured by High‐frequency Ultrasound

Cited by 3 publications

References 41 publications

Heme oxygenase-1 inducer hemin prevents vascular thrombosis

Heme oxygenase-1 inducer hemin prevents vascular thrombosis

Heme Oxygenase-1 Inducer Hemin Attenuates the Progression of Remnant Kidney Model

Linking Labile Heme with Thrombosis

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