Sodium butyrate alleviates pancreatic injury in acute pancreatitis by inhibiting the expression of HDAC1

• 1、School of Food Science and Technology, Jiangnan University, Wuxi, Jiangsu 214122
• 2、School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122

Abstract：Objective: To investigate the protective effects of sodium butyrate (SB) as a histone deacetylase (HDAC) inhibitor on acute pancreatitis (AP) in mice. Methods: Forty eight-week-old Balb/c mice were randomly divided into normal control group, model control group, low dose of sodium butyrate group (50 mg/kg), medium dose of sodium butyrate group (200 mg/kg) and high dose of sodium butyrate group (800 mg/kg). The model of AP in mice was established by intraperitoneal injection of caerulein and was given intragastric administration of SB for 7 days before model establishment. The level of serum amylase, lipase and pancreatic myeloperoxidase (MPO) was determined by commercial kit. The levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6 and monocyte chemotactic protein-1 (MCP-1) in pancreatic tissue were measured by enzyme-linked immune sorbent assay (ELISA). Histone deacetylases (HDACs) and NLRP3 inflammasome-related proteins were detected by Western blotting. Results: SB can effectively inhibit pancreas injury, as evidenced by the decrease of serum amylase and lipase and pancreatic MPO level, as well as the reduction of pancreatic edema and the improvement of pancreatic histopathological changes, in addition, the middle-dose SB group had the best anti-inflammatory effect. SB intervention significantly inhibited HDAC1 expression in pancreatic tissues. Furthermore, SB can inhibit the expression of NLRP3-regulated downstream proteins. Conclusions: SB can effectively relieve AP in mice and its mechanism may be related to the inhibition of HDAC1 expression and NLRP3 pathway-mediated inflammation.

Keywords： acute pancreatitis sodium butyrate histone deacetylase NLRP3