Ischemic Preconditioning Produces Comparable Protection Against Hepatic Ischemia/Reperfusion Injury Under Isoflurane and Sevoflurane Anesthesia in Rats

Jeong, Ji Seon; Kim, D.; Kim, K.Y.; Sun, Ruihong; Han, Seok Joo; Shin, Byung Seop; Kim, G.S.; Gwak, Mi Sook; Ko, Justine S.

doi:10.1016/j.transproceed.2017.07.002

Cited by 18 publications

(21 citation statements)

References 35 publications

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“…At the end of the reperfusion period, the rat was killed by exsanguination under anesthesia. While there is evidence that volatile anesthetics such as isofluorane and sevofluorane give some protection against IR injury, recent studies have shown that ischemic preconditioning can give substantial protection against IR injury over and above any provided by the volatile anesthetic itself (Bedirli et al, 2008;Jeong et al, 2017). These results indicate that, while isofluorane may have some effect on the progression of IR and recovery of the liver from IR, this is likely small, and in the present study is a constant factor in all experiments.…”

Section: Surgical Procedures For Ischemia and Reperfusion And Measurementioning

confidence: 47%

Evidence that decreased expression of sinusoidal bile acid transporters accounts for the inhibition by rapamycin of bile flow recovery following liver ischemia

Afroz

Jonkman

Jin

et al. 2018

European Journal of Pharmacology

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Rapamycin is employed as an immunosuppressant following organ transplant and, in patients with hepatocellular carcinoma, to inhibit cancer cell regrowth following liver surgery. Preconditioning the liver with rapamycin to induce the expression of antioxidant enzymes is a potential strategy to reduce ischemia reperfusion (IR) injury. However, pre-treatment with rapamycin inhibits bile flow, especially following ischemia. The aim was to investigate the mechanisms involved in this inhibition. In a rat model of segmental hepatic ischemia and reperfusion, acute administration of rapamycin by intravenous injection did not inhibit the basal rate of bile flow. Pre-treatment of rats with rapamycin for 24 h by intraperitoneal injection inhibited the expression of mRNA encoding the sinusoidal influx transporters Ntcp, Oatp1 and 2 and the canalicular efflux transporter Bsep, and increased expression of canalicular Mrp2. Dose-response curves for the actions of rapamycin on the expression of Bsep and Ntcp in cultured rat hepatocytes were biphasic, and monophasic for effects on Oatp1. In cultured tumorigenic H4IIE liver cells, several bile acid transporters were not expressed, or were expressed at very low levels compared to hepatocytes. In H4IIE cells, rapamycin increased expression of Ntcp, Oatp1 and Mrp2, but decreased expression of Oatp2. It is concluded that the inhibition of bile flow recovery following ischemia observed in rapamycin-treated livers is principally due to inhibition of the expression of sinusoidal bile acid transporters. Moreover, in tumorigenic liver tissue the contribution of tumorigenic hepatocytes to total liver bile flow is likely to be small and is unlikely to be greatly affected by rapamycin.

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Section: Surgical Procedures For Ischemia and Reperfusion And Measurementioning

confidence: 47%

Evidence that decreased expression of sinusoidal bile acid transporters accounts for the inhibition by rapamycin of bile flow recovery following liver ischemia

Afroz

Jonkman

Jin

et al. 2018

European Journal of Pharmacology

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“…In recent years, peroxisome proliferator activated receptor gamma (PPARγ), long noncoding RNAs (lncRNAs), and microRNAs (miRNAs) have been reported to play important roles to relieve hepatic I/R injury 6‐8 . In animal experiments, ischaemic pre‐conditioning and low‐temperature reperfusion alleviated hepatic I/R injury, but these preclinical findings are not yet translatable to clinical procedures 9,10 . Currently, there are few effective therapeutic strategies for protecting against I/R‐induced hepatic injury 2 …”

Section: Introductionmentioning

confidence: 99%

Remifentanil up‐regulates HIF1α expression to ameliorate hepatic ischaemia/reperfusion injury via the ZEB1/LIF axis

