Urinary trypsin inhibitor suppresses excessive generation of superoxide anion radical, systemic inflammation, oxidative stress, and endothelial injury in endotoxemic rats View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2010-08

AUTHORS

Ryo Tanaka, Motoki Fujita, Ryosuke Tsuruta, Kenji Fujimoto, Hiromi Shinagawa Aki, Kazumi Kumagai, Tetsuya Aoki, Akihiro Kobayashi, Tomonori Izumi, Shunji Kasaoka, Makoto Yuasa, Tsuyoshi Maekawa

ABSTRACT

OBJECTIVE AND DESIGN: The protective effects of ulinastatin, a human urinary trypsin inhibitor (UTI), against superoxide radical (O(2)(-*)) generation, systemic inflammation, lipid peroxidation, and endothelial injury were investigated in endotoxemic rats. MATERIALS AND TREATMENT: Twenty-one Wistar rats were allocated to a control group, a UTI group, and a sham group. A bolus of lipopolysaccharide (LPS; 3 microg/g) was administered intravenously to the control group, a bolus of LPS and UTI (5 U/g) to the UTI group, and a bolus of saline to the sham group. METHODS: The O(2)(-*) generated was measured as the current in the right atrium using an electrochemical O(2)(-*) sensor. Plasma nitrite, high mobility group box 1 (HMGB1), tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, malondialdehyde, and soluble intercellular adhesion molecule-1 (sICAM-1) were measured 360 min after LPS administration. RESULTS: The O(2)(-*) current increased in the control group and was significantly attenuated in the UTI group after 55 min (P < 0.05 at 55-60 min, P < 0.01 at 65-360 min). Plasma nitrite, HMGB1, TNF-alpha, IL-6, malondialdehyde, and sICAM-1 were attenuated in the UTI group. CONCLUSIONS: UTI suppressed excessive O(2)(-*) generation, systemic inflammation, lipid peroxidation, and endothelial injury in endotoxemic rats. More... »

PAGES

597-606

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00011-010-0166-8

DOI

http://dx.doi.org/10.1007/s00011-010-0166-8

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1027829754

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/20148283


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