MG132 Alleviates Liver Injury Induced by Intestinal Ischemia/Reperfusion in Rats: Involvement of the AhR and NFκB Pathways

Jing, Huirong; Shen, Gang; Wang, Guangzhi; Zhang, Feng; Li, Yubing; Luo, Fang; Yao, Jihong; Tian, Xiaofeng

doi:10.1016/j.jss.2011.09.001

Cited by 29 publications

(19 citation statements)

References 46 publications

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“…They postulated that MG-132 might play a preventive role in the development of cell and tissue injury. It was recently confirmed [21] in the rat model that intraperitoneal administration of MG-132 has a significant effect in protection against liver injury induced by intestinal ischaemia/reperfusion, most probably due to modulation of NFκB and Aryl hydrocarbon receptor pathways. A single intraperitoneal dose of MG-132 appears also to act effectively on the structures belonging to systems other than the gastrointestinal.…”

Section: Systemic Administration Of Proteasome Inhibitionmentioning

confidence: 87%

“…Both doses administered to the animals were based on the those previously reported in the literature. The higher dose was used in the studies of [9,24,50], and the lower dose in the studies of [1,21].…”

Section: Mg-132 Administrationmentioning

confidence: 99%

“…MG-132 properties, such as antiproliferative, anti-inflammatory, and induction of heat shock proteins, also make it the most widely used in the clinical impact of proteasome inhibition on the course of many processes at the cellular and tissue level, as well as having a link with studies of new proteasome inhibitors [15]. Literature reports indicate that under experimental conditions, intraperitoneal administration of MG-132 may play a beneficial role in the prevention and therapy of inflammatory diseases such as acute pancreatitis [9,24,50], inflammatory bowel disease [19], severe acute respiratory syndrome [28], and intestinal damage caused by ischaemia/reperfusion [1,21], and also partially prevents muscle atrophy associated with disuse [20]. However, data obtained on animal models are very controversial.…”

Section: Introductionmentioning

confidence: 99%

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Original article Nigrostriatal pathway degeneration in rats after intraperitoneal administration of proteasome inhibitor MG-132

Wójcik

Spodnik²,

Spodnik³

et al. 2014

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Section: Systemic Administration Of Proteasome Inhibitionmentioning

confidence: 87%

Section: Mg-132 Administrationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Original article Nigrostriatal pathway degeneration in rats after intraperitoneal administration of proteasome inhibitor MG-132

Wójcik

Spodnik²,

Spodnik³

et al. 2014

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“…NF- κ B is also a critical transcriptional factor regulating the genes involving cell survival and immune reactions. Moreover, NF- κ B plays a crucial role in the cellular stress such as inflammation and intracellular levels of reactive oxygen species [18, 21]. Under common circumstance, NF- κ B is a heterodimer, is located in the cytoplasm, and is combined to the inhibitory unit inhibitory κ B (I κ B).…”

Section: Discussionmentioning

confidence: 99%

The Protective Effects of Curcumin on Experimental Acute Liver Lesion Induced by Intestinal Ischemia-Reperfusion through Inhibiting the Pathway of NF-κB in a Rat Model

Jing

Yao

et al. 2014

Oxidative Medicine and Cellular Longevity

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Objective. In this study, we investigated the protective effect and mechanism of curcumin on a rat model of intestinal ischemia/reperfusion (I/R), which induces an acute liver lesion. Methods. Curcumin was injected into rats in the curcumin groups through left femoral vein. The same volume of vehicle (0.9% normal saline) was injected into sham and I/R groups. Blood and liver tissue were gathered for serological and histopathological determination. Results. Intestinal I/R led to severe liver injury manifested as a significant increase in serum AST and ALT levels; all of those were reduced by treatment with curcumin. Simultaneously, the activity of SOD in liver decreased after intestinal I/R, which was increased by curcumin treatment. On the other hand, curcumin reduced MPO activity of liver tissue, as well as serum IL-6 and TNF-α levels observably. This is in parallel with the decreased level of liver intercellular cell adhesion molecule-1 (ICAM-1) and nuclear factor-κB (NF-κB) expression. Conclusion. Our findings suggest that curcumin treatment attenuates liver lesion induced by intestinal I/R, attributable to the antioxidative and anti-inflammatory effect via inhibition of the NF-κB pathway.

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“…Initiators of this pathop hysiology are regulated by the transcript factor nuclear factor-κB. 4,5 Various methods with protective effects have been tested to ameliorate IRI. Conditioning (preconditioning, postconditioning, or remote conditioning) is among the therapeutic approaches used to enhance organ ischemia tolerance.…”

Section: Introductionmentioning

confidence: 99%

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Vrakas

Tsalis²,

Roidos³

et al. 2017

Exp Clin Transplant

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Objectives: Our study aimed to determine whether antithrombin plays a synergistic role in accentuating the effects of intestinal ischemic preconditioning. Materials and Methods: Fifty rats were randomly allocated to 5 groups (10 rats/group) as follows: sham treatment (group 1); ischemia-reperfusion (group 2); ischemic preconditioning followed by ischemiareperfusion (group 3); antithrombin + ischemia-reperfusion, similar to group 2 but including antithrombin administration (group 4); and antithrombin + ischemic preconditioning, similar to group 3 but including antithrombin administration (group 5). Blood samples and liver specimens were obtained for measurement of cytokines, myeloperoxidase, and malondialdehyde. Liver biopsies were examined by electron microscopy. Results: Intestinal ischemia-reperfusion induced a remote hepatic inflammatory response as evidenced by the striking increase of proinflammatory cytokines, myeloperoxidase, and malondialdehyde. Tumor necro sis factor-α levels in group 5 (12.48 ± 0.7 pg/mL) were significantly lower than in group 3 (13.64 ± 0.78 pg/mL; P = .014). Mean interleukin 1β was lower in group 5 (9.52 ± 0.67pg/mL) than in group 3 (11.05 ± 1.9 pg/mL; P > .99). Mean interleukin 6 was also significantly lower in group 5 (17.13 ± 0.54 pg/mL) than in group 3 (23.82 ± 1 pg/mL; P < .001). Myeloperoxidase levels were significantly higher in group 3 (20.52 ± 2.26 U/g) than in group 5 (18.59 ± 1.03 U/g; P = .025). However, malondialdehyde levels did not significantly improve in group 5 (4.55 ± 0.46 μmol) versus group 3 (5.17 ± 0.61 μmol; P = .286). Tumor necrosis factor-α, interleukin 6, and myeloperoxidase findings show that antithrombin administration further attenuated the inflammatory response caused by ischemia-reperfusion, suggesting a synergistic effect with ischemic preconditioning. These findings were confirmed by electron microscopy. Conclusions: The addition of antithrombin to ischemic preconditioning may act to attenuate or prevent damage from ischemia-reperfusion injury by inhi biting the release of cytokines and neutrophil infiltration.

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MG132 Alleviates Liver Injury Induced by Intestinal Ischemia/Reperfusion in Rats: Involvement of the AhR and NFκB Pathways

Cited by 29 publications

References 46 publications

Original article Nigrostriatal pathway degeneration in rats after intraperitoneal administration of proteasome inhibitor MG-132

Original article Nigrostriatal pathway degeneration in rats after intraperitoneal administration of proteasome inhibitor MG-132

The Protective Effects of Curcumin on Experimental Acute Liver Lesion Induced by Intestinal Ischemia-Reperfusion through Inhibiting the Pathway of NF-κB in a Rat Model

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