Neutrophil elastase inhibitor reduces neutrophil chemoattractant production after ischemia-reperfusion in rat liver

Yamaguchi, Yasuo; Akizuki, Eiji; Ichiguchi, Osamu; Matsumura, Fujio; Goto, Mataro; Miyanari, Nobutomo; Mori, Katsutaka; Yamada, Shinwa; Ogawa, Michio

doi:10.1053/gast.1997.v112.pm9024309

Cited by 61 publications

(56 citation statements)

References 2 publications

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“…These findings indicate that in addition to prostaglandin E1 and prostacyclin [13] which directly suppress the rise in [Ca 2+ ] i , other agents like corticosteroids may inhibit hepatic ischemia-reperfusion injury by suppressing the production of these extracellular mediators. In fact, corticosteroids have been shown to inhibit the generation of oxygen free radicals [24] , and reduce hepatic ischemia-reperfusion injury [25] . In the present study, we demonstrated that at a dose of 10 mg/kg, prednisolone inhibited degradation of talin, as well as calpain μ activation in the ischemic liver.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of prednisolone on ischemia-induced liver injury in rats

Wang¹,

Shen²,

Shi³

et al. 2008

WJG

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AIM:To investigate the effects of prednisolone on cell membrane bleb formation, calpain μ activation and talin degradation during hepatic ischemia-reperfusion injury in rats. METHODS:The hilar area of the left lateral and median lobes of rat liver (68%) was clamped for 60 min and followed by 120 min reperfusion. Prednisolone was administered at 1.0, 3.0, or 10 mg/kg at 30 min before ischemia. In addition to biochemical and microscopic analyses, activation of calpain μ was determined using specific antibodies against the intermediate (activated) form of calpain μ. Degradation of talin was also studied by Western blotting. RESULTS: In the control and prednisolone (1.0 mg/kg) groups, serum aspartate transaminase (AST) and alanine transaminase (ALT) level were elevated, and cell membrane bleb formation was observed after 120 min of reperfusion. Moreover, calpain μ activation and talin degradation were detected. Infusion of prednisolone at 3.0 or 10 mg/kg significantly suppressed serum AST and ALT, and prevented cell membrane bleb formation. At 10 mg/kg, prednisolone markedly suppressed calpain μ activation and talin degradation. CONCLUSION: Prednisolone can suppress ischemiareperfusion injury of the rat liver. Its cytoprotective effect is closely associated with the suppression of calpain μ activation and talin degradation.

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Section: Discussionmentioning

confidence: 99%

Protective effect of prednisolone on ischemia-induced liver injury in rats

Wang¹,

Shen²,

Shi³

et al. 2008

WJG

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“…Urinary trypsin inhibitor-1 and the elastase inhibitor ONO-5046 prevented this effect (23,24). Both inhibitors reduced chemokine formation, hepatic neutrophil accumulation, and liver injury during hepatic ischemia-reperfusion (23,24). In addition to these observations, many more effects of neutrophil serine proteases on the processing of cytokines, chemokines, growth factors, and their respective receptors, of complement receptors, CD14, ICAM-1, and many other cell surface receptors have been reported (22).…”

Section: Proteases and Neutrophil-induced Cell Killingmentioning

confidence: 93%

“…Furthermore, elastase can induce the formation of neutrophil-and monocyte chemoattractant chemokines in Kupffer cells (24). Urinary trypsin inhibitor-1 and the elastase inhibitor ONO-5046 prevented this effect (23,24). Both inhibitors reduced chemokine formation, hepatic neutrophil accumulation, and liver injury during hepatic ischemia-reperfusion (23,24).…”

Section: Proteases and Neutrophil-induced Cell Killingmentioning

confidence: 99%

Mechanisms of Liver Injury. II. Mechanisms of neutrophil-induced liver cell injury during hepatic ischemia-reperfusion and other acute inflammatory conditions

Jaeschke¹

2006

American Journal of Physiology-Gastrointestinal and Liver Physi

424

389

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“…For example, when isolated hepatocytes were exposed to PMN proteases in a hypoxic environment, damage occurred more rapidly than in an oxygen-replete environment (Luyendyk et al, 2005). Moreover, PMN protease inhibitors protected the liver from injury caused by ischemia-reperfusion, although this attenuation was accompanied by a decrease in circulating chemokines and hepatic PMN accumulation (Yamaguchi et al, 1997). Thus, PMN proteases might contribute to hepatocellular injury by mechanisms independent of direct hepatocyte killing (Yamaguchi et al, 1997(Yamaguchi et al, , 1999Soejima et al, 1999).…”

Section: Neutrophilsmentioning

confidence: 99%

“…Moreover, PMN protease inhibitors protected the liver from injury caused by ischemia-reperfusion, although this attenuation was accompanied by a decrease in circulating chemokines and hepatic PMN accumulation (Yamaguchi et al, 1997). Thus, PMN proteases might contribute to hepatocellular injury by mechanisms independent of direct hepatocyte killing (Yamaguchi et al, 1997(Yamaguchi et al, , 1999Soejima et al, 1999). It is possible that PMN proteases induce intracellular oxidative stress in hepatocytes, which could be exacerbated by glutathione peroxidase deficiency.…”

Section: Neutrophilsmentioning

confidence: 99%