Protective Effects of Calcitonin Gene-Related Peptide-Mediated p38 Mitogen-Activated Protein Kinase Pathway on Severe Acute Pancreatitis in Rats

Hu, Shaohui; Guang, Yi; Wang, Weixing

doi:10.1007/s10620-018-5345-4

Cited by 6 publications

(6 citation statements)

References 37 publications

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“…It is well documented that MPO activity is a key indicator reflecting the accumulation of polymorphonuclear neutrophils in the pancreatic tissues [ 29 , 30 ]. Decreased SOD activity is considered to be closely related to oxidative stress [ 31 , 32 ].…”

Section: Resultsmentioning

confidence: 99%

“…It is well documented that MPO activity is a key indicator reflecting the accumulation of polymorphonuclear neutrophils in the pancreatic tissues [29,30].…”

Section: Ctrp3 Over-expression Decreases Mpo Activity and Increases Smentioning

confidence: 99%

“…Severe acute pancreatitis (SAP), the most serious pathological type of AP, account for roughly 15% of all AP cases [9,10]. It is well documented that SAP is characterized by a rapid onset and a high mortality [11,12].…”

Section: Introductionmentioning

confidence: 99%

“…Severe AP (SAP), the most serious pathological type of AP, accounts for roughly 15% of all AP cases [ 9 , 10 ]. It is well documented that SAP is characterized by a rapid onset and a high mortality [ 11 , 12 ]. It is widely acknowledged that activation of NF-κB signaling pathway could induce inflammatory response during the pathogenesis of AP [ 13–15 ].…”

Section: Introductionmentioning

confidence: 99%

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CTRP3 ameliorates cerulein-induced severe acute pancreatitis in mice via SIRT1/NF-κB/p53 axis

Wei

et al. 2020

Bioscience Reports

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Severe acute pancreatitis (SAP) is a common and life-threatening clinical acute abdominal disease. C1q/tumor necrosis factor-related protein 3 (CTRP3), a novel paralog of adiponectin, has been identified as a crucial regulator in multiple types of inflammatory disorders. However, the biological role of CTRP3 in SAP remains poorly understood. This study aimed to characterize the role of CTRP3 in SAP and illuminate the potential mechanisms involved. In the current study, SAP mouse models were induced by seven hourly intraperitoneal injection of cerulein (50 μg/kg) and an immediate intraperitoneal injection of lipopolysaccharide (10 mg/kg) after the last cerulein administration. Histological examination and serological analysis demonstrated that SAP mouse models were successfully established. Herein, we found that CTRP3 expression was significantly decreased in the pancreatic tissues of SAP mice compared with normal control mice. Furthermore, we explored the effects of CTRP3 rescue in SAP mice and discovered that CTRP3 over-expression attenuated pathological lesions, inhibited inflammatory mediator release and repressed acinar cell apoptosis. Notably, mechanistic studies revealed that CTRP3 over-expression suppressed NF-κB p65 phosphorylation and p53 acetylation to alleviate cerulein-induced SAP in mouse models through activation of silent information regulator 1 (SIRT1), a nicotinamide adenine dinucleotide-dependent protein deacetylase. Collectively, our data indicate that CTRP3 may exert its protective effects in SAP mice via regulation of SIRT1-mediated NF-κB and p53 signaling pathways, implying a promising therapeutic strategy against SAP.

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Section: Resultsmentioning

confidence: 99%

“…It is well documented that MPO activity is a key indicator reflecting the accumulation of polymorphonuclear neutrophils in the pancreatic tissues [29,30].…”

Section: Ctrp3 Over-expression Decreases Mpo Activity and Increases Smentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

CTRP3 ameliorates cerulein-induced severe acute pancreatitis in mice via SIRT1/NF-κB/p53 axis

Wei

et al. 2020

Bioscience Reports

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“…It has been previously reported to improve pancreatic microcirculation (Zhang et al, 2018), in addition to exerting antiinflammatory and antioxidant effects in AP. Moreover, pretreatment with exogenous CGRP reduced oxidative stress and inflammatory response of severe AP by suppressing p38 MAPK pathway activity (Hu, Guang, & Wang, 2019). RUT has also been demonstrated to affect signal transduction in other inflammatory conditions.…”

