Nilotinib protects the murine liver from ischemia/reperfusion injury

Ocuin, Lee M.; Zeng, Shan; Cavnar, Michael J.; Sorenson, Eric C.; Bamboat, Zubin M.; Greer, Jonathan B.; Kim, Teresa S.; Popow, Rachel; DeMatteo, Ronald P.

doi:10.1016/j.jhep.2012.05.012

Cited by 48 publications

(46 citation statements)

References 50 publications

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“…JNK is related to the occurrence and development of tumors [25], ischemia-reperfusion (I/R) injury [26], immune inflammatory response [27], and other diseases. JNK is mainly localized in the cytoplasm.…”

Section: Discussionmentioning

confidence: 99%

Roles of the MST1-JNK signaling pathway in apoptosis of colorectal cancer cells induced by Taurine

Liu

Xia

Zhang

et al. 2018

Libyan Journal of Medicine

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The aim of this study was to observe the impact of the mammalian sterile 20-like kinase 1-c-Jun N-terminal kinase (MST1-JNK) signaling pathway on apoptosis in colorectal cancer (CRC) cells induced by Taurine (Tau). Caco-2 and SW620 cells transfected with p-enhanced green fluorescent protein (EGFP)-MST1 or short interfering RNA (siRNA)-MST1 were treated with Tau for 48 h. Apoptosis was detected by flow cytometry, and the levels of MST1 and JNK were detected by western blotting. Compared with the control group, 80 mM Tau could significantly induce apoptosis of CRC cells, and the apoptotic rate increased with increasing Tau concentration (P < 0.01). Meanwhile, the protein levels of MST1 and phosphorylated (p)-JNK in Caco-2 cells increased significantly (P < 0.01). The apoptotic rate of the p-EGFP-MST1 plasmid-transfected cancer cells was significantly higher than that of the control group (P < 0.05); however, the apoptotic rate of the p-EGFP-MST1+Tau group was increased further (P < 0.01). Silencing the MST1 gene could decrease the apoptotic rate of cancer cells, and Tau treatment could reverse this decrease. Blocking the JNK signaling pathway significantly reduced the Tau-induced apoptotic rate of CRC cells. Thus, the MST1-JNK pathway plays an important role in Tau-induced apoptosis of CRC cells.

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Section: Discussionmentioning

confidence: 99%

Roles of the MST1-JNK signaling pathway in apoptosis of colorectal cancer cells induced by Taurine

Liu

Xia

Zhang

et al. 2018

Libyan Journal of Medicine

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“…assessment of interleukin-6 (Il-6), tumor necrosis factor-α (TNF-α) and macrophage inflammatory protein-2 (MIP-2) levels IL-6, TNF-α and MIP-2 levels were estimated using the previously reported methods. 45,46 Blood was collected after reperfusion for 12 h and centrifuged at 3,600× g for 15 min to gain the sera. IL-6, TNF-α and MIP-2 levels were measured using commercially available kits.…”

Section: Liver Function Assessmentmentioning

confidence: 99%

“…Previous studies have shown that TNF-α, IL-6 and MIP-2 inflammatory cytokines and oxidative stress injury significantly increased HI/RI. 46,53 Some studies have affirmed that BMP-2 reduced TNF-α, IL-6 and oxidative stress injury in I/R injury. 15,16 In this study, BMP-2, BMP-2/PEG-b-PLL and BMP-2/ GA-PEG-b-PLL decreased TNF-α, IL-6 and MIP-2 inflammatory cytokines and oxidative stress injury in HI/RI ( Figure 6B-D).…”

mentioning

confidence: 99%

In vitro and in vivo protein release and anti-ischemia/<br />reperfusion injury properties of bone morphogenetic protein-2-loaded glycyrrhetinic acid-poly(ethylene glycol)-b-poly(L-lysine) nanoparticles

