Alcohol and the Pancreas

Schenker, Steven; Montalvo, Ralph

doi:10.1007/0-306-47148-5_3

Cited by 39 publications

(27 citation statements)

References 90 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the digestive apparatus, alcohol Figures are representative of each group: control, rats treated with absolute ethanol; ginseng A, rats administered orally with ginseng extract A at 10 mg/kg body weight 1 h prior to ethanol treatment; and ginseng B, rats administered orally with ginseng extract B at 10 mg/kg body weight 1 h prior to ethanol treatment has commonly been considered for its toxic effects on liver and pancreas [20][21]. However, relatively little attention has been paid to its actions within the stomach.…”

Section: Discussionmentioning

confidence: 99%

Ginseng, the Root of Panax ginseng C.A. Meyer, Protects Ethanol-Induced Gastric Damages in Rat through the Induction of Cytoprotective Heat-Shock Protein 27

et al. 2007

View full text Add to dashboard Cite

Ginseng, the root of Panax ginseng C.A. Meyer, has been reported to exert preventive effects on gastropathy via anti-oxidative and anti-inflammatory actions. In this study, we investigated the protective effects of ginseng against ethanol-induced gastric damages in rat. To examine the preventive effect of ginseng, rats received two different ginseng extracts, A and B, 1 h prior to the administration of ethanol. Pretreatment of rats with ginseng extract A and B attenuated the ethanol-induced gastric lesions by 111 AE 48 and 142 AE 47 mm 2 compared to control group (164 AE 54 mm 2 ). Significant induction of cytoprotective heat-shock proteins HSP27 and HSP70 was found in the ginseng-administrated rats, suggesting that the restoration of the proteins might contribute to prevention of ethanol-induced gastric injuries. It is, therefore, suggested that ginseng has a protective effect against ethanol-induced gastric damages by induction of heat-shock proteins 70 and 27.

show abstract

Section: Discussionmentioning

confidence: 99%

Ginseng, the Root of Panax ginseng C.A. Meyer, Protects Ethanol-Induced Gastric Damages in Rat through the Induction of Cytoprotective Heat-Shock Protein 27

et al. 2007

View full text Add to dashboard Cite

show abstract

“…Acute pancreatitis is an important disease that can be triggered by a variety of factors, including excessive alcohol consumption, [13][14][15][16] obstruction of the ampulla of Vater by gall stones, 17,18 and genetic factors. 19,20 Hereditary chronic pancreatitis is a rare form of early onset chronic pancreatitis, characterized by the onset of recurrent attacks of acute pancreatitis in childhood, and frequently progresses to chronic pancreatitis.…”

mentioning

confidence: 99%

Relationship of strain-dependent susceptibility to experimentally induced acute pancreatitis with regulation of Prss1 and Spink3 expression

Wang

Ohmuraya

Suyama

et al. 2010

Laboratory Investigation

View full text Add to dashboard Cite

To analyze susceptibility to acute pancreatitis, five mouse strains including Japanese Fancy Mouse 1 (JF1), C57BL/6J, BALB/c, CBA/J, and C3H/HeJ were treated with either a cholecystokinin analog, cerulein, or a choline-deficient, ethioninesupplemented (CDE) diet. The severity of acute pancreatitis induced by cerulein was highest in C3H/HeJ and CBA/J, moderate in BALB/c, and mildest in C57BL/6J and JF1. Basal protein expression levels of the serine protease inhibitor, Kazal type 3 (Spink3) were higher in JF1 and C57BL/6J mice than those of the other three strains under normal feeding conditions. After treatment with cerulein, expression level of Spink3 increased remarkably in JF1 and mildly in C57BL/6J, BALB/c, CBA/J, and C3H/HeJ strains. Increased proteinase, serine, 1 (Prss1) protein expression accompanied by increased trypsin activity with cerulein treatment was observed in susceptible strains such as CBA/J and C3H/HeJ. Similar results were obtained with a CDE diet. In the 3 kb Spink3 promoter region, 92 or 8 nucleotide changes were found in JF1 or C3H vs C57BL/6J, respectively, whereas in the Prss1 promoter region 39 or 46 nucleotide changes were found in JF1 or C3H vs C57BL/6J, respectively. These results suggest that regulation of Prss1 and Spink3 expression is involved in the susceptibility to experimentally induced pancreatitis. The JF1 strain, which is derived from the Japanese wild mouse, will be useful to examine new mechanisms that may not be found in other laboratory mouse strains. Over 450 inbred strains of mice have been described, 1 providing a wealth of different genotypes and phenotypes for studying human diseases. Actually, the use of various breeding strategies in combination with positional cloning and positional candidate gene approach has led to the discovery of many genes that underlie human disease. 2 The Japanese wild mouse, belonging to Mus musculus molossinus, has several genetic characteristics clearly distinguishable from the European wild mouse, derived from M.m. domesticus. These subspecies were separated about one million years ago and about 1% of their genome sequences are different. [3][4][5][6][7][8] Therefore, strains MSM/Ms 9 and Japanese Fancy Mouse 1 (JF1), 10 which were established from M.m. molossinus, are powerful genetic resources to analyze disease processes.Many inbred strains have been bred for specific phenotypes. C57BL/6J mice are susceptible to high-fat diet-induced type II diabetes. 11 JF1 mice are especially sensitive to high-fat diet-induced diabetes and obesity, whereas MSM/Ms mice are resistant. 12 To date, however, there is little information about the difference in severity of pancreatitis among inbred strains of mice.Acute pancreatitis is an important disease that can be triggered by a variety of factors, including excessive alcohol consumption, 13-16 obstruction of the ampulla of Vater by gall stones, 17,18 and genetic factors. 19,20 Hereditary chronic pancreatitis is a rare form of early onset chronic pancreatitis, characterized by the onset of recurrent...

