Abstract
Previous studies have focused on the effects of propylene glycol alginate sodium sulfate (PSS) against thrombosis, but the anti-inflammatory potential is unknown. Therefore, we specifically focused on the protective effects of PSS on cerulein-induced acute pancreatitis (AP) using a mouse model, and investigated the mechanism of PSS on autophagy and apoptosis via the Mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway. Cerulein (100 ug/kg) was used to induce AP by ten intraperitoneal injections at hourly intervals in Balb/C mice. Pretreatment with vehicle or PSS was carried out 1 h before the first cerulein injection and two doses (25 mg/kg and 50 mg/kg) of PSS were injected intraperitoneally. The severity of AP was assessed by pathological score, biochemistry, pro-inflammatory cytokine levels, myeloperoxidase (MPO) activity and MEK/ERK activity. Furthermore, pancreatic histological scores, serum amylase and lipase activities, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β interleukin (IL)-6 levels, and MPO activity were significantly reduced by PSS via up-regulated MEK/ERK activity. The representative molecules of apoptosis and autophagy, such as Bcl-2, Bax, Lc-3, Beclin-1, P62, were remarkably reduced. Taken together, these results indicate that PSS attenuates pancreas injury by inhibiting autophagy and apoptosis through a mechanism involving the MEK/ERK signaling pathway.
Highlights
Acute pancreatitis (AP) is an acute inflammation that begins with acinar activation and culminates in varying degrees of severity including multiple organ failure and death caused by consecutive extra-acinar events
We showed that Propylene glycol alginate sodium sulfate (PSS) can attenuate acute pancreatitis (AP) induced by cerulein through the inhibition of the release of pro‐inflammatory cytokines, apoptosis Signaling and autophagy
Our results demonstrated that the Mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) signal pathway mediated cell apoptosis and autophagy in cerulein-induced AP
Summary
Acute pancreatitis (AP) is an acute inflammation that begins with acinar activation and culminates in varying degrees of severity including multiple organ failure and death caused by consecutive extra-acinar events. The acinar activation, which occurs in pancreatic acinar cells, includes the activation of zymogens and the release of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6. TNF-a plays a pivotal role in the initiation and spread of inflammatory cascade to other organs and subsequent systemic complications. Besides exacerbating pancreatic acinar cell injury, TNF-a can induce infiltration of neutrophils and initiate or aggravate the cascade of other proinflammatory cytokines. It can be said, when AP occurs, TNF-α can initiate the inflammatory response [1]. The main mechanism involves the induction of a large number of inflammatory factors, such as IL-1 and IL-6, which can
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