Protective effect of ischemic preconditioning on hepatic ischemia-reperfusion injury in mice

Tsuyama, Hiroshi; Shimizu, Koïchi; Yoshimoto, Keiichi; Nezuka, Hideaki; Ito, Hideki; Yamamoto, Shinya; Hasebe, Ken; Onishi, Ichiro; Muraoka, Keiichi; Ninomiya, Itasu; Tani, Takashi; Hashimoto, Takeji; Yagi, Minoru; Miwa, Koichi

doi:10.1016/s0041-1345(00)01677-8

Cited by 17 publications

(16 citation statements)

References 10 publications

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“…Previous reports have also demonstrated suppression of increased liver enzymes following IPC [29,32,33] . In our study, IPC did not influence liver parameters, indicating only slight ischemiareperfusion injuries judged on conventional blood samples.…”

Section: Discussionmentioning

confidence: 75%

Cytokine Changes during Warm Ischemia and Reperfusion of the Pig Liver with or without Preconditioning

Kannerup

Grønbæk²,

Funch‐Jensen³

et al. 2009

Eur Surg Res

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Background: Hepatic inflow occlusion results in ischemia-reperfusion injury. The aim of the present porcine study was to investigate whether the pro- and anti-inflammatory cytokine response is involved in mediating the protective effect of ischemic preconditioning (IPC) during, and after warm liver ischemia. Methods: Fifteen randomized pigs – 7 non-IPC and 8 (IPC) – underwent laparotomy followed by 60 min of total ischemia with or without IPC continued by 3 h of reperfusion. Plasma cytokines (IL-6, IL-8, IL-10, and TNF-α) were measured during the study period as well as liver parameters (alanine-aminotransferase, alkaline phosphatase, bilirubin, and prothrombin time). Results: In the IPC group, IL-6 increased significantly during reperfusion compared to baseline and the non-IPC group. TNF-α increased nonsignificantly in the non-IPC group, while the levels remained stable in the IPC group. IL-8 and IL-10 increased in both groups after reperfusion. Only minor differences were observed in liver parameters. Conclusions: Warm liver ischemia with or without IPC activates inflammatory cytokines. IL-6 increased significantly in the IPC group compared to the non-IPC group, while the opposite was observed for TNF-α. These cytokine changes may be involved in the hepatoprotective mechanism induced by IPC.

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Section: Discussionmentioning

confidence: 75%

Cytokine Changes during Warm Ischemia and Reperfusion of the Pig Liver with or without Preconditioning

Kannerup

Grønbæk²,

Funch‐Jensen³

et al. 2009

Eur Surg Res

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“…A brief ischemic insult can also induce ischemic tolerance in the spinal cord [164] and other organs, such as the heart [165], liver [166] or kidneys [167]. The exact molecular mechanisms underlying delayed ischemic tolerance are not well understood, but requirements for de novo protein synthesis [168], activation of the proinflammatory transcription factor NF-ĸB [162], and induction of inflammatory cytokines such as TNF, IL-1, IL-6 and IL-8 have been demonstrated.…”

Section: Immune System Modulationmentioning

confidence: 99%

Inflammatory and Neuroimmunomodulatory Changes in Acute Cerebral Ischemia

Brea

Sobrino

Castillo³

2009

Cerebrovasc Dis

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Neuronal death produced by cerebral ischemia activates innate immunity by Toll-like receptors and triggers inflammatory response. This response is necessary to remove cell debris and to start regenerative process. However, inflammatory response could exacerbate cerebral damage and it is involved in secondary brain damage. Therefore, organisms have developed different mechanisms to regulate inflammatory response. An accurate balance between inflammation and anti-inflammation is necessary to assure the removal of cell debris and to avoid secondary cell damage. New therapeutic targets could be designed to obtain a correct modulation of the immune system and to reduce cerebral brain damage after cerebral ischemia. In this paper, we review the function of the immune system in cerebral ischemia, particularly inflammation and immunomodulation.

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“…Other studies have suggested that additional apoptosis-regulating genes, such as c-jun, are involved in the protective effect of IPC and that IPC reduces transcription and inhibits apoptosis (203,205,210,220). IL-6 is another possible mediator of the IPC effect; however, studies have reported diverging results, including reports of hepatoprotection when IL-6 is administered as well as reports of reduced levels of IL-6 after IPC compared with I/R alone (206,207). IPC results in lower TNF-α levels than I/R alone, but depleting TNF-/-mice of TNF-α ameliorates the protective effect of IPC (206,207,213).…”

Section: Ischemic Preconditioning (Ipc)mentioning

confidence: 99%

“…IL-6 is another possible mediator of the IPC effect; however, studies have reported diverging results, including reports of hepatoprotection when IL-6 is administered as well as reports of reduced levels of IL-6 after IPC compared with I/R alone (206,207). IPC results in lower TNF-α levels than I/R alone, but depleting TNF-/-mice of TNF-α ameliorates the protective effect of IPC (206,207,213). Thus, it appears that a low dose of TNF-α is required for the protective effect of IPC, as previously suggested (221).…”

Section: Ischemic Preconditioning (Ipc)mentioning

confidence: 99%

Methods to Reduce Liver Ischemia/Reperfusion Injury

Björnsson¹

2014

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Protective effect of ischemic preconditioning on hepatic ischemia-reperfusion injury in mice

Cited by 17 publications

References 10 publications

Cytokine Changes during Warm Ischemia and Reperfusion of the Pig Liver with or without Preconditioning

Cytokine Changes during Warm Ischemia and Reperfusion of the Pig Liver with or without Preconditioning

Inflammatory and Neuroimmunomodulatory Changes in Acute Cerebral Ischemia

Methods to Reduce Liver Ischemia/Reperfusion Injury

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