Cyclooxygenase-2 is Overexpressed in Chronic Pancreatitis

Schultze-Seemann, Wolfgang; Schlosser, Sophia; Ramadani, Marco; Gansauge, Frank; Gansauge, Susanne; Beger, H. G.

doi:10.1097/00006676-200207000-00008

Cited by 73 publications

(67 citation statements)

References 25 publications

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“…During AP, the cell membrane ruptures, intestinal bacteria enter the blood, and circulatory, respiratory, urinary, and digestive system abnormalities occur. The results were consistent with previous reports that systemic inflammatory response syndrome (SIRS) and multiple organ failure (MOF) are caused by AP (Schlosser et al, 2002;Isenmann, Rau, Beger, 2001;Buter et al, 2002). When rheum was administered to the rats, multiple metabolic abnormalities such as the occurrence of amines were not observed, even though several metabolic pathways were impacted.…”

Section: Other Metabolitessupporting

confidence: 91%

Metabolic analysis of the effect of rheum on a taurocholate-induced acute pancreatitis rat model

Chen

Shen

Yang

et al. 2017

Braz. J. Pharm. Sci.

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The effects of rheum on serum parameters in a taurocholate-induced acute pancreatitis (AP) rat model were investigated using pathological and biochemical tests, and a proton nuclear magnetic resonance ( 1 H NMR)-based metabonomic strategy. Healthy rats and rats with AP were either treated with rheum (7.5% at a dose of 1.5 g/kg) or left untreated. Serum samples were collected from the AP and rheum-treated groups at 6, 12, and 24 h after treatment. The effect of rheum on pathological changes in the pancreatic was investigated to validate the AP model. We obtained 1 H NMR spectra and analyzed the results using the partial least squares discriminant method. The results of the pathological and metabolic analyses revealed an amelioration of multiple metabolic abnormalities and an increase in the aerobic respiration ratio after treatment, compared with the AP groups. These results were attributed to improvements in energy supply and the elimination of metabolic products. The study also promoted NMR-based metabonomic analysis as a feasible method of assessing traditional Chinese drugs.

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Section: Other Metabolitessupporting

confidence: 91%

Metabolic analysis of the effect of rheum on a taurocholate-induced acute pancreatitis rat model

Chen

Shen

Yang

et al. 2017

Braz. J. Pharm. Sci.

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“…The constitutively expressed COX-1 appears to regulate many normal physiologic functions in several cell types, whereas the inducible COX-2 enzyme mediates the inflammatory response. Aberrant COX-2 expression was initially described in colorectal cancer and has now been detected in many human tumors including breast and pancreatic cancers [33,96]. Epidemiological studies have shown that the risk of developing cancers of the colon, breast, esophagus, and stomach is lowered following the ingestion of nonsteroidal anti-inflammatory drugs (NSAIDs) [71].…”

Section: Importance Of Epigenetic Mechanisms As Targets For Chemoprevmentioning

confidence: 99%

The roles of polyphenols in cancer chemoprevention

2006

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Abstract.Oxidative stress imposed by reactive oxygen species (ROS) plays a crucial role in the pathophysiology associated with neoplasia, atherosclerosis, and neurodegenerative diseases. The ROS-induced development of cancer involves malignant transformation due to altered gene expression through epigenetic mechanisms as well as DNA mutations. Considerable attention has been focused on identifying naturally occurring antioxidative phenolic phytochemicals that are able to decrease ROS levels, but the efficacies of antioxidant therapies have been equivocal at best. Several studies have shown that some antioxidants exhibit prooxidant activity under certain conditions and potential carcinogenicity under others, and that dietary supplementation with large amounts of a single antioxidant may be deleterious to human health. This article reviews the intracellular signaling pathways that respond to oxidative stress and how they are modulated by naturally occurring polyphenols. The possible toxicity and carcinogenicity of polyphenols is also discussed.

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“…Furthermore, NS398, a selective COX-2 inhibitor, reduced the growth of PSCs by PANC-1 CM. Several studies have indicated that COX-2 expression is high in both chronic pancreatitis and PDAC therefore suggesting a potential role in fibrosis (6,29). COX-2 levels are also known to positively correlate with the aggressiveness of PDAC (30) and that blocking COX-2 significantly reduces pancreatic tumor size and metastatic potential (31) in animal models.…”

Section: Discussionmentioning

confidence: 99%

“…By immunohistochemistry (IHC), COX-2 was found to be highly expressed in chronic pancreatitis (6), pancreatic adenocarcinoma (7,(13)(14)(15) and pancreatic intraepithelial neoplasia (PanIN) (16). The expression of COX-2 in chronic pancreatitis is primarily localized in the cytoplasm of pancreatic acinar cells, islet cells, and ductal cells (6), while in pancreatic adenocarcinoma it is localized primarily to cancer cells (7). Transgenic over-expression of COX-2 in the pancreas led to the development of pancreatic fibrosis and even cellular transformation (17).…”

Section: Introductionmentioning

confidence: 99%

PGE2 regulates pancreatic stellate cell activity via the EP4 receptor

et al. 2013

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Objectives-Pancreatic stellate cells are source of dense fibrotic stroma, a constant pathological feature of chronic pancreatitis (CP) and pancreatic adenocarcinoma (PDAC). We observed correlation between levels of cyclooxygenase-2 (COX-2) and its product prostaglandin E2 (PGE 2 ) and the extent of pancreatic fibrosis. Aim of this study was to delineate the effects of PGE 2 on immortalized human pancreatic stellate cells (HPSC) and to identify the receptor involved. The authors have no any potential conflict of interest including any financial, personal, or other relationships with other people or organizations that could inappropriately influence this work. MethodsPublisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptPancreas. Author manuscript; available in PMC 2014 April 01. by LC/MS/MS. HPSC proliferation was assessed by MTS assay; migration by Boyden chamber assay and invasion using an invasion chamber. Transient silencing was obtained by siRNA.Results-HPSC express COX-2 and synthesize PGE 2 . PGE 2 stimulated HPSC proliferation, migration and invasion; stimulated expression of both ECM and MMP genes. HPSC expressed all four EP receptors. Only blocking the EP4 receptor resulted in abrogation of PGE 2 mediated HPSC activation. Specificity of EP4 for the effects of PGE 2 on stellate cells was confirmed using specific antagonists.Conclusion-Our data indicate that PGE 2 regulates PSC profibrotic activities via EP4 receptor thus suggesting EP4 receptor as useful therapeutic target for pancreatic cancer to reduce desmoplasia.

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Cyclooxygenase-2 is Overexpressed in Chronic Pancreatitis

Abstract: Our results support the hypothesis that COX-2 may be involved in inflammatory responses in chronic pancreatitis and in the progression of this chronic inflammatory disease.

Cited by 73 publications

References 25 publications

Metabolic analysis of the effect of rheum on a taurocholate-induced acute pancreatitis rat model

Metabolic analysis of the effect of rheum on a taurocholate-induced acute pancreatitis rat model

The roles of polyphenols in cancer chemoprevention

PGE2 regulates pancreatic stellate cell activity via the EP4 receptor

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