Attenuation of Liver and Lung Injury after Hepatic Ischemia and Reperfusion by a Cytokine-Suppressive Agent, FR167653

Hato, Shinji; Urakami, Atsushi; Yamano, Tetsuo; Uemura, Takashi; Ota, Tsuguhito; Hirai, Ryuji; Shimizu, Nobuyoshi

doi:10.1159/000049707

Cited by 24 publications

(20 citation statements)

References 29 publications

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“…These cytokines play important roles in the induction of polymorphonuclear neutrophil (PMN) activation and infiltration, and induce not only localized hepatic injury but also remote organ injury. In the study of Hato et al [46] , neutrophil accumulation and the content of cytokines, including TNF-␣ , and IL-1 ␤ , were increased in the reperfused liver. Similarly, Tsuchihashi et al [47] , who studied the role of cytokines in I/R injury of the liver tissue, suggested that I/R led to the expression of TNF-, IL-1 ␤ , IL-6, in the reperfused rat liver model, and the expressed cytokines are expected to aggravate I/R injury.…”

Section: Discussionmentioning

confidence: 91%

Alpha-Lipoic Acid Protects against Hepatic Ischemia-Reperfusion Injury in Rats

et al. 2007

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Background and Aim: To evaluate the protective effect of alpha-lipoic acid in reducing oxidative damage after severe hepatic ischemia/reperfusion (IR) injury. Methods: Wistar albino rats were subjected to 45 min of hepatic ischemia, followed by 60 min reperfusion period. Lipoic acid (100 mg/kg i.p.) was administered 15 min prior to ischemia and immediately before reperfusion period. At the end of the reperfusion period aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) activity, and cytokine, TNF-α and IL-1β levels were determined in serum samples. Malondialdehyde (MDA), and glutathione (GSH) levels and myeloperoxidase (MPO) activity were determined in the liver tissue samples while formation of reactive oxygen species was monitored by using chemiluminescence (CL) technique with luminol and lucigenin probes. Tissues were also analyzed histologically. Results: Serum ALT, AST, and LDH activities and TNF-α and IL-1β levels were elevated in the I/R group, while this increase was significantly lower in the group of animals treated concomitantly with lipoic acid. Hepatic GSH levels, significantly depressed by I/R, were elevated back to control levels in lipoic acid-treated I/R group. Furthermore, increases in tissue luminol and lucigenin CL, MDA levels and MPO activity due to I/R injury were reduced back to control levels with lipoic acid treatment. Conclusion: Since lipoic acid administration alleviated the I/R-induced liver injury and improved the hepatic structure and function, it seems likely that lipoic acid with its antioxidant and oxidant-scavenging properties may be of potential therapeutic value in protecting the liver against oxidative injury due to ischemia-reperfusion.

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Section: Discussionmentioning

confidence: 91%

Alpha-Lipoic Acid Protects against Hepatic Ischemia-Reperfusion Injury in Rats

et al. 2007

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“…Therefore, it seems reasonable to propose that hepatic ischemia/ reperfusion (I/R) injury leads to the release of the cytokines. In the study of Hato et al (2001) neutrophil accumulation and the content of cytokines, including TNF-α and IL-1β, were increased in the reperfused liver. Similarly, Tsuchihashi et al (2006) who studied the role of cytokines in I/R injury of the liver tissue, suggested that I/R led to the expression of TNF-α, IL-1β, IL-6 in the reperfused rat liver model, and the expressed cytokines are expected to aggravate I/R injury.…”

Section: Discussionmentioning

confidence: 95%

Grape seed extract treatment reduces hepatic ischemia‐reperfusion injury in rats

Şehirli

Ozel

Dulundu

et al. 2007

Phytotherapy Research

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This study was designed to determine the possible protective effect of grape seed extract (GSE), a widely used antioxidant dietary supplement, on hepatic ischemia/reperfusion (I/R) injury. Wistar albino rats were subjected to 45 min of hepatic ischemia, followed by a 60 min reperfusion period. GSE was administered in a dose of 50 mg/kg/day orally for 15 days before I/R injury and repeated before the reperfusion period. Liver samples were taken for histological examination or determination of hepatic malondialdehyde (MDA), glutathione (GSH) and myeloperoxidase (MPO) activity. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were determined to assess liver functions. Lactate dehydrogenase (LDH) and cytokines (TNF-α α α α α and IL-1β β β β β ) were also assayed in serum samples for the evaluation of generalized tissue damage. Ischemia/reperfusion caused a significant decrease in hepatic GSH, and significant increases in MDA level, and MPO activity. Serum AST and ALT levels, as well as LDH activity and plasma TNF-α α α α α and IL-1β β β β β levels were also elevated in the I/R group. Treatment with GSE reversed all these biochemical parameters as well as histological alterations induced by I/R. In conclusion, GSE reduced I/R-induced organ injury through its ability to balance the oxidant-antioxidant status, to inhibit neutrophil infiltration and to regulate the release of inflammatory mediators.