Section: Discussionmentioning

confidence: 99%

Rutaecarpine alleviates acute pancreatitis in mice and AR42J cells by suppressing the MAPK and NF‐κB signaling pathways via calcitonin gene‐related peptide

Huang

Wang

Guo

et al. 2021

Phytotherapy Research

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Acute pancreatitis (AP) is an acute inflammatory condition of the pancreas. Previous studies have shown that rutaecarpine (RUT), an important alkaloid component of Evodia rutaecarpa, exhibits certain protective effects against AP in rats by upregulating calcitonin gene-related peptide (CGRP). However, the molecular mechanism of RUT in AP remains unknown. This study aimed to investigate the effects of RUT on ceruleininduced AP in vivo and in vitro, and to explore the underlying molecular mechanisms.In cerulein/LPS-treated wild-type mice, but not CGRP gene knock-out mice, RUT significantly ameliorated pancreatic inflammation by alleviating histopathological changes, reducing IL-6 and TNF-α levels, and increasing in IL-10 levels. Moreover, RUT improved AP by suppressing the MAPK and NF-κB signaling pathways. These effects were mostly mediated through CGRP. Cell-based studies revealed that RUT significantly improved cell viability while suppressing the apoptosis of AR42J cells with cerulein-induced AP, downregulating IL-6 and TNF-α, stimulating IL-10 release, and inhibiting MAPK, NF-κB, and STAT3 signaling activation, all in a CGRP-dependent manner. RUT ameliorated cerulein/LPS-induced AP inflammatory responses in mice and AR42J cells in a CGRP-dependent manner and thus may represent a potential therapeutic option for AP patients. Our study provides valuable insights for AP drug development.

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Putative molecular targets for vitamin A in neutralizing oxidative stress in acute and chronic pancreatitis — a systematic review

Burzyński

Fichna

Tarasiuk

2023

Naunyn-Schmiedeberg's Arch Pharmacol

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Acute pancreatitis (AP) and chronic pancreatitis (CP) are debilitating diseases of gastrointestinal tract and constitute great threat for human health in high-income countries. Recent studies emphasize the impact of oxidative stress on development of these pathologies, and numerous authors evaluate the effect of the antioxidant therapy on the course of AP and CP. Though several antioxidative agents were discovered in the past decades, vitamins remain canonical antioxidants. Despite the fact that vitamin A is known for its antioxidative effect, there is little data about the impact of vitamin A on oxidative stress in the pathogenesis of AP and CP. The scope of the review is to evaluate molecular targets for vitamin A, which may be involved in oxidative stress occurring in the course of AP and CP. Our research of available literature revealed that several mechanisms are responsible for attenuation of oxidative stress in AP and CP, including Nrf2, MAPK, AMPK, TLR3, and TLR4. Furthermore, these factors are at least partially expressed in vitamin A-dependent manner, though further investigations are required for elucidating in detail the role of vitamin A in defense against reactive oxygen species. Our review revealed that vitamin A might influence the expression of several molecular pathways involved in antioxidative defense and cytoprotection; thus, its administration during AP and CP may change the course of the disease.

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Protective Effects of Calcitonin Gene-Related Peptide-Mediated p38 Mitogen-Activated Protein Kinase Pathway on Severe Acute Pancreatitis in Rats

Cited by 6 publications

References 37 publications

CTRP3 ameliorates cerulein-induced severe acute pancreatitis in mice via SIRT1/NF-κB/p53 axis

CTRP3 ameliorates cerulein-induced severe acute pancreatitis in mice via SIRT1/NF-κB/p53 axis

Rutaecarpine alleviates acute pancreatitis in mice and AR42J cells by suppressing the MAPK and NF‐κB signaling pathways via calcitonin gene‐related peptide

Putative molecular targets for vitamin A in neutralizing oxidative stress in acute and chronic pancreatitis — a systematic review

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