Ulinastatin attenuates reperfusion injury in the isolated blood-perfused rabbit heart

Cao, Zhili; Okazaki, Yukio; Naito, Kozo; Ueno, Tetsuya; Natsuaki, Masafumi; Itoh, Tsuyoshi

doi:10.1016/s0003-4975(99)01433-2

Cited by 33 publications

(35 citation statements)

References 14 publications

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“…Urinary trypsin inhibitor (Ulinastatin, UTI), a protease inhibitor, has been known to prevent global I/R injury in various tissues including the heart [4,5,6,7]. Its protective effect on I/R injury is partly mediated by inhibition of lysosomal enzymes and free radicals [8] or reduction in Ca 2+ overload [9].…”

Section: Introductionmentioning

confidence: 99%

Urinary Trypsin Inhibitors Afford Cardioprotective Effects through Activation of PI3K-Akt and ERK Signal Transduction and Inhibition of p38 MAPK and JNK

Kim

Yoo²,

Jeong³

et al. 2009

Cardiology

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Background: We determined the effect of urinary trypsin inhibitors (UTI) in regional myocardial ischemia/reperfusion (I/R) injury and its underlying mechanisms involving the role of prosurvival kinases such as phosphatidylinositol-3-OH kinases (PI3K)-Akt and extracellular signal-regulated kinases (ERK 1/2) and apoptotic kinases such as p38 and JNK. Methods: The rats were anesthetized and subjected to an I/R insult consisting of 30-min left anterior descending coronary artery (LAD) occlusion followed by reperfusion. Infarct size was measured after 120 min of reperfusion. UTI was given alone or along with wortmannin (inhibitor of PI3K) or PD098059 (inhibitor of ERK1/2) before LAD occlusion. The phosphorylation of Akt, ERK1/2, p38 and JNK was determined by immunoblotting after 5 min of reperfusion. UTI was administered 10 min before LAD occlusion, and wortmannin and PD098059 were administered 20 min before LAD occlusion. Results: UTI significantly reduced the infarct size compared with the control. Wortmannin or PD098059 alone did not affect the infarct size, but they abolished the UTI-induced cardioprotective effect. UTI significantly reduced the phosphorylation of p38 and JNK, while it enhanced that of Akt and ERK1/2. Conclusions: UTI has a protective effect against regional myocardial I/R injury through activation of survival kinases PI3K-Akt and ERK1/2 and attenuation of p38 and JNK.

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Section: Introductionmentioning

confidence: 99%

Urinary Trypsin Inhibitors Afford Cardioprotective Effects through Activation of PI3K-Akt and ERK Signal Transduction and Inhibition of p38 MAPK and JNK

Kim

Yoo²,

Jeong³

et al. 2009

Cardiology

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“…Seventy-two rats were randomly divided into three groups with 24 rats in each group: group 1, the sham group, where rats were not treated with either LPS/D-gal or ulinastatin; group 2, the control group, where rats were treated with only LPS/D-gal, and group 3, the treated group, where rats were pre-treated with ulinastatin and then injected with LPS/D-gal. Rats in each group were killed at different time points after LPS/D-gal treatment with six rats in each time point (6,12,24,36, and 48 h after LPS/D-gal treatment). Acute liver injury in rats was established by intraperitoneal administration of D-gal (800 mg/kg) and LPS (4 lg/kg) once.…”

Section: Animal Modelmentioning

confidence: 99%

“…Ulinastatin is known to reduce elastase from neutrophils [4] and to inhibit the accumulation and adhesion of neutrophils from ischemia to reperfusion injury [5]. In addition, ulinastatin is able to modulate the expression of adhesion molecules in endothelial cells [6]. Recently, several studies documented that ulinastatin has a protective effect on ischemia/reperfusion injury in the liver.…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Ulinastatin on Acute Liver Failure Induced by Lipopolysaccharide/d-Galactosamine

et al. 2011

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“…Also, UTI can alleviate coagulatory disturbance accompanied by sepsis such as an increase in the serum level of fibrinogen and fibrinogen degradation products [33]. Likewise, UTI has a protective effect against ischemiareperfusion injury in the liver [35], kidney [36], heart [37], and lung [38] in vivo via the actions of its radical scavenging elements [39]. As for its mechanism, UTI reduces C-X-C chemotactic molecule production during liver ischemia/reperfusion in vivo [40].…”

Section: Anti-inflammatory Potential Of Uti In In Vitro In Vivo Andmentioning

confidence: 99%

Urinary Trypsin Inhibitor, an Alternative Therapeutic Option for Inflammatory Disorders

Inoue¹,

Takano²

2011

Inflammatory Diseases - A Modern Perspective

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Ulinastatin attenuates reperfusion injury in the isolated blood-perfused rabbit heart

Cited by 33 publications

References 14 publications

Urinary Trypsin Inhibitors Afford Cardioprotective Effects through Activation of PI3K-Akt and ERK Signal Transduction and Inhibition of p38 MAPK and JNK

Urinary Trypsin Inhibitors Afford Cardioprotective Effects through Activation of PI3K-Akt and ERK Signal Transduction and Inhibition of p38 MAPK and JNK

Protective Effects of Ulinastatin on Acute Liver Failure Induced by Lipopolysaccharide/d-Galactosamine

Urinary Trypsin Inhibitor, an Alternative Therapeutic Option for Inflammatory Disorders

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