Urinary trypsin inhibitor reduces inflammatory response in kidney induced by Lipopolysaccharide

Ueki, Masaaki; Taie, Satoshi; Chujo, Kousuke; Asaga, Takehiko; Iwanaga, Yasuyuki; Ono, Junichiro; Maekawa, Nobuhiro

doi:10.1263/jbb.104.315

Cited by 30 publications

(20 citation statements)

References 32 publications

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“…Lipopolysaccharide [18], alcohol [19], methamphetamine [20], glycerol [21], and many other drugs can induce renal injury, including oxidative stress and inflammation in mice and rats. D-gal-treated mice have been often used in antioxidative pharmacology research.…”

Section: Discussionmentioning

confidence: 99%

Troxerutin protects the mouse kidney from d-galactose-caused injury through anti-inflammation and anti-oxidation

Fan

Zhang

Zheng

et al. 2009

International Immunopharmacology

121

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Section: Discussionmentioning

confidence: 99%

Troxerutin protects the mouse kidney from d-galactose-caused injury through anti-inflammation and anti-oxidation

Fan

Zhang

Zheng

et al. 2009

International Immunopharmacology

121

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“…In addition, UTI protects mitochondrial function by reducing the calcium overload in injured cells and exhibits protective effects against ischemia-reperfusion (I/R) injury in the heart, lung, liver and kidney (9). Furthermore, previous studies have demonstrated that UTI can alleviate LPS-induced lung and kidney injury by inhibiting inflammatory responses in these organs (10,11). Thus, we hypothesized that UTI may protect against cerebral I/R injury following CPR and inhibit TLR4-induced inflammatory responses in the brain following resuscitation.…”

Section: Introductionmentioning

confidence: 98%

Postconditioning improvement effects of ulinastatin on brain injury following cardiopulmonary resuscitation

Sui

2014

Experimental and Therapeutic Medicine

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The aim of the present study was to determine the effects of ulinastatin (UTI) on brain injury in rats subjected to cardiopulmonary resuscitation (CPR) following asphyxial cardiac arrest (CA) and identify the underlying mechanisms. In total, 100 healthy male Wistar rats were randomly divided into control and treatment groups (n=50). After 4 min of asphyxial CA, all the rats were immediately subjected to CPR. The treatment group animals were administered 15 mg/kg UTI at the onset of resuscitation. The mortality rate in the two groups was recorded at 24 h post-resuscitation. In addition, neurological function was evaluated at 24, 48 and 72 h post-resuscitation using a neurological deficit scale (NDS). Furthermore, the effects of UTI on the Toll-like receptor 4 (TLR4) signaling pathway in brain tissues were determined by assessing TLR4 mRNA expression, nuclear factor (NF)-κB activity and tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels at 1, 3, 6, 12, 24, 48 and 72 h post-resuscitation. After 24 h, the mortality rate significantly decreased in the treatment group when compared with the control animals (10 vs. 30%; P<0.05). Additionally, an overt improvement was observed in the NDS score following UTI treatment when compared with the control (P<0.01). Finally, statistically significant decreases in the levels of TLR4 mRNA expression, NF-κB activity and TNF-α and IL-6 were observed in the treatment group at each time point (P<0.01). Therefore, UTI treatment at the onset of CPR significantly inhibits the TLR4 signaling pathway, thereby alleviating the inflammatory responses following resuscitation and improving neurological function.

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“…Recent studies have demonstrated that UTI inhibits the induction of cytokines and adhesion molecules, as well as that of lysosomal enzymes [15][16][17][18]. We have also reported that UTI inhibits the increases in renal tissue levels of TNF α, cytokine-induced neutrophil chemoattractant-1, and myeloperoxidase, as well as inhibiting increases in BUN and serum creatinine levels, after lipopolysaccharide stimulation [19]. It is thought that UTI improves the microcirculation by inhibiting interactions among these mediators, neutrophils, and endothelial cells.…”

Section: Discussionmentioning

confidence: 56%

Urinary trypsin inhibitor ameliorates renal tissue oxygenation after ischemic reperfusion in rats

et al. 2008

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Urinary trypsin inhibitor reduces inflammatory response in kidney induced by Lipopolysaccharide

Cited by 30 publications

References 32 publications

Troxerutin protects the mouse kidney from d-galactose-caused injury through anti-inflammation and anti-oxidation

Troxerutin protects the mouse kidney from d-galactose-caused injury through anti-inflammation and anti-oxidation

Postconditioning improvement effects of ulinastatin on brain injury following cardiopulmonary resuscitation

Urinary trypsin inhibitor ameliorates renal tissue oxygenation after ischemic reperfusion in rats

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