Key result
DSC alleviates caerulein-induced acute pancreatitis by inhibiting NF-κB, STAT3, and NLRP3 inflammasome activation.
Why the study?
Inflammation is the main cause of pancreatic damage in acute pancreatitis, but the potential beneficial effect of the novel danshensu derivative DSC in AP has not been demonstrated.
Does DSC alleviate pancreatic inflammation and damage in mice with caerulein-induced acute pancreatitis?
Does DSC alleviate pancreatic inflammation and damage in mice with caerulein-induced acute pancreatitis?
DSC alleviates pancreatic inflammation and damage in experimental acute pancreatitis by inhibiting NF-κB, STAT3, and NLRP3 inflammasome activation.
DSC may support preclinical testing in acute pancreatitis; leaves open translation to human disease and clinical trials.
Acute pancreatitis (AP), a common abdominal inflammatory disorder, is characterized by premature intracellular activation of digestive proteases within pancreatic acini and a consecutive systemic inflammatory response. Although the mechanism remains to be fully understood, inflammation is the main cause of pancreatic damage in AP. A novel compound [4-(2-acetoxy-3-((R)-3-(benzylthio)-1-methoxy-1-oxopropan-2-ylamino)-3-oxopropyl)-1,2-phenylene diacetate (DSC)], derived from danshensu, exhibits anti-inflammatory and anti-apoptotic properties in vitro. However, its potential beneficial effect in AP has not been demonstrated. This study aimed to investigate the effects and underlying mechanisms of DSC in experimental AP in mice. We found that DSC suppressed inflammatory responses in AP by inhibiting the activation of nuclear factor-κB (NF-κB), signal transducer and activator of transcription 3 (STAT3) and nucleotide-binding domain leucine-rich repeat containing family, pyrin domain-containing 3 (NLRP3) inflammasome. Furthermore, treatment with DSC modulated the infiltration of neutrophils and the phenotypes of macrophages in mice induced with AP. Interestingly, we found that the expression of nuclear factor-erythroid 2 related factor 2 (Nrf2) and its regulated antioxidant enzyme heme oxygenase-1 (HO-1), which modulate inflammatory activities, was significantly increased in DSC-treated groups. Together, our findings demonstrate that DSC alleviates pancreatic inflammation and damage in AP by inhibiting the activation of NF-κB, STAT3 and NLRP3 inflammasome and modulating immune cell responses.
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Ren et al. (2018) studied Acute Pancreatitis. DSC (Danshensu derivative) vs. Caerulein alone or Dexamethasone was evaluated on Pancreatic inflammation and damage (edema, amylase, lipase, histology). DSC alleviated pancreatic inflammation and damage in caerulein-induced acute pancreatitis by inhibiting NF-κB, STAT3, and NLRP3 inflammasome activation and modulating immune cell responses.
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