Ischemic preconditioning enhances hepatocyte proliferation in the early phase after ischemia under hemi-hepatectomy in rats

Jin, Liming; Jin, Shuifang; Liu, Yuan; Zhou, Lin; Xie, Haiyang; Yan, Sheng; Xu, Xiao; Zheng, Shusen

doi:10.1016/s1499-3872(12)60217-3

Cited by 11 publications

(10 citation statements)

References 34 publications

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“…This was confirmed by the decreased serum ALT and AST levels observed in the IPC group compared with the I/R group. In agreement with our findings, remote ischemic preconditioning (RIP) and N-acetylcysteine with RIP, as well as other ischemic preconditioning methods have been shown to exert protective effects against reperfusion injury in rats (26)(27)(28). Of note, in our study, IPC reversed the I/R-induced increase in MDA activity, as well as the I/R-induced decrease in SOD activity in the liver tissue, as mentioned above.…”

Section: Discussionsupporting

confidence: 93%

Ischemic preconditioning increases GSK-3β/β-catenin levels and ameliorates liver ischemia/reperfusion injury in rats

Yan

Li²,

Tian

et al. 2015

International Journal of Molecular Medicine

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Ischemic preconditioning (IPC) ameliorates ischemia/reperfusion (I/R) injury in a number of organs, and the glycogen synthase kinase-3β (GSK-3β)/β-catenin signaling pathway regulates I/R-induced proliferation and apoptosis in the central nervous system and heart. However, the function of this signaling pathway in IPC during liver I/R remains unclear. Thus, in this study, we aimed to investigte the role of the GSK-3β/β-catenin pathway during I/R and following ischemic preconditioning. For this purpose, 30 Sprague-Dawley rats were randomly divided into the sham-operated, the I/R and the IPC groups (n=10). Following reperfusion, liver pathology, as well as alanine aminotransferase (ALT), aspartate aminotransferase (AST), maleic dialdehyde (MDA) and superoxide dismutase (SOD) levels were assessed. Western blot analysis was performed to quantify the GSK-3β, Ser9-phospho-GSK-3β (p-GSK-3β), cytosolic and nuclear β-catenin, vascular endothelial growth factor (VEGF), Bcl-2 and survivin levels. In addition, the Bcl-2 and survivin mRNA levels were assessed by RT-qPCR. Compared with the sham-operated group, I/R increased serum ALT, AST and MDA activity and decreased SOD levels, while IPC significantly decreased serum ALT, AST and MDA activity and increased SOD levels, compared with the I/R group. Simultaneously, I/R increased p-GSK-3β protein expression, and decreased Bcl-2 and survivin protein and mRNA levels. IPC further increased the protein expression of p-GSK-3β, and also increased cytosolic and nuclear β-catenin and VEGF expression compared with the I/R group; the expression of Bcl-2 and survivin was also increased by IPC, both at the mRNA and protein level. The total GSK-3β expression remained unaltered in all the groups. In conclusion, our data demonstrate that IPC exerts protective effects against liver injury induced by I/R and activates the GSK-3β/β-catenin signaling pathway.

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Section: Discussionsupporting

confidence: 93%

Ischemic preconditioning increases GSK-3β/β-catenin levels and ameliorates liver ischemia/reperfusion injury in rats

Yan

Li²,

Tian

et al. 2015

International Journal of Molecular Medicine

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“…Since the liver has an abundant blood supply, hepatic portal occlusion is often adopted in order to reduce hemorrhage during the operation; however, this method may lead to hepatic IRI (14). In the present study, in order to generate a rat model of hepatic acute IRI, an atraumatic vascular clamp was used to completely block the first porta hepatis, which was reopened following 35 min in order to recover the hepatic blood inflow.…”

Section: Discussionmentioning

confidence: 99%

Effects of melatonin on liver function and lipid peroxidation in a rat model of hepatic ischemia/reperfusion injury

