Heat Shock Preconditioning Ameliorates Liver Injury Following Normothermic Ischemia–Reperfusion in Steatotic Rat Livers

Yamagami, Kazuhiko; Yamamoto, Yūzō; Kume, Makoto; Kimoto, Sayuri; Yamamoto, Hidekazu; Ozaki, Nobuhiro; Yamamoto, Masayuki; Sugiyama, Yasuyuki; Toyokuni, Shinya; Yamaoka, Yoshio

doi:10.1006/jsre.1998.5403

Cited by 57 publications

(42 citation statements)

References 28 publications

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“…It has been similarly reported in the liver that ischemic or heat shock preconditioning exerts a protective effect on hepatic ischemia-reperfusion injury. [10][11][12][13][14][15][16][17][18]24 Although little is known about the molecular basis of the preconditioning, oxidative stress seems to be one of the causes. Peralta et al 15,25 and Yin et al 26 have reported the role of nitric oxide and free radicals during ischemic preconditioning in the liver.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, HSPs induced by the stresses may also play a critical role for the subsequent hepatic injury. [17][18][19] In Pringle' s maneuver in liver surgery and liver transplantation, the ischemia-reperfusion is an unavoidable process and the protection against liver damage induced by the operation is one of the major problems. Ischemia-reperfusion injury is considered to be related to the generation of free oxygen radicals, which is also implicated in the cellular response to several agents associated with pathophysiological and pathological stresses.…”

Section: Discussionmentioning

confidence: 99%

“…Yamaoka' s group has recently reported that ischemic or heat shock preconditioning induces HSP72 in the liver and the induced HSP72 may reduce the succeeding ischemia-reperfusion injury. 17,18 Similarly, Marber et al 19 reported in the heart that brief ischemia or heat stress induced HSP72 and the HSP72 was associated with resistance to myocardial infarction. 19 The possibility of initiating the stress response by pharmacological preconditioning has been reported.…”

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confidence: 98%

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Doxorubicin preconditioning: A protection against rat hepatic ischemia-reperfusion injury

Itō

Ozasa²,

Sanada

et al. 2000

Hepatology

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Doxorubicin produces clinically useful responses in a variety of human cancers. However, the toxicity of doxorubicin has limited its usefulness. This side effect is mainly due to the doxorubicin-mediated free radical formation. Administration of doxorubicin (10 mg/kg body weight) to rats intravenously induces heme oxygenase-1 (HO-1) in the liver. The levels of HO-1 protein were first detected at 6 hours and peaked at about 18 to 24 hours after the injection. It is known that HO-1 plays a protective role against the oxidative injury. Therefore, we have examined the protective effect of doxorubicin preconditioning against the hepatic ischemia-reperfusion injury. Partial hepatic ischemia was produced in the left and medium lobes for 45 minutes followed by 120 minutes reperfusion. When low doses of doxorubicin (1 mg/kg body weight) was intravenously administered to rats 2 days before the ischemia, the serum alanine transaminase (ALT) levels in the preconditioning rat were clearly improved compared with those in the rat without preconditioning. Under this situation, zincprotoporphyrin IX, a specific inhibitor of HO-1, was injected subcutaneously to rats at 3 and 16 hours before the ischemia, the ALT levels were not improved by doxorubicin preconditioning. Histopathologic examination also supported these results. Although the HO-1 protein level was fairly low 2 days after the doxorubicin administration, significant amounts of HO-1 protein were detected. Our results indicated that the induction of HO-1 played a protective role against hepatic ischemia-reperfusion injury and that doxorubicin preconditioning is more clinically useful than other preconditioning methods. (HEPATOLOGY 2000;31:416-419.)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 98%

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Doxorubicin preconditioning: A protection against rat hepatic ischemia-reperfusion injury

Itō

Ozasa²,

Sanada

et al. 2000

Hepatology

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“…3 Recent studies have shown that the same phenomenon could also be observed in the liver. [4][5][6][7][8][9][10] In particular, 10-minute interruption of liver blood supply in anesthetized rats followed by 10 minutes of reperfusion reduces transaminases released during a subsequent 90-minute period of ischemia and 90-minute reoxygenation. 5 A similar effect has also been observed in steatosic livers following heat shock preconditioning.…”

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confidence: 99%

“…5 A similar effect has also been observed in steatosic livers following heat shock preconditioning. 7 Furthermore, ischemic preconditioning before cold preservation prevents reperfusion injury of liver endothelial cells 9 and increases rat survival after liver transplant. 6 Experiments performed using isolated hepatocyte suspensions show that the hepatoprotective action of liver preconditioning observed in vivo can be reproduced in vitro.…”

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Signal pathway involved in the development of hypoxic preconditioning in rat hepatocytes

