Effect of Adiponectin and Ghrelin on Apoptosis of Barrett Adenocarcinoma Cell Line

Konturek, Peter C.; Burnat, Grzegorz; Rau, Tilman T.; Hahn, Eckhart G.; Konturek, Stanisław J.

doi:10.1007/s10620-007-9922-1

Cited by 90 publications

(76 citation statements)

References 29 publications

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“…HippisleyCox et al [109] Population based Kaye et al [111] Population based Bhutta et al [112] Population based Beales et al [37] Casecontrol Because adiponectin and ghrelin can interfere in vitro with EAC cell apoptosis [126] , obesity, a parameter overlooked by most observational studies [40,41,43] , mandates further attention.…”

Section: Beneficial Effectmentioning

confidence: 99%

Role of chemoprophylaxis with either NSAIDs or statins in patients with Barrett’s esophagus

Tsibouris

Vlachou

Isaacs

2014

WJGPT

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The incidence of esophageal adenocarcinoma, a poor prognosis neoplasia, has risen dramatically in recent decades. Barrett's esophagus represents the best-known risk factor for esophageal adenocarcinoma development. Non-steroidal anti-inflammatory drugs through cyclooxygenase-2 inhibition and prostaglandin metabolism regulation could control cell proliferation, increase cell apoptosis and regulate the expression of growth and angiogenic factors. Statins can achieve equivalent effects through prenylation and subsequently control of cellular signaling cascades. At present, epidemiological studies are small and underpowered. Their data could not justify either medication as a chemo-preventive agent. Population based studies have shown a 43% reduction of the odds of developing an esophageal adenocarcinoma, leaving out or stating a 25% reduction in patients consuming non-aspirin nonsteroidal antiinflammatory drugs and a 50% reduction in those patients consuming aspirin. They have also stated a 19% reduction of esophageal cancer incidence when statins have been used. Observational studies have shown that non-steroidal anti-inflammatory drugs could reduce the adenocarcinoma incidence in patients with Barrett's esophagus by 41%, while statins could reduce the risk by 43%. The cancer preventive effect has been enhanced in those patients taking a combination of non-steroidal anti-inflammatory drugs and statins (a 74% decrease). Observational data are equivocal concerning the efficacy of non-steroidal anti-inflammatory drug subclasses. Non-steroidal anti-inflammatory drugs clearly have substantial potential for toxicity, while statins are rather safe drugs. In conclusion, both non-steroidal anti-inflammatory drugs and statins are promising chemopreventive agents and deserve further exploration with interventional studies. In the meanwhile, their use is justified only in patients with cardiovascular disease.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved.Key words: Esophageal adenocarcinoma; Barrett's esophagus; Non-steroidal anti-inflammatory drugs; Aspirin; Statins; Cancer chemoprevention Core tip: Esophageal adenocarcinoma remains a major burden upon health. Experimental studies have suggested that non-steroidal anti-inflammatory drugs and statins may have useful actions against esophageal cancer cells. This review of observational studies shows that non-steroidal anti-inflammatory drugs reduced adenocarcinoma incidence in patients with Barrett' s esophagus by 41%, while statins reduced the risk by 43%. The cancer preventive effect is enhanced in those patients taking a combination of non-steroidal anti-inflammatory drugs and statins (a 74% decrease). Non-steroidal anti-inflammatory drugs clearly have substantial potential for toxicity, while statins are rather safe drugs. Their combination offers promise for chemoprevention and further interventional studies are warranted.Tsibouris P, Vlachou E, Isaacs PET. Role of chemoprophylaxis REVIEWOnline Submissions: http://www.wjgnet.com/esps/

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Section: Beneficial Effectmentioning

confidence: 99%

Role of chemoprophylaxis with either NSAIDs or statins in patients with Barrett’s esophagus

Tsibouris

Vlachou

Isaacs

2014

WJGPT

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“…Unlike leptin, adiponectin levels are decreased in obesity, and low levels of adiponectin have been associated with an increased risk of BE and EAC (Rubenstein et al, 2008;Yildirim et al, 2009). Its role in the development of cancer is believed to be protective through antiproliferative (Ogunwobi and Beales, 2008a) and pro-apoptotic effects (Konturek et al, 2008). Adiponectin leads to a dose-dependent increase in the rate of apoptosis in esophageal cancer cell lines, which can be explained by a dose dependent increase and decrease in mRNA and protein expression of pro-apoptotic BAX and anti-apoptotic Bcl-2, respectively (Konturek et al, 2008).…”

Section: Adiposity and Adipokinesmentioning

confidence: 99%

“…Its role in the development of cancer is believed to be protective through antiproliferative (Ogunwobi and Beales, 2008a) and pro-apoptotic effects (Konturek et al, 2008). Adiponectin leads to a dose-dependent increase in the rate of apoptosis in esophageal cancer cell lines, which can be explained by a dose dependent increase and decrease in mRNA and protein expression of pro-apoptotic BAX and anti-apoptotic Bcl-2, respectively (Konturek et al, 2008). Its anti-proliferative effects may be mediated through its actions on adiponectin receptor-1 as well as activation of adenosine monophosphate activated protein kinase and serine/threonine phosphatases, which ultimately lead to modulation of p53 and p21 (Ogunwobi and Beales, 2008a); (Rubenstein et al, 2009).…”

