Intermittent Ischemic Preconditioning Protects Against Hepatic Ischemia-Reperfusion Injury and Extensive Hepatectomy in Steatotic Rat Liver

Sikalias, Nikolaos; Karatzas, Theodore; Alexiou, Konstantinos; Mountzalia, Lamprini; Demonakou, Maria; Kostakis, Ioannis D.; Zacharioudaki, Argyro; Papalois, Αpostolos; Kouraklis, Gregory

doi:10.1080/08941939.2017.1334844

Cited by 15 publications

(13 citation statements)

References 71 publications

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“…It has been reported that programmed transient ischemia-reperfusion during shock, or during resuscitation also has protective effects [16]. Second, the protective effect of IPC is more prominent in primary hepatic I/RI in special cases, such as fatty and senile liver [10,13,29]. This study showed that RIPC-activated autophagy plays a role in hepatoprotection after hemorrhagic shock, but to what extent autophagy is the underlying mechanism and whether RIPC plays a more prominent role in special groups need further investigation.…”

Section: Discussionmentioning

confidence: 99%

Remote Ischemic Preconditioning Attenuates Hepatic Ischemia/Reperfusion Injury after Hemorrhagic Shock by Increasing Autophagy

Zhou¹,

Li²,

Sun³

et al. 2021

Int. J. Med. Sci.

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Section: Discussionmentioning

confidence: 99%

Remote Ischemic Preconditioning Attenuates Hepatic Ischemia/Reperfusion Injury after Hemorrhagic Shock by Increasing Autophagy

Zhou¹,

Li²,

Sun³

et al. 2021

Int. J. Med. Sci.

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“…They have been used as animal models, mice and rats in genetic, nutritional and mixed models for the development of NAFLD ( 2 , 29 – 32 ). NAFLD developmental dietary models are rather more reliable research tools.…”

Section: Discussionmentioning

confidence: 99%

“…The most frequently used experimental models of NAFLD concern the choline or choline/ methionine- free diet ( 2 , 30 , 46 ). The absence of choline disrupts the synthesis of phosphatidylcholine in the liver, leading to accumulation of triglycerides in the hepatocyte and development of hepatic steatosis ( 2 , 14 , 29 , 2 ). Feeding with a choline-free diet causes severe chronic-dependent hepatic steatosis, characterized by inflammation, with or without mild fibrosis, while prolonged feeding can cause even neoplasia ( 2 , 14 , 28 – 30 , 46 ).…”

Section: Discussionmentioning

confidence: 99%

Histopathological changes and onset of severe hepatic steatosis in rats fed a choline‑free diet

et al. 2018

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Hepatic steatosis significantly increases morbidity and mortality associated with major liver surgery. Several rodent models of hepatic steatosis have been previously reported, which aimed to investigate the effect of various pharmaceutical agents and interventional procedures on the pathophysiology of steatotic liver. The aim of the present study was to investigate the time frame of severe hepatic steatosis in rats after they were fed a choline-free diet and any associated histopathological changes. The duration of feeding with a choline-free diet required to develop severe hepatic steatosis was investigated in Wistar rats. The severity of hepatic steatosis in liver specimens was evaluated at 8, 10, 12 and 14 weeks following the onset of the choline-free diet. Comparisons were made with rats receiving standardized laboratory food. Feeding rats for 12–13 weeks with a choline-free diet led to 66% fatty liver infiltration, which exceeded 68% after 14 weeks. Prior to 8 weeks, the fatty infiltration reached 43%, with a gradual increase revealing a stronger rate from 8–12 weeks and a gradual decline after 14 weeks. At 12–13 weeks the fatty infiltration was considered representative of severe hepatic steatosis. Macrovesicular fatty infiltration revealed a significant increase at a steady rate between 8 and 14 weeks, with evidence of the onset of lobular inflammation and steatohepatitis after 14 weeks of feeding with the choline-free diet. Microvesicular fatty infiltration demonstrated a lower growth rate between 8 and 12 weeks while maintaining a steady rate between 12 and 14 weeks. Mixed fatty infiltration maintained its steady rate of hepatic parenchyma from 8.8–9.5%. Rats fed with the standard laboratory diet did not demonstrate fatty infiltration >4.5%, so they did not develop hepatic steatosis. Developing an ideal model of hepatic steatosis is a particular challenge. The findings of the present study indicate that severe hepatic steatosis in rodents may lead to the development of steatohepatitis after feeding with a choline-free diet for at least 14 weeks. This model is of particular interest in experimental liver surgery and associated surgical maneuvers, and is easily reproducible.

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“…A number of animal and clinical studies have assessed the protective efficacy of IPC in liver transplantation and hepatectomy 16,17 . Some animal studies showed hepatic protection of RIPer from warm IRI 14,18 .…”

Section: Introductionmentioning

confidence: 99%

Impact of combined ischemic preconditioning and remote ischemic perconditioning on ischemia-reperfusion injury after liver transplantation

Wang

et al. 2018

Sci Rep

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Ischemic preconditioning (IPC) and remote ischemic perconditioning (RIPer) confer protective effects against liver ischemia-reperfusion injury (IRI), but data about RIPer applying in liver transplantation is lacking. The study aimed to evaluate whether the combination of IPC and RIPer provides reinforced protective effects. C57BL/6 mice (160 pairs) were allocated into four groups: control, subjected to liver transplantation only; IPC, donor hilar was clamped for 10 min followed by 15 min of reperfusion; RIPer, three cycles of occlusion (5 min) and opening (5 min) of femoral vascular bundle were performed before reperfusion; IPC + RIPer, donors and recipients were subjected to IPC and RIPer respectively. Liver tissues were obtained for histological evaluation, TUNEL staining, malondialdehyde assays, GSH-Px assays, and NF-κB p65 protein and Bcl-2/Bax mRNA analyses. Blood samples were used to evaluate ALT, AST, TNF-α, NOx levels and flow cytometry. We found that protective efficacy of RIPer is less than IPC in terms of ALT, TNF-α, GSH-Px and NOx at 2 h postoperation, but almost equivalent at 24 h and 72 h postoperation. Except for Suzuki scores, ALT, Bcl-2/Bax mRNA ratio, other indices showed that combined treatment brought enhanced attenuation in IRI, compared with single treatment, through additive effects on antioxidation, anti-apoptosis, modulation of microcirculation disturbance, and inhibition of innate immune response. This study suggested a combined strategy that could enhance protection against IRI in clinical liver transplantation, otherwise, provided a hint that RIPer’s mechanism might be partly or totally different from IPC in humoral pathway.

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Intermittent Ischemic Preconditioning Protects Against Hepatic Ischemia-Reperfusion Injury and Extensive Hepatectomy in Steatotic Rat Liver

Abstract: Hepatic steatosis and IRI after major liver surgery largely affect morbidity and mortality. Intermittent IPC, 24 hours before IRI and extensive hepatectomy, presents higher 30-day survival and improved liver function parameters.

Cited by 15 publications

References 71 publications

Remote Ischemic Preconditioning Attenuates Hepatic Ischemia/Reperfusion Injury after Hemorrhagic Shock by Increasing Autophagy

Remote Ischemic Preconditioning Attenuates Hepatic Ischemia/Reperfusion Injury after Hemorrhagic Shock by Increasing Autophagy

Histopathological changes and onset of severe hepatic steatosis in rats fed a choline‑free diet

Impact of combined ischemic preconditioning and remote ischemic perconditioning on ischemia-reperfusion injury after liver transplantation

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