• Yukang Song, Shixing Miao, Yexuzi Li, and Hui Fu.
• Department of Medical Intensive Care Unit, The First People's Hospital of Wenling, Taizhou, Zhejiang, China.
• J. Cell. Biochem. 2019 Jan 1; 120 (1): 417-424.

AbstractSepsis is a syndrome of life-threatening multiorgan dysfunction caused by host response dysregulation to infection. Ulinastatin (UTI), a serine protease inhibitor, possesses anti-inflammatory properties and has been suggested to modulate lipopolysaccharide-induced sepsis. However, little is known about the mechanism underlying its effects on sepsis. In the current study, we investigated the protective effect of UTI on liver injury in a cecal ligation and puncture (CLP)-induced sepsis of C57BL/6 mouse model and explored the possible mechanisms. Mice underwent CLP as sepsis models and were randomized into five groups including the sham group, UTI group, CLP group, UTI-L group, and UTI-H group. UTI was intraperitoneally administered at doses of UTI 1500 U/100 g (UTI-L group) or 3000 U/100 g (UTI-H group), before CLP. The mice were killed, and immunohistochemical changes, cytokine levels, and antioxidant enzyme activities were detected. Our results showed that UTI ameliorated CLP-mediated increases in serum aspartate aminotransferase and alanine aminotransferase activities, histological activity index, degenerative region ratio, and infiltrated inflammatory cell numbers. Moreover, UTI also decreased nitrotyrosine and 4-hydroxynonenal, activated caspase-3, and activated poly (ADP-ribose) polymerase (PARP) levels and inhibited the mitogen-activated protein kinase pathway activation in liver tissues. Our results indicated that UTI could inhibit CLP-induced liver injury by suppressing inflammation and oxidation. Our results indicated that UTI may serve as a potential therapeutic agent for sepsis.© 2018 Wiley Periodicals, Inc.

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