Abstract
Catalpol, an iridoid glucoside extracted from the traditional Chinese herbal medicine, Rehmannia glutinosa, is reported to exert neuroprotective, anti-inflammatory, anti-tumor and anti-apoptotic effects. The main aim of the present study was to investigate whether catalpol ameliorates experimental acute pancreatitis (AP) induced by sodium taurocholate (STC). AP was induced in rats via retrograde injection of 4% STC (0.1 mL/100 g) into the biliopancreatic duct. Rats were pre-treated with saline or catalpol (50 mg/kg) 2 h before STC injection. At 12, 24 and 48 h after injection, the severity of AP was evaluated using biochemical and morphological analyses. Pretreatment with catalpol led to a significant reduction in serum amylase and lipase activities, pancreatic histological damage, myeloperoxidase (MPO) activity, interleukin (IL)-1β, IL-6 and TNF-α levels, and activation of nuclear factor kappa B (NF-κB). Moreover, administration of catalpol increased the viability of pancreatic acinar cells and inhibited NF-κB expression in vitro. Our results collectively support the potential of catalpol as a highly effective therapeutic agent for treatment of AP.
Highlights
Acute pancreatitis (AP) is a severe inflammatory condition of the pancreas caused by multiple factors
The optimal effective dose of catalpol was evaluated based on the levels of serum amylase and lipase, two biochemical indicators closely related to pancreatic damage
We examined the effect of catalpol in a well-characterized model of acute pancreatitis (AP) induced by sodium taurocholate (STC), which is similar to human AP in view of the typical inflammation performance
Summary
Acute pancreatitis (AP) is a severe inflammatory condition of the pancreas caused by multiple factors. It is generally believed that the severity of pancreatitis is determined by initial events in pancreatic acinar cells. These events, including activation of zymogens and release of proinflammatory cytokines, such as interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α, result in recruitment of inflammatory cells, such as neutrophils and macrophages, leading to further acinar cell injury and inflammation of chemical mediators [3,4]. The transcription factor, NF- B, a key regulator of cytokine induction, activates AP early on in acinar cells and promotes the expression of multiple proinflammatory genes [5,6,7,8]. Recent studies showed that the severity of pancreatitis in transgenic mice is increased through activation of NF- B in acinar cells [9], and the inflammatory response and severity of AP can be attenuated through inhibition of NF- B activity [8,10]
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