Fang¹,

Liu²,

Jiang³

et al. 2017

IJN

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Here, we describe a bone morphogenetic protein-2 (BMP-2) nanocarrier based on glycyrrhetinic acid (GA)-poly(ethylene glycol) (PEG)-b-poly( l -lysine) (PLL). A protein nanocarrier was synthesized, characterized and evaluated as a BMP-2 delivery system. The designed nanocarrier was synthesized based on the ring-opening polymerization of amino acid N-carboxyanhydride. The final product was measured with 1 H nuclear magnetic resonance. GA-PEG-b-PLL nanocarrier could combine with BMP-2 through electrostatic interaction to form polyion complex (PIC) micelles. BMP-2 could be rapidly and efficiently encapsulated through the GA-PEG-b-PLL nanocarrier under physiological conditions, exhibiting efficient encapsulation and sustained release. In addition, the GA-PEG-b-PLL-mediated BMP-2 delivery system could target the liver against hepatic diseases as it has GA-binding receptors. The anti-hepatic ischemia/reperfusion injury (anti-HI/RI) effect of BMP-2/GA-PEG-b-PLL PIC micelles was investigated in rats using free BMP-2 and BMP-2/PEG-b-PLL PIC micelles as controls, and the results showed that BMP-2/GA-PEG-b-PLL PIC micelles indicated significantly enhanced anti-HI/RI property compared to BMP-2 and BMP-2/PEG-b-PLL. All results suggested that GA-PEG-b-PLL could be used as a potential BMP-2 nanocarrier.

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“…One of them is Nilotinib (receptor tyrosine kinase inhibitor), and its protective role against liver cell damage. One recent study has shown that Nilotinib lowers both liver Jun Nterminal kinases (JNK) activation and neural progenitor cells (NPC) p 38 mitogen-activated protein kinase (MAPK) activation in mice, and may be useful in ameliorating liver IRI in humans (79). All of the aforementioned methods are summarized in Table 2.…”

Section: Nilotinibmentioning

confidence: 99%

Hepatic Ischemia and Reperfusion Injury and Trauma: Current Concepts

Papadopoulos¹,

Siempis²,

Theodorakou³

et al. 2013

Arch Trauma Res

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Context: Ischemia-reperfusion injury is a fascinating topic which has drawn a lot of interest in the last several years. Hepatic ischemia reperfusion injury may occur in a variety of clinical situations. These include transplantation, liver resection, trauma, and vascular surgery. Evidence Acquisition: The purpose of this review was to outline the molecular mechanisms underlying hepatic I/R injury and present the latest approaches, both surgical and pharmacological, regarding the prevention of it. A comprehensive electronic literature search in MEDLINE/PubMed was performed to identify relative articles published within the last 2 years. Results: The basic mechanism of hepatic ischemia -reperfusion injury is one of blood deprivation during ischemia, followed by the return of flow during reperfusion. It involves a complex series of events, such as mitochondrial deenergization, adenosine-5'-triphosphate depletion, alterations of electrolyte homeostasis, as well as Kupffer cell activation, oxidative stress changes and upregulation of proinflammatory cytokine signaling. The great number of variable pathways, with several mediators interacting with each other, leads to a high number of candidates for potential therapeutic intervention. As far as surgical approaches are concerned, the modification of existing clamping techniques and the ischemic preconditioning are the most promising techniques till recently. In the search for novel techniques of protecting against hepatic ischemia reperfusion injury, many different strategies have been used in experimental models. The biggest part of this research lies around antioxidant therapy, but other potential solutions have been explored as well. Conclusions:The management of hepatic trauma, in spite of the fact that it has become increasingly nonoperative, there still remains the possibility of hepatic resection in the hepatic trauma setting, especially in severe injuries. Hence, clinicians should be familiar with the concept of hepatic ischemia-reperfusion injury and respond appropriately and timely.Keywords: Reperfusion Injury; Ischemia; Pathophysiology; Prevention Implication for health policy/practice/research/medical education: Hepatic ischemia and reperfusion injury is a complex phenomenon which is commonplace in clinical practice such as the operative management of hepatic trauma, liver transplantation and liver resection. Hence, surgeons should be familiar with it and apply the necessary methods to prevent it.

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Nilotinib protects the murine liver from ischemia/reperfusion injury

Cited by 48 publications

References 50 publications

Roles of the MST1-JNK signaling pathway in apoptosis of colorectal cancer cells induced by Taurine

Roles of the MST1-JNK signaling pathway in apoptosis of colorectal cancer cells induced by Taurine

In vitro and in vivo protein release and anti-ischemia/<br />reperfusion injury properties of bone morphogenetic protein-2-loaded glycyrrhetinic acid-poly(ethylene glycol)-b-poly(L-lysine) nanoparticles

Hepatic Ischemia and Reperfusion Injury and Trauma: Current Concepts

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