COX-2 inhibition results in alterations in nuclear factor (NF)-κB activation but not cytokine production in acute pancreatitis

Slogoff, Michele; Ethridge, Richard T.; Rajaraman, Srinivasan; Evers, B. Mark

doi:10.1016/j.gassur.2003.11.023

Cited by 25 publications

(16 citation statements)

References 55 publications

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“…VEHIC 1w group) showed increased COX-2, TNF-a and IL-6 mRNA levels, as well as an increased number of laryngeal cells immunoreactive to COX-2. These data are in accordance with studies including other inflammatory conditions, where these molecules were also significantly increased [26,27]. TNF-a and IL-6 induce COX-2 expression [28] and are known to induce the release of the pro-inflammatory neuropeptides SP and CGRP in different tissues [26,29].…”

Section: Discussionsupporting

confidence: 90%

“…However, no changes were observed in the IL-6, IL-1b and IL-10 mRNA levels. This could be conflicting data because Etoricoxib inhibits the nuclear factor kappa B (NF-jB) [24,25,27,30,31], an important mediator in many inflammatory conditions, and thus the levels of these interleukins were expected to be altered. These results may be explained by the occurrence of alternative pathways of cytokine production, possibly by alterations of the activity of cellular kinases, such as Erk, p38 MAPK or Cdks [32,33].…”

Section: Discussionmentioning

confidence: 99%

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The selective COX-2 inhibitor Etoricoxib reduces acute inflammatory markers in a model of neurogenic laryngitis but loses its efficacy with prolonged treatment

et al. 2010

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

The selective COX-2 inhibitor Etoricoxib reduces acute inflammatory markers in a model of neurogenic laryngitis but loses its efficacy with prolonged treatment

et al. 2010

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“…Slogoff et al, using a cerulein model of AP, showed that IL-6 levels were elevated in mice treated with COX-2 inhibitors, despite attenuated pancreatic inflammation and a decrease in NF-κB activation. 38 This finding suggests that the stimulus for IL-6 secretion remained intact, despite a lower NF-κB activity; however, it did not elucidate whether IL-6 is linked to the amelioration of AP in mice. In the present report, although serum levels of IL-6 were diminished, this was not associated with any benefit regarding the pancreatic histologic damage.…”

Section: Discussionmentioning

confidence: 89%

Inhibition of Cyclooxygenase-2 in Experimental Severe Acute Pancreatitis

Almeida

Jukemura

Coelho

et al. 2006

Clinics

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BACKGROUND:The standard treatment for acute pancreatitis (AP) is still based on supportive care. The search for a new drug that could change the natural history of the disease is a continuing challenge for many researchers. The aim of this study is to evaluate the effect of a cyclooxygenase-2 (COX-2) inhibitor on experimental AP in rats. METHODS:The animals were divided into 2 groups: Group 1 (n = 30)-animals with taurocholate-induced AP treated with parecoxib (40 mg/kg). Group 2 (n = 30)-animals with taurocholate-induced AP that received saline. The COX-2 inhibitor (parecoxib) was injected immediately after AP induction, through the penis dorsal vein. The parameters evaluated were histology, serum levels of amylase, IL-6 and IL-10, and mortality rate. RESULTS: The serum levels of IL-6 and IL-10 in the parecoxibtreated group were lower than the control group. The amylase serum levels and the mortality rate remained unchanged in the treated animals. Histologic morphology also was unaltered, except for fat necrosis, which was higher in parecoxib-treated rats. CONCLUSION: Inhibition of Cox-2 decreases the systemic release of inflammatory cytokines, but has a poor effect on the direct pancreas injury caused by taurocholate.

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“…( 1998) found that infection of HT -29 colon cancer cells with an NF-ICB superrepressor significantly decreased COX-2 mRNA and prote in expression in response to TNF-u st imul ation. Slogoff et al (2004) described inhibition of late-phase NF-ICB act ivation via COX-2 inhibition. It has also been demonstrated that Akl can modulate the stabi lity of COX-2 mRNA (Shao et aJ., 2000).…”

Section: Summary Of Pathwaysmentioning

confidence: 99%

Chronic Inflammation and Pathogenesis of GI and Pancreatic Cancers

Jackson

Evers

2006

Cancer Treatment and Research

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Abstract:Keywords:The pathogenesis of cancer represents a complex and multifactorial process requiring a number of acquired and genetic defects. It is becoming increasingly apparent that many cancers originate from a chronic inflammatory process, The topic of this review is the inflammatory response and development of gastrointestinal (GI) and pancreatic cancers, Here, we describe the development of various gastric colorectal and pancreatic cancers through an inflammatory process. The tumor microenvironment which predisposes to tissue destruction, subsequent attempts at healing and accumulation of cellular damage with loss of cell cycle control mechanisms is discussed. Components of the tumor microenvironment that are important in the final common pathway leading to cancer include the tumor stroma, tumor-associated macrophages, cytokines and chemokines and reactive oxygen and nitrogen species. Common signaling pathways that link inflammation with cancer are described and include the COX-2, NF-KB and phosphatidyl inositol 3-kinase (PI3K) pathways. Finally, therapies that can be directed to the inflammatory process as either treatment or prevention of these cancers will be discussed including novel inhibitors of signaling pathways which are currently in development.

show abstract

COX-2 inhibition results in alterations in nuclear factor (NF)-κB activation but not cytokine production in acute pancreatitis

Cited by 25 publications

References 55 publications

The selective COX-2 inhibitor Etoricoxib reduces acute inflammatory markers in a model of neurogenic laryngitis but loses its efficacy with prolonged treatment

The selective COX-2 inhibitor Etoricoxib reduces acute inflammatory markers in a model of neurogenic laryngitis but loses its efficacy with prolonged treatment

Inhibition of Cyclooxygenase-2 in Experimental Severe Acute Pancreatitis

Chronic Inflammation and Pathogenesis of GI and Pancreatic Cancers

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