Zhou

Mei

et al. 2020

J Cellular Molecular Medi

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Ischaemia/reperfusion (I/R)‐induced hepatic injury is regarded as a main reason of hepatic failure after transplantation or lobectomy. The current study aimed to investigate how the opioid analgesic remifentanil treatment affects I/R‐induced hepatic injury and explore the possible mechanisms related to HIF1α. Initially, an I/R‐induced hepatic injury animal model was established in C57BL/6 mice, and an in vitro hypoxia‐reoxygenation model was constructed in NCTC‐1469 cells, followed by remifentanil treatment and HIF1α silencing treatment. The levels of blood glucose, lipids, alanine transaminase (ALT) and aspartate transaminase (AST) in mouse serum were measured using automatic chemistry analyser, while the viability and apoptosis of cells were detected using CCK8 assay and flow cytometry. Our results revealed that mice with I/R‐induced hepatic injury showed higher serum levels of blood glucose, lipids, ALT and AST and leukaemia inhibitory factor (LIF) expression, and lower HIF1α and ZEB1 expression (P < .05), which were reversed after remifentanil treatment (P < .05). Besides, HIF1α silencing increased the serum levels of blood glucose, lipids, ALT and AST (P < .05). Furthermore, hypoxia‐induced NCTC‐1469 cells exhibited decreased HIF1α and ZEB1 expression, reduced cell viability, as well as increased LIF expression and cell apoptosis (P < .05), which were reversed by remifentanil treatment (P < .05). Moreover, HIF1α silencing down‐regulated ZEB1 expression, decreased cell viability, and increased cell apoptosis (P < .05). ZEB1 was identified to bind to the promoter region of LIF and inhibit its expression. In summary, remifentanil protects against hepatic I/R injury through HIF1α and downstream effectors.

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“…Some strategies, including ischemic preconditioning, ischemic postconditioning, and machine perfusion, are already used to attenuate the damage induced by reperfusion. During the period of the perfusion, a short-term ischemic preconditioning, to make the organism adaptive to the subsequent long ischemia, is an effective endogenous protective phenomenon, but the mechanism is poorly understood [ 14 ]. De Almeida et al illuminated that hepatic preconditioning ameliorated liver IRI by reducing lipid peroxidation [ 15 ].…”

Section: Current Strategies For Ameliorating Liver Ischemia-reperfmentioning

confidence: 99%

Novel Targets for Treating Ischemia-Reperfusion Injury in the Liver

Yang

Chen

Meng

et al. 2018

IJMS

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Liver ischemia-reperfusion injury (IRI) is a major complication of hemorrhagic shock, liver transplantation, and other liver surgeries. It is one of the leading causes for post-surgery hepatic dysfunction, always leading to morbidity and mortality. Several strategies, such as low-temperature reperfusion and ischemic preconditioning, are useful for ameliorating liver IRI in animal models. However, these methods are difficult to perform in clinical surgeries. It has been reported that the activation of peroxisome proliferator activated receptor gamma (PPARγ) protects the liver against IRI, but with unidentified direct target gene(s) and unclear mechanism(s). Recently, FAM3A, a direct target gene of PPARγ, had been shown to mediate PPARγ’s protective effects in liver IRI. Moreover, noncoding RNAs, including LncRNAs and miRNAs, had also been reported to play important roles in the process of hepatic IRI. This review briefly discussed the roles and mechanisms of several classes of important molecules, including PPARγ, FAM3A, miRNAs, and LncRNAs, in liver IRI. In particular, oral administration of PPARγ agonists before liver surgery or liver transplantation to activate hepatic FAM3A pathways holds great promise for attenuating human liver IRI.

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Ischemic Preconditioning Produces Comparable Protection Against Hepatic Ischemia/Reperfusion Injury Under Isoflurane and Sevoflurane Anesthesia in Rats

Cited by 18 publications

References 35 publications

Evidence that decreased expression of sinusoidal bile acid transporters accounts for the inhibition by rapamycin of bile flow recovery following liver ischemia

Evidence that decreased expression of sinusoidal bile acid transporters accounts for the inhibition by rapamycin of bile flow recovery following liver ischemia

Remifentanil up‐regulates HIF1α expression to ameliorate hepatic ischaemia/reperfusion injury via the ZEB1/LIF axis

Novel Targets for Treating Ischemia-Reperfusion Injury in the Liver

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