Carini¹,

Cesaris²,

Splendore³

et al. 2001

Hepatology

102

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Ischemic preconditioning improves liver resistance to hypoxia and reduces reperfusion injury following transplantation. However, the intracellular signals that mediate the development of liver hypoxic preconditioning are largely unknown. We have investigated the signal pathway leading to preconditioning in freshly isolated rat hepatocytes. Hepatocytes were preconditioned by 10-minute incubation under hypoxic conditions followed by 10 minutes of reoxygenation and subsequently exposed to 90 minutes of hypoxia. Preconditioning reduced hepatocyte killing by hypoxia by about 35%. A similar protection was also obtained by preincubation with chloro-adenosine or with A 2A -adenosine receptor agonist CGS21680, whereas A 1 -adenosine receptor agonist N-phenyl-isopropyladenosine (R-PIA) was inactive. Conversely, the development of preconditioning was blocked by A 2 -receptor antagonist 3,7-dimethyl-1-propargylxanthine (DMPX), but not by A 1 -receptor antagonist 8-cyclopenthyl-1,3-dipropylxanthine (DPCPX). In either preconditioned or CGS21680-treated hepatocytes a selective activation of ␦ and protein kinase C (PKC) isoforms was also evident. Inhibition of heterotrimeric G i protein or of phospholypase C by, respectively, pertussis toxin or U73122, prevented PKC activation as well as the development of preconditioning. MEK inhibitor PD98509 did not interfere with preconditioning that was instead blocked by p38 MAP kinase inhibitor SB203580. The direct activation of p38 MAPK by anisomycin A mimicked the protection against hypoxic injury given by preconditioning. Consistently, an increased phosphorylation of p38 MAPK was observed in preconditioned or CGS21680-treated hepatocytes, and this effect was abolished by PKC-blocker, chelerythrine. We propose that a signal pathway involving A 2A -adenosine receptors, G i -proteins, phospholypase C, ␦-and -PKCs, and p38 MAPK, is responsible for the deve- The term ischemic preconditioning refers to the resistance to ischemic injury acquired by tissue following one or more brief periods of ischemia followed by reperfusion. 1,2 Ischemic preconditioning was first described in the myocardium, 1 but has been shown in several other organs, including the brain, the skeletal muscles, and the small intestine. 3 In the heart, ischemic preconditioning occurs in 2 phases: an early phase (early preconditioning) that immediately follows the transient hypoxia and lasts 2 to 3 hours and a late phase (late preconditioning), which begins 12 to 24 hours from the transient ischemia and lasts for about 3 to 4 days. 3 Recent studies have shown that the same phenomenon could also be observed in the liver. [4][5][6][7][8][9][10] In particular, 10-minute interruption of liver blood supply in anesthetized rats followed by 10 minutes of reperfusion reduces transaminases released during a subsequent 90-minute period of ischemia and 90-minute reoxygenation. 5 A similar effect has also been observed in steatosic livers following heat shock preconditioning. 7 Furthermore, ischemic preconditioning before cold preserva...

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Induction of the Stress Response In Vivo Decreases Nuclear Factor–Kappa B Activity in Jejunal Mucosa of Endotoxemic Mice

Pritts

Wang²,

Sun³

et al. 2000

Arch Surg

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Background: Results of previous studies suggest that the stress response protects cells and tissues by regulating proinflammatory mediators. The transcription factor nuclear factor-kappa B (NF-B), normally sequestered in the cytoplasm by its inhibitory protein, IB, regulates many genes involved in inflammatory responses to critical illness. Endotoxemia is associated with increased NF-B activity in intestinal mucosa, but the effect of the stress response on endotoxin-induced NF-B activation in intestinal mucosa is not known. Hypothesis: Induction of the stress response inhibits NF-B DNA binding activity in jejunal mucosa during endotoxemia. Methods: The stress response was induced in mice by hyperthermia (42°C) or injection with sodium arsenite (10 mg/kg). After 2 to 5 hours, mice were injected with endotoxin (lipopolysaccharide, 12.5 mg/kg) or a corresponding volume of sterile saline. One hour later, jejunal mucosa was harvested for preparation of nuclear and cytoplasmic extracts. Results: Mucosal levels of heat shock protein-72 increased after hyperthermia or treatment with sodium arsenite, consistent with induction of the stress response. The increase in NF-B DNA binding activity and decrease in IB-␣ levels seen after endotoxin injection were inhibited by previous induction of the stress response. Conclusion: The protective effects of the stress response in vivo might, at least in part, be due to inhibited NF-B activation.

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Heat Shock Preconditioning Ameliorates Liver Injury Following Normothermic Ischemia–Reperfusion in Steatotic Rat Livers

Cited by 57 publications

References 28 publications

Doxorubicin preconditioning: A protection against rat hepatic ischemia-reperfusion injury

Doxorubicin preconditioning: A protection against rat hepatic ischemia-reperfusion injury

Signal pathway involved in the development of hypoxic preconditioning in rat hepatocytes

Induction of the Stress Response In Vivo Decreases Nuclear Factor–Kappa B Activity in Jejunal Mucosa of Endotoxemic Mice

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