2006•Journal of Hepatopancreatobiliary SurgeryRequires access

Protective role of heme oxygenase-1 on the liver ischemia/reperfusion injury

Zheng-yang Hu

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Abstract

Objective To investigate the protein expression of heme oxygenase-1(HO-1) after liver ischemia/reperfusion(I/R) and its influences. Methods The model of partial hepatic ischemia were established in Balb/C mice. 36 mice were divided at random into sham-operation group(S), liver ischemia/reperfusion group (I/R), and induce of HO-1(hemin) pretreatment group (HM). The protein expression of HO-1 was observed using immunohistochemical technique and assessed semi-quantitatively. The activity of serum aspartate transaminase (AST) and alanine transaminase(ALT) were assessed. The liver malondialdehyde(MDA) content, SOD activity and liver histpathological changes were detected respectively. Results Compared with that in S group, the expression of HO-1 was significantly increased in I/R group(p0.01). In I/R group, the liver enzymes and MDA content were obviously higher than those in S group (p0.01), but they were decreased obviously when pretreated with hemin. the SOD activity were significantly increased in I/R group, but redued in HM group. Under microscope, the histopathologic results revealed that the injury in HM group was mild compared with that in I/R group. Conclusion The HO-1 protein induced by hemin pretreatment may contribute to the protection on liver I/R injury.

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Objective To investigate the protein expression of heme oxygenase-1(HO-1) after liver ischemia/reperfusion(I/R) and its influences. Methods The model of partial hepatic ischemia were established in Balb/C mice. 36 mice were divided at random into sham-operation group(S), liver ischemia/reperfusion group (I/R), and induce of HO-1(hemin) pretreatment group (HM). The protein expression of HO-1 was observed using immunohistochemical technique and assessed semi-quantitatively. The activity of serum aspartate transaminase (AST) and alanine transaminase(ALT) were assessed. The liver malondialdehyde(MDA) content, SOD activity and liver histpathological changes were detected respectively. Results Compared with that in S group, the expression of HO-1 was significantly increased in I/R group(p0.01). In I/R group, the liver enzymes and MDA content were obviously higher than those in S group (p0.01), but they were decreased obviously when pretreated with hemin. the SOD activity were significantly increased in I/R group, but redued in HM group. Under microscope, the histopathologic results revealed that the injury in HM group was mild compared with that in I/R group. Conclusion The HO-1 protein induced by hemin pretreatment may contribute to the protection on liver I/R injury.

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Available abstract

Objective To investigate the protein expression of heme oxygenase-1(HO-1) after liver ischemia/reperfusion(I/R) and its influences. Methods The model of partial hepatic ischemia were established in Balb/C mice. 36 mice were divided at random into sham-operation group(S), liver ischemia/reperfusion group (I/R), and induce of HO-1(hemin) pretreatment group (HM). The protein expression of HO-1 was observed using immunohistochemical technique and assessed semi-quantitatively. The activity of serum aspartate transaminase (AST) and alanine transaminase(ALT) were assessed. The liver malondialdehyde(MDA) content, SOD activity and liver histpathological changes were detected respectively. Results Compared with that in S group, the expression of HO-1 was significantly increased in I/R group(p0.01). In I/R group, the liver enzymes and MDA content were obviously higher than those in S group (p0.01), but they were decreased obviously when pretreated with hemin. the SOD activity were significantly increased in I/R group, but redued in HM group. Under microscope, the histopathologic results revealed that the injury in HM group was mild compared with that in I/R group. Conclusion The HO-1 protein induced by hemin pretreatment may contribute to the protection on liver I/R injury.

Key concepts: Hemin, Malondialdehyde, Aspartate transaminase, Heme oxygenase, Alanine transaminase, Reperfusion injury, Heme, Ischemia

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