show abstract

“…However, the defense systems may be overcome, leading to the phenomenon known as "oxidative stress" (Ames et al, 1993;Anisimov, 1998;Harman, 1988). In recent years, this has become recognized or suggested as participating in the development of senescence, carcinogenesis, and a wide variety of diseases, either aging-dependent or independent (Ames et al, 1993;Ando et al, 1998;Anisimov, 1998;Busciglio et al, 1998;Facchinetti et al, 1998;Feher et al, 1998;Feig et al, 1994;Floyd, 1990;Harman, 1988;Hasselwander and Young, 1998;Hogg, 1998;Kaplowitz and Tsukamoto, 1996;Kasai, 1997;Minamoto et al, 1999;Peterhans, 1997;Reiter, 1998;Saugstad, 1998;Schenker and Montalvo, 1998;Singal et al, 1998;Stadtman and Berlett, 1998;Thomson et al, 1998;Zs-Nagy et al, 1988).…”

mentioning

confidence: 99%

Age and Organ Dependent Spontaneous Generation of Nuclear 8-Hydroxydeoxyguanosine in Male Fischer 344 Rats

Nakae

Akai

Kishida

et al. 2000

Laboratory Investigation

View full text Add to dashboard Cite

SUMMARY: 8-Hydroxydeoxyguanosine (8-OHdG) is a major oxidative DNA adduct playing roles in senescence, carcinogenesis and various disease processes. High-performance liquid chromatography with an electrochemical detection (HPLC-ECD) method has been widely used to assess organ levels of 8-OHdG, and a recently introduced immunohistochemical approach has made it possible to clarify intra-organ localization. In the present study, these methods were employed to reveal age-dependent changes in nuclear 8-OHdG within various tissues of male Fischer 344 rats between 18 fetal days and 104 weeks of age. 8-OHdG was detected in the nuclei of cerebellar small granule and small cortical cells, cerebral nerve cells, and choroid plexus epithelia of the brain and ependymal cells of the spinal cord; parenchymal cells in the anterior lobe of the pituitary and adrenal glands (mainly cortex); bronchial epithelium of the lung; intra-hepatic bile duct, pancreatic duct, glandular gastric and intestinal epithelial cells; renal tubular epithelial cells (mainly medulla); and spermatogonia and spermatocytes of the testis and seminal vesicle epithelia. The nuclear 8-OHdG levels were high (more than two lesions per 10 6 deoxyguanosines) from 7 days to 104 weeks of age in the brain, 3 to 6 weeks in the adrenal gland, 6 to 104 weeks in the lung, and 3 to 52 weeks in the testis. In the other organs, the nuclear 8-OHdG levels remained low throughout. These findings provide a basis for research dealing with oxidative stress by indicating organ-specific and age-but not aging-dependent changes in the localization of spontaneously generated nuclear 8-OHdG in intact rats. The immunohistochemical approach has advantages for assessing variation of 8-OHdG formation at the cellular level not accessible to the HPLC-ECD method. (Lab Invest 2000, 80:249-261).

show abstract

Alcohol and the Pancreas

Cited by 39 publications

References 90 publications

Ginseng, the Root of Panax ginseng C.A. Meyer, Protects Ethanol-Induced Gastric Damages in Rat through the Induction of Cytoprotective Heat-Shock Protein 27

Ginseng, the Root of Panax ginseng C.A. Meyer, Protects Ethanol-Induced Gastric Damages in Rat through the Induction of Cytoprotective Heat-Shock Protein 27

Relationship of strain-dependent susceptibility to experimentally induced acute pancreatitis with regulation of Prss1 and Spink3 expression

Age and Organ Dependent Spontaneous Generation of Nuclear 8-Hydroxydeoxyguanosine in Male Fischer 344 Rats

Contact Info

Product

Resources

About