An injury of the liver caused by ischemia-reperfusion in rat liver.

Egashira, Toru; Nagai, Takayuki; Kimba, Yoshihira; Murayama, Fumie; Goto, Shinichiro; Kudo, Yoshikuni; Sudo, Shinji; Kono, Takuya; Yamanaka, Yasumitsu

doi:10.1254/fpj.97.6_339

Cited by 11 publications

(3 citation statements)

References 26 publications

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“…As previously described (22,23), the MDA levels, which are derived from lipid peroxidation in liver tissue, increased after 60 min of reperfusion following 15 min of ischemia. However, when 100,000 U/kg of ULN was administered before ischemia, the MDA level increase was significantly suppressed (Fig.…”

Section: Lipid Peroxide Level In Liver Tissuesupporting

confidence: 67%

Protective Effect of Ulinastatin against Liver Injury Caused by Ischemia-Reperfusion in Rats.

1992

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ABSTRACT-The effects of ulinastatin (ULN), a human urinary protease inhibitor, on liver injury caused by ischemia-reperfusion were studied in rats. In the liver ischemia-reperfusion model, ULN sup pressed the elevation of serum transaminase levels and tissue lipid peroxide levels in the liver. ULN did not exhibit a radical-trapping action on the superoxide and hydroxyl radicals as measured by electron spin resonance (ESR). ULN suppressed formylmethionyl-leucyl-phenylalanine (FMLP) and phorbol myristate acetate (PMA)-induced superoxide production from polymorphonuclear leukocytes (PMNs) as measured by the cytochrome c assay. ULN did not inhibit either xanthine oxidase (XO) activity or the conversion of xanthine dehydrogenase (XDH) to XO during the ischemic period. ULN also strong ly protected against the hypotonic hemolysis of rat erythrocytes. These results suggest that ULN's mem brane stabilizing action and suppressive effect against PMNs superoxide production might be attributed to its suppressive effect on the liver's lipid peroxidation caused by ischemia-reperfusion.

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Section: Lipid Peroxide Level In Liver Tissuesupporting

confidence: 67%

Protective Effect of Ulinastatin against Liver Injury Caused by Ischemia-Reperfusion in Rats.

1992

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“…Our warm ischemia-reperfusion model was non-lethal in the normal liver 90 min and fatty liver ischemia groups, and it could be evaluated without secondary liver injury due to unrelated factors such as circulatory and respiratory failure. The blood ALT activity increased at R1h in normal livers in an ischemia-duration-dependent manner; it decreased at R6h in the group with less than 30 min of ischemia but did not recover in the I90 group, consistent with the findings a previous report [23]. ALT activity in fatty livers was similar to that in the I90/R1h group; however, it surpassed that in the I90/R6h group.…”

Section: Discussionsupporting

confidence: 90%

Warm Ischemia Induces Spatiotemporal Changes in Lysophosphatidylinositol That Affect Post-Reperfusion Injury in Normal and Steatotic Rat Livers

Shibata

Hayasaka

Sakamoto

et al. 2023

JCM

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Warm ischemia-reperfusion injury is a prognostic factor for hepatectomy and liver transplantation. However, its underlying molecular mechanisms are unknown. This study aimed to elucidate these mechanisms and identify the predictive markers of post-reperfusion injury. Rats with normal livers were subjected to 70% hepatic warm ischemia for 15, 30, or 90 min, while those with steatotic livers were subjected to 70% hepatic warm ischemia for only 30 min. The liver and blood were sampled at the end of ischemia and 1, 6, and 24 h after reperfusion. The serum alanine aminotransferase (ALT) activity, Suzuki injury scores, and lipid peroxidation (LPO) products were evaluated. The ALT activity and Suzuki scores increased with ischemic duration and peaked at 1 and 6 h after reperfusion, respectively. Steatotic livers subjected to 30 min ischemia and normal livers subjected to 90 min ischemia showed comparable injury. A similar trend was observed for LPO products. Imaging mass spectrometry of normal livers revealed an increase in lysophosphatidylinositol (LPI (18:0)) and a concomitant decrease in phosphatidylinositol (PI (18:0/20:4)) in Zone 1 (central venous region) with increasing ischemic duration; they returned to their basal values after reperfusion. Similar changes were observed in steatotic livers. Hepatic warm ischemia time-dependent acceleration of PI (18:0/20:4) to LPI (18:0) conversion occurs initially in Zone 1 and is more pronounced in fatty livers. Thus, the LPI (18:0)/PI (18:0/20:4) ratio is a potential predictor of post-reperfusion injury.

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“…2). Such abnormal leak ages of hepatic enzymes suggest that structural and func tional disorders in the hepatic microsomes also occurred, which were shown in our previous studies and by Frederiks et al (14,[17][18][19]. Therefore we examined the effects of Dic Na and a-toc.…”

Section: Discussionmentioning

confidence: 67%

Effect of Diclofenac, a Non-Steroidal Anti-Inflammatory Drug, on Lipid Peroxidation Caused by Ischemia-Reperfusion in Rat Liver

Takayama

Egashira

Yamanaka

1994

Japanese Journal of Pharmacology

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ABSTRACT-The present study investigated the effects of diclofenac sodium (Dic Na) on lipid peroxidation (LPO) and liver injury in ischemia-reperfused rats. LPO was estimated from the levels of phosphatidylcholine hydroperoxide (PCOOH), a primary peroxidative product of phosphatidylcholine. Hepatic ischemia-reperfusion induced significant elevation of plasma PCOOH and caused liver injury in rats. Rats were treated daily with Dic Na or a-tocopherol (a-toc.), p.o., for 5 days and once at 1 hr prior to induction of ischemia. Both substances prevented LPO from decreasing the plasma PCOOH level, and they significantly suppressed the elevation of serum GOT and LDH, in a dose-dependent manner. Dic Na was able to scavenge the stable free radical 1,1-diphenyl-2-picrylhydrazyl (DPPH), but did not show radical-trapping ability for superoxide anion (02-) or hydroxyl radicals (• OH), nor a suppressive ability for the NADPH-dependent LPO of microsomes. In contrast, a-toc. trapped both DPPH and 02-, but not • OH , and it inhibited the NADPH dependent LPO in vitro. These results suggest that Dic Na may suppress liver injury caused by ischemia-reperfusion through stable radical scavenging and the inhibition of super oxide production in activated phagocytes, both of which may restrain the induction and progression of oxidative stress.

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An injury of the liver caused by ischemia-reperfusion in rat liver.

Cited by 11 publications

References 26 publications

Protective Effect of Ulinastatin against Liver Injury Caused by Ischemia-Reperfusion in Rats.

Protective Effect of Ulinastatin against Liver Injury Caused by Ischemia-Reperfusion in Rats.

Warm Ischemia Induces Spatiotemporal Changes in Lysophosphatidylinositol That Affect Post-Reperfusion Injury in Normal and Steatotic Rat Livers

Effect of Diclofenac, a Non-Steroidal Anti-Inflammatory Drug, on Lipid Peroxidation Caused by Ischemia-Reperfusion in Rat Liver

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