Why could ethyl pyruvate attenuate severe acute pancreatitis?
Excessive activation of inflammatory mediator cascade during SAP is a major cause of distant organ injury and the high mortality. Cytokines such as TNF-alpha and IL-1 beta are released early in the development of systemic inflammatory response. This leaves a narrow therapeutic window for administration of therapeutics and delayed delivery of that anti-inflammatory therapeutics is not effective after the inflammatory mediator cascade has developed. A research article was published on 28 July 2008 in the World Journal of Gastroenterology addresses this question. The research team led by Prof. Wang from Centre of Pancreatic Surgery of Xiehe Hospital, Tongji Medical College, Huazhong University of Science and Technology, demonstrated that the serum levels of HMGB1 began to rise significantly at 12 h, and maintained at high levels up to 48 h after induction of experimental SAP in rats. The delayed kinetics indicated that HMGB1 may provide a broader therapeutic window for treating this letha
