Phytochemicals with protective effects against acute pancreatitis: a review of recent literature

Abstract

Context Acute pancreatitis (AP) is an acute abdominal inflammatory disease with episodes ranging from mild to fulminant symptoms which could include necrosis, systemic inflammation and multiple organ dysfunction. Increasing experimental evidence demonstrates that specific bioactive ingredients from natural plants have a favourable therapeutic effect on AP. Objective The objective of this review is to summarize the protective effects and potential mechanisms of action of phytochemicals on the attenuation of AP. Methods Experimental studies in vivo or in vitro between January 2016 and June 2021 were sought in PubMed and Web of Science using the following search terms: (‘phytochemicals’ OR ‘medicinal plant’ OR ‘traditional medicine’) AND (‘pancreatitis’ OR ‘pancreatic damage’ OR ‘pancreatic injury’). Data concerning the basic characteristics of phytochemicals, therapeutic dose and potential molecular mechanisms related to AP were extracted in this study. Results A total of 30 phytochemicals with potential therapeutic effects were reviewed and summarized systematically. According to their molecular pathways in AP, the underlying mechanisms of the phytochemicals were illustrated in detail. Discussion and conclusions The phytochemicals with anti-inflammatory and antioxidant abilities may be efficient candidate drugs for AP treatment. Importantly, more preclinical investigations are needed to illustrate the efficacy of future phytochemicals.

Wistin Exerts an Anti-Inflammatory Effect via Nuclear Factor-κB and p38 Signaling Pathways in Lipopolysaccharide-Stimulated RAW264.7 Cells

“…The MAPK pathway (ERK, JNK, and p38) regulates pro-inflammatory mediators [ 41 ]. In particular, p38 can induce NF-κB activation to induce the expression of pro-inflammatory cytokines [ 51 ]. p38 MAPK activates mitogen- and stress-activated protein kinases (MSK), which can activate NF-κB (p65 subunit) signaling [ 52 ].…”

Ameliorative Effects of Gut Microbial Metabolite Urolithin A on Pancreatic Diseases

“…The pathogenesis of AP is associated with complex intra-acinar events, such as autophagy, oxidative stress, mitochondrial dysfunction, and ER stress [46]. Furthermore, inflammatory responses, including the recruitment of immune cells, activation of damage-related molecular patterns, and release of various inflammatory cytokines and chemokines, have been partly involved in the development of AP [47]. Based on recent studies on the effects of natural active substances on AP, three major signaling pathways, including NF-κB, Nrf2, and MAPK, have received great interest and attention from researchers and industries [47].…”

“…Furthermore, inflammatory responses, including the recruitment of immune cells, activation of damage-related molecular patterns, and release of various inflammatory cytokines and chemokines, have been partly involved in the development of AP [47]. Based on recent studies on the effects of natural active substances on AP, three major signaling pathways, including NF-κB, Nrf2, and MAPK, have received great interest and attention from researchers and industries [47]. (1) During the development of AP, NF-κB is rapidly activated in pancreatic acinar cells, followed by significant increases in inflammatory cytokines and chemokines, which can affect vascular permeability and lead to thrombosis, bleeding, and tissue necrosis [48,49].…”

“…It also down-regulates the expression and secretion of malonic dialdehyde (MDA), myeloperoxidase (MPO), C-reaction protein (CRP), and other inflammatory proteins. (3) Three predominant members of the MAPK family, c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38 MAPK, are upregulated to mitigate early AP progression by reducing pancreatic acinar cells damage and inhibiting inflammation [47].…”

Alteration of Peripheral Resistin and the Severity of Acute Pancreatitis: A Meta-Analysis

“…Pancreatic injury is mild and self-limiting in approximately 80% of patients with AP that would find their health after brief hospitalization. Unfortunately, the other 20% of patients with AP would develop lethal severe acute pancreatitis (SAP) that requires intensive care ( 2 , 3 ). Despite improvements in treatment measurements and supportive care, SAP remains one of the important causes of death during the past decade ( 4 ).…”