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“…Nevertheless, transient interruption of hepatic inflow is sometimes necessary during partial hepatectomy (10,14). The lung is one of the most susceptible organs to systemic inflammation-related injury, secondary to liver ischemiareperfusion (7,16,36), intestinal ischemia-reperfusion (6, 37), and renal ischemia-reperfusion (11,17).…”

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confidence: 99%

High tidal volume ventilation induces lung injury after hepatic ischemia-reperfusion

Ota¹,

Nakamura²,

Yazawa³

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

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mia-reperfusion not only damages the affected organ but also leads to remote organ injuries. Hepatic inflow interruption usually occurs during hepatic surgery. To investigate the influence of liver ischemiareperfusion on lung injury and to determine the contribution of tidal volume settings on liver ischemia-reperfusion-induced lung injury, we studied anesthetized and mechanically ventilated rats in which the hepatic inflow was transiently interrupted twice for 15 min. Two tidal volumes, 6 ml/kg as a low tidal volume (IR-LT) and 24 ml/kg as a high tidal volume (IR-HT), were assessed after liver ischemia-reperfusion, as well as after a sham operation, 6 ml/kg (NC-LT) and 24 ml/kg (NC-HT). Both the IR-HT and IR-LT groups had a gradual decline in the systemic blood pressure and a significant increase in plasma TNF-␣ concentrations. Of the four groups, only the IR-HT group developed lung injury, as assessed by an increase in the lung wet-to-dry weight ratio, the presence of significant histopathological changes, such as perivascular edema and intravascular leukocyte aggregation, and an increase in the bronchoalveolar lavage fluid TNF-␣ concentration. Furthermore, only in the IR-HT group was airway pressure increased significantly during the 6-h reperfusion period. These findings suggest that liver ischemia-reperfusion caused systemic inflammation and that lung injury is triggered when high tidal volume ventilation follows liver ischemia-reperfusion. acute lung injury; ventilator-induced lung injury; lung protective strategy; cytokines ISCHEMIA-REPERFUSION NOT ONLY damages the affected organ itself but can also cause systemic inflammation (32, 34). Such systemic inflammation may lead to remote organ injury and morbidity (20). Nevertheless, transient interruption of hepatic inflow is sometimes necessary during partial hepatectomy (10,14). The lung is one of the most susceptible organs to systemic inflammation-related injury, secondary to liver ischemiareperfusion (7,16,36), intestinal ischemia-reperfusion (6, 37), and renal ischemia-reperfusion (11,17).Acute lung injury (ALI), or acute respiratory distress syndrome (ARDS), is an important cause of mortality in critically ill patients. The mortality rate from ALI or ARDS is ϳ40 -50% (4, 31). In some cases, ALI or ARDS can be caused by extrapulmonary factors, such as systemic inflammation (5, 25) and sepsis (30,35). ALI/ARDS patients ventilated with low tidal volume ventilation have a lower mortality rate than those ventilated with high tidal volume ventilation (3, 4). There are in vivo and ex vivo studies that have analyzed the effect of tidal volume on ventilator-induced lung injury (VILI) following LPS administration (2, 28, 33) and cecal ligation and perforation (23); both of these induce severe systemic inflammation. As far as we know, there are no published papers that have explored the effect of different tidal volumes on VILI in connection with liver ischemia-reperfusion.To evaluate the effects of ventilation on lung injury induced by systemic inflammation follo...

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Attenuation of Liver and Lung Injury after Hepatic Ischemia and Reperfusion by a Cytokine-Suppressive Agent, FR167653

Cited by 24 publications

References 29 publications

Alpha-Lipoic Acid Protects against Hepatic Ischemia-Reperfusion Injury in Rats

Alpha-Lipoic Acid Protects against Hepatic Ischemia-Reperfusion Injury in Rats

Grape seed extract treatment reduces hepatic ischemia‐reperfusion injury in rats

High tidal volume ventilation induces lung injury after hepatic ischemia-reperfusion

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