Urinary trypsin inhibitor: anti-inflammatory effects in septic mice and molecular insights in bacterial lipoprotein-induced THP-1 cells.

Introduction: Excessive release of inflammatory cytokines in severe infections significantly contributes to the onset and progression of sepsis, a condition linked to elevated mortality rates in intensive care units. However, the lack of effective sepsis treatment strategies remains a significant challenge in critical care medicine. The use of anti-inflammatory agents against sepsis has advantages. Urinary trypsin inhibitor (UTI), a serine protease inhibitor obtained from the urine of healthy males, finds broad application in patients with inflammatory conditions such as shock, pancreatitis, and trauma. This investigation aimed to examine the impact and underlying mechanism of UTI in mice with sepsis and THP-1 cells stimulated by bacterial lipoprotein (BLP). Material and methods: C57BL/6J mice were divided into the control, sham operation, cecal ligation and puncture (CLP), and UTI + CLP groups. Histological staining was performed to assess heart and lung injury. Transmission electron microscopy was performed to analyze myocardial mitochondrial injury. The creatine kinase-myoglobin binding and aspartate aminotransferase isoenzyme were detected by evaluating heart injury. Serum interleukin 1 Results: The CLP group exhibited elevated levels of creatine kinase-myoglobin binding, aspartate aminotransferase, and IL-1 Conclusions: UTI can effectively inhibit BLP-induced activation of the NF-