Abstract
Background Naringenin (Nar) is a type of flavonoid and has been shown to have anti-inflammatory and antioxidative properties. However, the effects of Nar on acute pancreatitis (AP) have not been well studied. In this study, we aimed to investigate the function of Nar in a mouse model of AP. Methods Mild acute pancreatitis (MAP) was induced by caerulein (Cae), and severe acute pancreatitis (SAP) was induced by L-arginine in mice. Nar was administered intraperitoneally at doses of 25, 50, or 100 mg/kg following MAP induction and at a dose of 100 mg/kg following SAP induction. The serum levels of cytokines, lipase, and amylase were determined, and pancreatic and pulmonary tissues were harvested. Results The serum levels of amylase, lipase, and cytokines were significantly decreased in both MAP and SAP models after Nar treatment. The malondialdehyde (MDA) levels of the pancreatic tissue was significantly reduced in both MAP and SAP after Nar treatment. In contrast, glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), total sulfhydryl (T-SH), and non-proteinsulthydryl (NP-SH) were markedly increased in both MAP and SAP after Nar treatment. The injury in pancreatic and pulmonary tissues was markedly improved as evidenced by the inhibited expression of myeloperoxidase, nod-like receptor protein 3, and interleukin 1 beta as well as the enhanced expression of nuclear factor erythroid 2-related factor 2/heme oxygenase-1 in pancreatic tissues. Conclusions Nar exerted protective effects on Cae-induced MAP and L-arginine-induced SAP in mice, suggesting that Nar may be a potential therapeutic intervention for AP.
Highlights
Acute pancreatitis (AP) is an acute and life-threatening inflammatory disease that commonly damages peripancreatic tissues and other distant organs, leading to nearly 250,000 inpatient admissions at a cost of approximately $2.2 billion in the United States annually [1]
At the standard induction dose of Cae (50 μg/kg), the pancreatic tissues were mainly characterized as obvious edema, inflammatory cell infiltration, and necrosis, while the pancreatic injuries in Nar-treated (100 mg/kg and 50 mg/kg) mice were significantly reduced compared with the Mild acute pancreatitis (MAP) group (Figure 1(a))
Our results showed that the expression of nod-like receptor protein 3 (NLRP3) was remarkably elevated in both models, and administration of Nar (100 mg/kg) significantly reduced the NLRP3 expression in pancreatic tissues compared with the MAP and severe acute pancreatitis (SAP) groups (P < 0 001 and P < 0 05, resp.) (Figures 5(a) and 5(b))
Summary
Acute pancreatitis (AP) is an acute and life-threatening inflammatory disease that commonly damages peripancreatic tissues and other distant organs, leading to nearly 250,000 inpatient admissions at a cost of approximately $2.2 billion in the United States annually [1]. SAP, due to excessive release of inflammatory factors and increased oxidative stress response, can cause distant organ damage, especially acute lung injury. The effects of Nar on acute pancreatitis (AP) have not been well studied. Mild acute pancreatitis (MAP) was induced by caerulein (Cae), and severe acute pancreatitis (SAP) was induced by L-arginine in mice. The serum levels of cytokines, lipase, and amylase were determined, and pancreatic and pulmonary tissues were harvested. The serum levels of amylase, lipase, and cytokines were significantly decreased in both MAP and SAP models after Nar treatment. The malondialdehyde (MDA) levels of the pancreatic tissue was significantly reduced in both MAP and SAP after Nar treatment. Nar exerted protective effects on Cae-induced MAP and L-arginine-induced SAP in mice, suggesting that Nar may be a potential therapeutic intervention for AP
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