In 1909, The existence of ulinary trypsin inhibitor in urine was first reported by Beuer and Reich. In 1985, Ulinastatinwas marketed in Japan and applied in the clinical treatment of diseases caused by cell lysosomal membrane rupture, hydrolytic enzyme overflow and hyperfunction (e.g., acute pancreatitis). Studies have shown that UTI has neuroprotective effects and has beneficial effects on neuropathic pain (NP), which may be a new measure to prevent and treat NP. In this paper, the neuroprotective effect of Ulinastatin and its effect on NP are reviewed.

　　Pharmacological characteristics of Ulinastatin and its common clinical fields

　　Ulinastatin has been isolated and purified from healthy male urine and has been used clinically in Asia for over 20 years. UTI is a broad-spectrum serine protease inhibitor, and its low molecular weight degradants have strong inhibition of hydrolases. Under physiological conditions, UTI exists in the human body. UTI concentration changes when the body is exposed to infection, shock, tumor, pregnancy, surgery, or glucocorticoid administration.

　　Ulinastatin is synthesized primarily in the liver and is metabolized by the kidneys and excreted in urine. Clinically, UTI was administered intravenously and the drugs were metabolized by the kidney. Clinical applications include acute pancreatitis, sepsis, complex multiple trauma, shock, ischemia-reperfusion injury, acute lung injury, and malignant tumor. The main mechanisms are anti-inflammatory (inhibiting the production and release of inflammatory factors, activation and focusing of inflammatory cells), reduction of intracellular lysosomal membrane damage, reduction of vascular permeability, improvement of immune function (promoting immunoglobulin production, improving immune suppression), regulation of oxidative stress and apoptosis. The main pathways involved are p38MAPK, JNK, STAT-3, mTOR, NF- B, etc.