Bucillamine improves hepatic microcirculation and reduces hepatocellular injury after liver warm ischaemia-reperfusion injury

Junnarkar, Sameer P; Tapuria, Niteen; Dutt, Neelanjana; Fuller, Barry; Seifalian, Alexander M.; Davidson, Brian R

doi:10.1111/j.1477-2574.2009.00054.x

Cited by 7 publications

(7 citation statements)

References 38 publications

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“…We have previously shown that bucillamine has a protective effect against liver IRI, which is related to its maintenance of the liver microcirculation 38 . This study has confirmed our previous findings that bucillamine can reduce warm IRI in the liver, and has studied the possible mechanism.…”

Section: Discussionsupporting

confidence: 89%

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Attenuation of warm ischemia–reperfusion injury in the liver by bucillamine through decreased neutrophil activation and Bax/Bcl‐2 modulation

Junnarkar

Tapuria

Mani

et al. 2010

J of Gastro and Hepatol

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Section: Discussionsupporting

confidence: 89%

“…This also correlates with the decreased histological grading of IRI seen on bucillamine infusion. This co‐related with our earlier observation of increased non‐viable nuclei with propidium iodide on intravital microscopy and its attenuation by bucillamine infusion 38 …”

Section: Discussionsupporting

confidence: 87%

Attenuation of warm ischemia–reperfusion injury in the liver by bucillamine through decreased neutrophil activation and Bax/Bcl‐2 modulation

Junnarkar

Tapuria

Mani

et al. 2010

J of Gastro and Hepatol

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“…During the transplantation, IRI is an unavoidable pathological process in the donor liver and is closely related to the primary non-function of the grafted liver [2]. Existing research [6,11] shows that liver IRI is divided into 2 stages: early injury and late injury, with very complicated mechanisms. Early injury on hepatocytes is directly induced by the cytokines, such as TNF-α, IL-1, and IL-6 released by activated KCs and a large amount of ROS.…”

Section: Discussionmentioning

confidence: 99%

“…Effective prevention and treatment for the IRI in the grafted liver can improve the function of the grafted liver and increase the success rate of liver transplantation. Thus, it is currently one of the hot topics in the field of liver surgery [4–6]. A large number of studies have shown that ischemic preconditioning, which refers to one or more transient IR episodes induced in body tissues or organs that confers a state of endogenous protection of body tissue and cells against subsequent long-term ischemic injuries [7], and drug pretreatment, including more than 8 kinds of drugs [8], can be helpful in the prevention and treatment of the grafted liver IRI [9,10].…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Apoptosis of Kupffer Cells Induced by Zoledronate Liposomes Following Hepatic Ischemia-Reperfusion Injury

Zhao

Han

et al. 2018

Ann Transplant

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BackgroundThe goal of this study was to observe the effect of the apoptosis of Kupffer cells (KCs) selectively induced by zoledronate liposomes following the hepatic ischemia-reperfusion injury (IRI) in the rat liver transplantation model and to explore its mechanisms.Material/MethodsThe rat liver transplantation model was established using the improved Kamada method. Male Sprague Dawley rats were randomly divided into 3 groups: no liver transplantation or drug treatment (Group A); donor rats were injected with 1 mL normal saline through the tail vein for 3 continuous days before transplantation, and the donor liver was preserved in cold for 2 hours (Group B); donor rats were injected with 1 mL zoledronate liposomes (0.001 mg/mL) through the tail vein for 3 continuous days before transplantation, and the donor liver was preserved in cold for 2 hours (Group C). At 24 hours after transplantation, the receiving rats were sacrificed for sampling.ResultsCompared with Group C and Group A, the bile secretion flow was dramatically decreased in Group B, whereas the serum liver function index [alanine aminotransferase (ALT), glutamate aminotransferase (AST), and γ-glutamyl transpeptidase (γ-GT)] was significantly increased (P<0.01), and the pathological injury area was obviously increased. Compared with Group B, the levels of serum interleukin1 (IL-1), tumor necrosis factor-α (TNF-α), and the apoptotic index in Group C were significantly decreased (P<0.05), and Suzuki scores of congestion, vacuolar degeneration, and necrosis were all reduced (P<0.05).ConclusionsThe apoptosis of KCs selectively induced by zoledronate liposomes inhibited the inflammatory cascade reaction induced by KC activation and reduced the release of cytokines and decreased the extent of IRI in the liver transplantation in animal model.

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“…There is experimental evidence that some pharmacological interventions [46,47] protect against liver IR injury in the animal model. In humans, a systematic review of randomized controlled trials assessing the role of pharmacologic interventions in decreasing IR injury after liver resections showed that some interventions such as methyl prednisolone decrease the enzyme markers of liver parenchymal injury after liver resections but without demonstrating evidence of clinical benefit [13] .…”

Section: Pharmacologic Interventions To Decrease Ir Injurymentioning

confidence: 99%

Current protective strategies in liver surgery

Gurusamy

González²,

Davidson³

2010

WJG

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During liver resection surgery for cancer or liver transplantation, the liver is subject to ischaemia (reduction in blood flow) followed by reperfusion (restoration of blood flow), which results in liver injury [ischemia-reperfusion (IR) or IR injury]. Modulation of IR injury can be achieved in various ways. These include hypothermia, ischaemic preconditioning (IPC) (brief cycles of ischaemia followed by reperfusion of the organ before the prolonged period of ischaemia i.e. a conditioning response), ischaemic postconditioning (conditioning after the prolonged period of ischaemia but before the reperfusion), pharmacological agents to decrease IR injury, genetic modulation of IR injury, and machine perfusion (pulsatile perfusion). Hypothermia decreases the metabolic functions and the oxygen consumption of organs. Static cold storage in University of Wisconsin solution reduces IR injury and has prolonged organ storage and improved the function of transplanted grafts. There is currently no evidence for any clinical advantage in the use of alternate solutions for static cold storage. Although experimental data from animal models suggest that IPC, ischaemic postconditioning, various pharmacological agents, gene therapy, and machine perfusion decrease IR injury, none of these interventions can be recommended in clinical practice. This is because of the lack of randomized controlled trials assessing the safety and efficacy of ischaemic postconditioning, gene therapy, and machine perfusion. Randomized controlled trials and systematic reviews of randomized controlled trials assessing the safety and efficacy of IPC and various pharmacological agents have demonstrated biochemical or histological improvements but this has not translated to clinical benefit. Further well designed randomized controlled trials are necessary to assess the various new protective strategies in liver resection.

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Bucillamine improves hepatic microcirculation and reduces hepatocellular injury after liver warm ischaemia-reperfusion injury

Abstract: Bucillamine reduces the hepatocellular injury of liver ischaemia reperfusion and improves parenchymal perfusion.

Cited by 7 publications

References 38 publications

Attenuation of warm ischemia–reperfusion injury in the liver by bucillamine through decreased neutrophil activation and Bax/Bcl‐2 modulation

Attenuation of warm ischemia–reperfusion injury in the liver by bucillamine through decreased neutrophil activation and Bax/Bcl‐2 modulation

Protective Effects of Apoptosis of Kupffer Cells Induced by Zoledronate Liposomes Following Hepatic Ischemia-Reperfusion Injury

Current protective strategies in liver surgery

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