Preconditioning with tin-protoporphyrin IX attenuates ischemia/reperfusion injury in the rat kidney

Kubo, Takashi; Tamaki, Tohru; Tanaka, Mitsuko; Uchida, Yasushi; Tsuchihashi, Seiichiro; Kawamura, Akio; Kakita, Akira

doi:10.1046/j.1523-1755.2003.00882.x

Cited by 61 publications

(44 citation statements)

References 43 publications

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“…It should be noted however, that hemin might not be simply an inducer of HO-1, but also of HO-2. 45 However, we think a role of HO-2 in our results unlikely because HO-2 expression was unmodified after CS and/or hemin exposure. Furthermore, we ensure that the effects of hemin were reversed by the HO inhibitor SnPP, which markedly reduced HO activity (Figure 1C), and opposite effects to those induced by hemin were observed by specific inhibition of HO-1 expression by an in vivo siRNA strategy.…”

Section: Discussionmentioning

confidence: 73%

Heme Oxygenase-1 Prevents Airway Mucus Hypersecretion Induced by Cigarette Smoke in Rodents and Humans

Almolki

Guénégou

Gołda

et al. 2008

The American Journal of Pathology

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We investigated the role of heme oxygenase-1 (HO-1), a powerful anti-inflammatory and anti-oxidant enzyme, in modulating cigarette smoke (CS)-induced mucus secretion. In both rats and mice, 5-day CS exposure increased HO-1 expression and activity, mucus secretion, MUCIN 5AC (MUC5AC) gene and protein expression, and local inflammation, along with up-regulation of dual oxidase 1 gene expression and both the activity and phosphorylation of the epidermal growth factor receptor, which is involved in MUC5AC induction. Pharmacological induction of HO-1 prevented these actions and inhibition of HO-1 expression by a specific siRNA potentiated them. In French participants to the European Community Respiratory Health Survey II (n ‫؍‬ 210, 30 to 53 years of age, 50% males) exposed to CS, a significant increase in the percentage of participants with chronic sputum was observed in those harboring at least one allele with a long (GT) n in the HO-1 promoter gene (>33 repeats), which is associated with a low level of HO-1 protein expression, compared with those with a short number of (GT)n repeats (21.7% versus 8.6% , P ‫؍‬ 0.047). No such results were observed in those who had never smoked (n ‫؍‬ 297). We conclude that HO-1 has a significant protective effect against airway mucus hypersecretion in animals and humans exposed to CS.

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Section: Discussionmentioning

confidence: 73%

Heme Oxygenase-1 Prevents Airway Mucus Hypersecretion Induced by Cigarette Smoke in Rodents and Humans

Almolki

Guénégou

Gołda

et al. 2008

The American Journal of Pathology

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“…8 The difficulty encountered in interpreting studies based on the use of metalloporphyrin HO inhibitors may be illustrated by studies using these inhibitors to evaluate the role of the HO system in renal ischemic injury: in this disease model, depending on the study, contrasting conclusions are reached in which the HO system is considered either a protectant against or a contributor to renal injury. 42,43 The Vol. 170,No.…”

Section: Discussionmentioning

confidence: 99%

Renal Hemodynamic, Inflammatory, and Apoptotic Responses to Lipopolysaccharide in HO-1−/− Mice

Tracz

Juncos

Grande

et al. 2007

The American Journal of Pathology

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؉/؉ mice. We conclude that HO-1 deficiency exhibits a heightened and dysregulated inflammatory response to LPS accompanied by greater impairment in renal hemodynamic response and widespread apoptosis of immune cells. Because polymorphisms in the HO-1 gene with diminished HO activity predispose to human disease, we speculate that our findings may be relevant to the clinical outcome in patients with sepsis syndromes.