Deng

Liu

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. The present study aimed to investigate the effects of melatonin (MT) on liver function and lipid peroxidation following hepatic ischemia-reperfusion injury (IRI). A total of 66 male Sprague-Dawley rats were randomly assigned into three groups: Normal control (N) group, ischemia-reperfusion (IR) group and the MT-treated group. A hepatic IRI model was developed by blocking the first porta hepatis, and subsequently restoring hepatic blood inflow after 35 min. Following reperfusion, changes in the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) were detected by a chemical method at various time points. In the MT group, the MDA levels were significantly reduced (P<0.05) at all time points, as compared with the IR group. Furthermore, SOD activity was significantly increased (P<0.05) in the MT group, as compared with the IR group at all time points; and the levels of GSH in the MT group were significantly higher (P<0.05) than those of the IR group at 2, 4, and 8 h post-reperfusion. The levels of ALT, AST and LDH were significantly reduced in the MT group at each time point, as compared with that of the IR group (P<0.05). In conclusion, MT exhibits potent antioxidant properties that may create favorable conditions for the recovery of liver function following IRI. IntroductionIn order to effectively control bleeding during hepatobiliary surgery, hepatic portal occlusion is often used, as it can temporarily interrupt the portal vein and hepatic artery inflow. This method is widely accepted since it is clinically simple, practical and effective; however, there is an inherent risk of subsequent liver ischemia-reperfusion injury (IRI). Therefore, in recent years, clinical research in the field of hepatic surgery has focused on how to reduce blood loss and improve the safety of hepatic portal occlusion, whilst simultaneously reducing the risk of liver IRI.Previous studies investigating tissues and organs such as the brain, heart, kidney and retina have demonstrated that numerous free radicals are produced during IRI, when the endogenous radical scavengers cannot function appropriately, leading to cell damage (1,2). Therefore, investigating effective drugs that alleviate IRI-induced functional liver damage, and improve the postoperative survival rate, has become a research hotspot in the field of hepatic surgery. Melatonin (MT) is a neural endocrine hormone that is secreted by the pineal gland (PG), which exerts known antioxidant, antitoxic, anti-stress and anti-inflammatory effects (3,4). Previous studies have demonstrated that MT has a protective role in IRI of the brain, heart, kidney and retina (5); however, its protective effects in liver IRI and the underlying mechanism require further research. An animal model of hepatic portal occlusion was used in the present study. MT was administered in advance, and the influence and significance of MT on antioxidant capacity, lipid peroxidation ...

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“…Hemorrhage control procedures performed during surgical operations on blood-rich liver cause I/R damage [18]. In recent years, clinical researches made on the field of hepatic surgery have focused on how to reduce blood loss and I/R damage more safely [19].…”

Section: Discussionmentioning

confidence: 99%

The effect of Liv-52 on liver ischemia reperfusion damage in rats

Cimen¹,

Eken²,

Çimen³

et al. 2019

Preprint

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Background: Liver ischemia reperfusion (I/R) damage is frequently seen in clinical hepatobiliary surgeries and there is no effective treatment for it. Liv-52, known to have hepatoprotective effects, is a natural antioxidant drug licensed by Ministry of Health of India. Therefore, the aim of our study is to investigate the effect of Liv-52 on liver damage induced by I/R in rats. Methods: Albino Wistar male rats were divided into three groups; liver I/R (IR), 20 mg/kg Liv-52 + liver ischemia reperfusion (LIR) and sham operation applied to control group (HG). Liv-52 was administered to the LIR group (n-6) one hour prior to I/R application and distilled water was given orally to IR (n-6) and HG (n-6) groups as a solvent. In animals, ischemia was determined as one hour, and reperfusion was identified as six hours. Results: Increased levels of alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase, malondialdehyde, myeloperoxidase, and decreased levels of superoxide dismutase, and glutathione related enzymes caused by I/R application have been converged to healthy group level with Liv-52 treatment and the damage occurred in liver tissue has been improved histopathologically. Conclusions: Liv-52 may be beneficial for preventing liver I/R damage in pre-surgery application.

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Ischemic preconditioning enhances hepatocyte proliferation in the early phase after ischemia under hemi-hepatectomy in rats

Cited by 11 publications

References 34 publications

Ischemic preconditioning increases GSK-3β/β-catenin levels and ameliorates liver ischemia/reperfusion injury in rats

Ischemic preconditioning increases GSK-3β/β-catenin levels and ameliorates liver ischemia/reperfusion injury in rats

Effects of melatonin on liver function and lipid peroxidation in a rat model of hepatic ischemia/reperfusion injury

The effect of Liv-52 on liver ischemia reperfusion damage in rats

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