THE EFFECTS OF SIVELESTAT SODIUM ON SEVERE ACUTE
PANCREATITIS COMPLICATIONS
KEXING ZHOU #, SIQUAN ZHANG #*, SHUGUO LI, JIAYU HAN, YAN YAO, XI ZHAO, QINYAO QI
Intensive Care Unit, Xixi Hospital, Hangzhou, 310023, China
*corresponding author: zhangsiquancare@yeah.net
#Authors with equal contribution
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Abstract:
Acute pancreatitis represents a medical emergency and untreated can lead to serious complications. This study aimed to
investigate the therapeutic effect of sivelestat sodium on the renal injury induced by severe acute pancreatitits and its
mechanism of action. Ninety Sprangue-Dawley male rats were randomly divided into 3 groups: a sham operation group (SO
group), an acute pancreatitis model group (SAP group) and sivelestat sodium treatment group (SS group), 30 rats per group.
The rats from each group were randomly divided into three subgroups (6 h, 12 h and 24 h time points evaluation), 10 animals
per subgroup. At each time point, serum amylase (AMY), creatinine (Cr), blood urea nitrogen (BUN), serum TNF-α, IL-6,
and neutrophil elastase (NE) levels were determined, pancreas and kidney tissue were evaluated histopathologically and NFkB
activity was determined in the renal tissue. In the SAP and SS groups, the levels of AMY, Cr, BUN, NE, TNF-α, IL-6
were increased compared with the SO group. The pathological scores of pancreas and kidney were increased in the SAP and
SS groups compared to the SO group at each time point (p < 0.05). In addition, the level of NF-kB activation in renal tissue
was gradually increased (p < 0.05). Compared with the SAP group, in SS rats the levels of AMY, Cr, BUN, NE, TNF-α, IL-6
decreased significantly at each time point. NF-kB activity was lower in the SS group compared with SAP also the integrity of
pancreatic and renal tissue was less affected than in the case of SAP rats (p < 0.05). Sivelestat sodium can effectively
improve the function of damaged kidney in the course of severe acute pancreatitis. Its mechanism of action is related to the
reduction of inflammatory factors like TNF-α and IL-6, through the inhibition of NE release and to the blockage NF-kB
pathway activators in the renal tissue, in order to avoid secondary inflammatory injuries of the tissue.






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