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“…HO-1 plays an important role in the maintenance of renal function and in the protection of tubular cells, especially in the segment of the nephron susceptible to ischemic or toxic injury, as demonstrated by its protective function in in vivo and in vitro experimental models (11,13) . The protective function of HO-1 is believed to be associated with the action of one or more of the subproducts resulting from heme degradation: bilirubin, ferritin and carbon monoxide (14) . Curiously, administration of ZnPP, a highly specific and selective HO-1 and HO-1 inhibitor, did not result in alterations in renal function or in interference with the redox mechanism.…”

Section: Discussionmentioning

confidence: 99%

Proteção funcional da enzima heme-oxigenase-1 na lesão renal aguda isquêmica e tóxica

Dezoti

Watanabe

Pinto³

et al. 2009

Acta paul. enferm.

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Original ArticleProteção funcional da enzima heme-oxigenase-1 na lesão renal aguda isquêmica e tóxica Protección funcional de la enzima heme-oxigenasa-1 en la lesión renal aguda isquémica y tóxica RESUMOObjetivos: Verificar a proteção funcional da heme-oxigenase (HO-1), por meio do uso do seu indutor (Hemin) e seu inibidor químico (protoporfirina de zinco-ZnPP) na lesão renal aguda isquêmica e tóxica pela Polimixina B (PmxB) em ratos. Material: Foram utilizados ratos Wistar, adultos e machos divididos em 8 grupos: SHAM (controle), Isquemia (Isq), Isq+Hemin (indutor de HO-1), Isq+ZnPP (inibidor de HO-1), SALINA (controle), Polimixina B (PmxB), PmxB+Hemin, PmxB+ZnPP. Métodos: Jaffé (clearance de creatinina, Clcr) e FOX-2 (peróxidos urinários). Resultados: A isquemia (30´) dos pedículos reais e a administração de PmxB reduziu o Clcr com manutenção do fluxo urinário. Os peróxidos urinários se elevaram em ambas as lesões. A administração do Indutor de HO-1 determinou melhora da função renal e redução dos níveis de peróxidos urinários. Conclusão: Os resultados deste estudo demonstraram que a isquemia e a PmxB induzem LRA oxidativa. O indutor de HO-1 atenuou a lesão em ambos os modelos por atenuação do mecanismo redox. Descritores: Rim/lesões; Heme-oxigenase-1 RESUMEN Objetivos: Verificar la protección funcional de la heme-oxigenasa (HO-1), por medio del uso de su inductor (Hemin) y su inhibidor químico (protoporfirina de zinc-ZnPP) en la lesión renal aguda isquémica y tóxica producida por la Polimixina B (PmxB) en ratas. Material: Fueron utilizadas ratas Wistar, adultas y machos divididos en 8 grupos: SHAM (control), Isquemia (Isq), Isq+Hemin (indutor de HO-1), Isq+ZnPP (inibidor de HO-1), SALINA (control), Polimixina B (PmxB), PmxB+Hemin, PmxB+ZnPP. Métodos: Jaffé (clearance de creatinina, Clcr) y FOX-2 (peróxidos urinarios). Resultados: La isquemia (30´) de los pedículos reales y la administración de PmxB redujo el Clcr con manutención del flujo urinario. Los peróxidos urinarios se elevaron en ambas lesiones. La administración del Inductor de HO-1 determinó mejora de la función renal y reducción de los niveles de peróxidos urinarios. Conclusión: Los resultados de este estudio demuestran que la isquemia y la PmxB inducen AKL por la elevación de los peróxidos urinarios. El inductor de HO-1 atenuó la lesión en ambos modelos por atenuación del mecanismo redox. Descriptores: Riñón/lesión; Hemo-oxigenase-1

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Preconditioning with tin-protoporphyrin IX attenuates ischemia/reperfusion injury in the rat kidney

Cited by 61 publications

References 43 publications

Heme Oxygenase-1 Prevents Airway Mucus Hypersecretion Induced by Cigarette Smoke in Rodents and Humans

Heme Oxygenase-1 Prevents Airway Mucus Hypersecretion Induced by Cigarette Smoke in Rodents and Humans

Renal Hemodynamic, Inflammatory, and Apoptotic Responses to Lipopolysaccharide in HO-1−/− Mice

Proteção funcional da enzima heme-oxigenase-1 na lesão renal aguda isquêmica e tóxica

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