Section: Adiposity and Adipokinesmentioning

confidence: 99%

“…Ghrelin levels have been shown to be inversely related to adiposity and EAC risk (de Martel et al, 2007), but the biomolecular mechanism underlying this association has not been completely elucidated. There may be an anti-inflammatory component to the mechanism, as evidence suggests that ghrelin inhibits the increased production of COX-2 and interleukin-1β (IL-1β) by tumor necrosis factor alpha (TNFα) (Konturek et al, 2008). In addition, ghrelin stimulates gastric motility by stimulating the vagus nerve and myenteric neurons.…”

Section: Adiposity and Adipokinesmentioning

confidence: 99%

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Gastroesophageal Reflux Disease: Molecular Predictors in Neoplastic Progression of Barrett's Esophagus

François¹,

Khan²,

Yang³

et al. 2012

Gastroesophageal Reflux Disease

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“…13 In addition to modulating gastric acid secretion and accelerating gastric emptying, 8,9 it has been reported to protect the gastric mucosa from acute gastric injury. 5,[14][15][16][17] Thus, ghrelin and DA-9601 seem to have similar gastro-protective effects. The aim of this study was to examine possible interaction between DA-9601 and ghrelin in acute gastric injury induced by ethanol or indomethacin.…”

Section: Introductionmentioning

confidence: 99%

Augmenting Effect of DA-9601 on Ghrelin in an Acute Gastric Injury Model

Baek

Lee²,

Jun³

et al. 2011

Gut Liver

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Background/Aims: Acute gastric injury by alcohol or indomethacin has been reported to be prevented by DA-9601, an extract of the herb Artemisia asiatica. Ghrelin, an endogenously produced gastrointestinal peptide hormone, has also been demonstrated to play a role in gastric mucosal defense. The aim of this study was to investigate the effects of DA-9601 on ghrelin in an acute gastric injury model induced by alcohol or indomethacin. Methods: A total of 140 SpragueDawley rats were divided into two groups, a placebo group and a DA-9601-pretreated group. Thirty minutes later, half of the rats in each group received ethanol injury and the other half received indomethacin injury. Levels of serum ghrelin and gastric mucosal ghrelin mRNA were measured by ELISA and RT-PCR, respectively. Results: Immediately after ethanol administration, ghrelin increased in both groups pretreated with DA-9601 and placebo. However, the increase occurred more rapidly and was higher in the DA-9601-pretreated rats than in the controls that did not receive DA-9601-pretreatment. Similarly, from 30 minutes to 2 hours after indomethacin administration, the DA-9601-pretreated rats showed a significant increase in serum and gastric mucosal ghrelin concentrations, whereas placebo-pretreated rats showed only a mild increase. Conclusions: DA-9601 potentiates the endogenous production and secretion of ghrelin in acute gastric injury models induced by ethanol or indomethacin. (Gut Liver 2011;5:52-56) Key Words: DA-9601; Ghrelin; Acute gastric injury INTRODUCTIONThe gastric mucosa defends its structural integrity against many noxious substances such as alcohol and nonsteroidal anti-inflammatory drugs (NSAIDs) via pre-epithelial, epithelial and sub-epithelial factors that include the mucus barrier, bicarbonate secretion, epithelial tight junctions, prostaglandin (PG) synthesis, cell restitution, and mucosal blood flow.1 Alcohol ingestion may lead to gastric mucosal lesions by penetrating the gastric mucosa and causing mucosal inflammation, erosions and ulcer formation. 2-4 Alcohol-induced gastric injury is mediated by free radicals, which is supported by the fact that ethanol administration depletes cells of major antioxidants such as superoxide dismutase, catalase, and glutathione peroxidase. Gastric injury induced by NSAIDs such as indomethacin is mediated by nonselective inhibition of the cyclooxygenase pathways, which results in decreased PG synthesis. DA-9601, an extract of Artemisia asiatica, has been reported to have anti-inflammatory, antioxidative and cytoprotective effects and therefore to play a protective role in experimentallyinduced gastrointestinal damage and hepatic and pancreatic lesions. [5][6][7][8][9] However, the underlying mechanisms of its gastric mucosal protective effects have not been fully elucidated. Another gastro-protective agent, ghrelin, which is made endogenously, has been recently found as one of the gut hormones. It affects the secretory and motor functions of gut as well as energy homeostasis by controlling appetite...

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Effect of Adiponectin and Ghrelin on Apoptosis of Barrett Adenocarcinoma Cell Line

Cited by 90 publications

References 29 publications

Role of chemoprophylaxis with either NSAIDs or statins in patients with Barrett’s esophagus

Role of chemoprophylaxis with either NSAIDs or statins in patients with Barrett’s esophagus

Gastroesophageal Reflux Disease: Molecular Predictors in Neoplastic Progression of Barrett's Esophagus

Augmenting Effect of DA-9601 on Ghrelin in an Acute Gastric Injury Model

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