Effect of Non-Alcoholic Compounds of Alcoholic Drinks on the Pancreas

Feick, Peter; Gerloff, Andreas; Singer, Manfred V.

doi:10.1159/000104237

Cited by 16 publications

(14 citation statements)

References 21 publications

(22 reference statements)

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“…It has been shown to reduce the incidence of a variety of carcinogen-induced tumors 20 . The anticarcinogenic effect of EA was shown in several types of cancers [21][22][23][24][25] . In our study we observed, EA at 25-200µM strikingly reduced the cell viability of U251 cells, suggesting the anti-proliferative efficacy.…”

Section: Discussionmentioning

confidence: 99%

Ellagic acid inhibits proliferation and induces apoptosis in human glioblastoma cells

et al. 2016

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PURPOSE:To investigate the anticancer activity of ellagic acid (EA) in U251 human glioblastoma cells and its possible molecular mechanism. METHODS:The cells were treated with EA at various concentrations for different time periods. Cell viability and cell proliferation were detected by cell counting kit-8(CCK-8) assay and live/dead assay respectively. Cell apoptosis were measured with Annexin V-FITC/PI double staining method by flow cytometry and Mitochondrial membrane potential assay separately. Cell cycle was measured with PI staining method by flow cytometry. The expressions of Bcl-2, Survivin, XIAP, Caspase-3, Bax, JNK, p-JNK, ERK1/2, p-ERK1/2, p38, p-p38, DR4, DR5, CHOP and GRP78-related proteins were detected by western blot after EA treatment. RESULTS:Cell viability and proliferation of glioblastoma cells treated with EA were significantly lower than the control group. EA caused robust apoptosis of the glioblastoma cells compared to the control group. EA significantly decreased the proportion at G0/ G1 phases of cell cycling accompanied by increased populations at S phase in U251 cell lines. And the expressions of anti-apoptotic proteins were dramatically down-regulated. CONCLUSION:Ellagic acid potentially up-regulated DR4, DR5 and MAP kinases (JNK, ERK1/2 and p38). EA also caused significant increase in the expressions of CHOP and GRP78. Our findings suggest that EA would be beneficial for the treatment of glioblastoma.

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Section: Discussionmentioning

confidence: 99%

Ellagic acid inhibits proliferation and induces apoptosis in human glioblastoma cells

et al. 2016

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“…2,21,22 Moreover, quercetin has been shown to inhibit amylase release induced by agonists such as cholecystokinin, carbachol, phorbol ester tetra decanoylphorbol-13--acetate. [23][24][25] A recent study has shown that one hour after the last dose of cerulein administration, quercetin treatment attenuates the development of AP in mice. The aim of the present study was to evaluate the protective and therapeutic effects of quercetin on pancreatic injury in cerulein-induced acute pancreatitis in rats.…”

Section: Methodsmentioning

confidence: 99%

The effect of quercetin on cerulein-induced acute pancreatitis

Kahraman¹,

Vurmaz²,

Koca³

et al. 2017

Medical Express

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OBJECTIVE:The aim of this study was to evaluate the protective and therapeutic effects of quercetin on pancreatic injury in cerulein-induced acute pancreatitis. METHOD: Thirty-two rats were randomly divided into four groups, eight per group: (CT): untreated controls, (CER) treated with cerulein, 50 μg/kg body weight; (Q+CER) pre-treatment with quercetin, 100 mg/kg body weight, followed by cerulein, 50 μg/kg; (CER+Q) post-treatment, cerulein followed by quercetin, same doses. Cerulein was divided into four doses, given at 1-hour intervals by intraperitoneal injection. Quercetin was given either 1-hour before (in pre-treatment group) or 1-hour after (in post-treatment group) cerulein. Pancreatic malondialdehyde (MDA), carbonyl, myeloperoxidase (MPO), tumor necrosis factor-alpha (TNF-a), interleukin-6 (IL-6), reduced and oxidized glutathione (GSH and GSSG, respectively) were measured. Histology of the pancreas was studied. RESULTS: (1) MDA, carbonyl, MPO, TNF-a and IL-6 levels were significantly higher in CER vs CT rats. (2) MDA, carbonyl, MPO and TNF-α decreased significantly in pre-treated rats vs. CER. (3) MDA, MPO, TNF-α, IL-6 were significantly lower in post-treated rats vs. CER. (4) The reduced vs. oxidized glutathione ratio (GSH/GSSG) of was significantly lower CER vs. CT rats. (5) Pre-and post-treatment with quercetin significantly increased this ratio. (6) Pancreatic histology showed that quercetin had no significant effect on the histological image of the pancreas CONCLUSION: These results suggest that quercetin can attenuate the severity of cerulein-induced acute pancreatitis by acting as an antioxidant and anti-inflammatory agent and combating oxidative stress. Further studies are needed to clearly explain its utility on acute pancreatitis.

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“…Wiadomo, że alkohol etylowy wprowadzony dożylnie hamuje międzytrawienną aktywność zewnątrzwydziel-niczą tego narządu. Jednak w warunkach normalnych, kiedy napoje alkoholowe są przyjmowane doustnie, najczęściej zresztą razem z pokarmami, ich wpływ na egzokrynną czynność trzustki zależy nie tylko od stę-żenia etanolu, lecz także od oddziaływania składników niealkoholowych [82,83]. W badaniach Hajnala i wsp.…”

Section: Wpływ Napojów Alkoholowych Na Trzustkęunclassified

Alcohol and the digestive system – should it always be blamed?

Kasicka-Jonderko¹

2012

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Effect of Non-Alcoholic Compounds of Alcoholic Drinks on the Pancreas

Abstract: unknown, caution is required in attempting to define alcoholic etiology of pancreatitis without considering the effect of non-alcoholic compounds of alcoholic beverages.

Cited by 16 publications

References 21 publications

Ellagic acid inhibits proliferation and induces apoptosis in human glioblastoma cells

Ellagic acid inhibits proliferation and induces apoptosis in human glioblastoma cells

The effect of quercetin on cerulein-induced acute pancreatitis

Alcohol and the digestive system – should it always be blamed?

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