Disease relevance of 16,16-dimethylprostaglandin E2

• Persistence of ketosis despite suppression of lipolysis by 16,16-dimethylprostaglandin E2 in experimental diabetic ketoacidosis in rats [1].
• We investigated the effect on in vivo administration of 16,16-dimethyl-prostaglandin E2 (di-M-PGE2) alone and in combined treatment with alpha-beta interferon (IFN) on NK activity in normal, cyclophosphamide (CY)-treated, tumor bearing or irradiated and bone marrow reconstituted mice and on B-16 melanoma growth [2].
• We studied the effect of the intravenous infusion of 16,16-dimethylprostaglandin E2 methyl ester (di-M-PGE2) and somatostatin on bombesin-stimulated gastric acid secretion, plasma gastrin and plasma pancreatic polypeptide in four chronic gastric fistula dogs [3].
• We evaluated the ability of 16,16-dimethyl-prostaglandin E2 (PGE2 to augment mucosal hyperplasia following massive small bowel resection in the rat [4].
• We examined the effects of 16,16 dimethylprostaglandin E2 (DMPGE2) on the development of diabetic ketoacidosis (DKA) in rats [5].

High impact information on 16,16-dimethylprostaglandin E2

• 16,16-dimethyl-prostaglandin E2: antisecretory and protective efforts on human gastric mucosa [6].
• Treatment of NSCLC cells with exogenous 16,16-dimethylprostaglandin E2 significantly increased EP4 receptor, CD44, and MMP-2 expression and matrigel invasion [7].
• 3. Further evidence for the EP-receptor mediating excitation and relaxation was provided by the action of the EP2-/EP3-receptor selective prostanoids rioprostil, AY23626 and misoprostol, and the EP1-/EP2-receptor selective agonist 16,16-dimethylprostaglandin E2 [8].
• This study investigated the hypothesis that pharmacologic preservation of intestinal structure and function by orally administered 16,16-dimethyl-prostaglandin E2 would prevent bacterial translocation in intravenously fed rats [9].
• The magnitude of prostaglandin [16,16-dimethylprostaglandin E2 (DMPGE2)] protection against ethanol action has been evaluated by studying the intracellular events leading to synthesis, modification, intracellular retention, and secretion of mucus glycoprotein in the rat gastric mucosal cell culture [10].

Biological context of 16,16-dimethylprostaglandin E2

• Cytoprotection by 16,16-dimethylprostaglandin E2. Role of gastric juice and mucus gel layer [11].
• The H2 receptor antagonist ranitidine completely blocked the effects of histamine (100 mumol/l) on [3H]Leu incorporation into cellular and released AIM (IC50 37 and 32 mumol/l, respectively) but had no inhibitory effect on the 16,16-dimethylprostaglandin-E2 - and forskolin-stimulated tracer incorporation [12].
• The 16,16-dimethylprostaglandin E2 (dmPGE2)-induced diarrhea was analyzed in cecectomized rats prepared by resecting the cecum and its vasculature without disturbing the ileocecal junction. dmPGE2 (0.1-1.0 mg/kg, p.o.) dose-dependently increased the number of defecation episodes and induced a soft and watery stool in cecectomized rats [13].
• E series prostaglandins and their biologically active analogue, 16,16-dimethylprostaglandin E2 (dimethylprostaglandin E2), have inhibited hormone-stimulated glycogenolysis in hepatocytes cultured from male rats (Okumura, T., Sago, T. and Saito, K. (1988) Biochim. Biophys. Acta 958, 179-187) [14].

Anatomical context of 16,16-dimethylprostaglandin E2

• The effect of somatostatin and 16,16-dimethyl-prostaglandin E2 on bombesin-stimulated canine gastric acid, plasma gastrin and pancreatic polypeptide secretion [3].
• Gastric surface epithelial cell damage induced by restraint and water-immersion stress in rats. Protective effects of 16,16-dimethyl-prostaglandin E2 [15].
• Oral and subcutaneous administration of 16,16-dimethylprostaglandin E2 (16,16-dimethyl PGE2) resulted in an increase in the dry weight of the stomach and small intestine of the female rat [16].
• The present investigation determined the role of microtubules (a major cytoskeletal component) in GI injury induced by ethanol (EtOH) and its prevention by 16,16-dimethylprostaglandin E2 (dmPGE2) using cells from a human colonic cell line known as Caco-2 cells [17].

Associations of 16,16-dimethylprostaglandin E2 with other chemical compounds

• Results demonstrate that orally administered 16,16-dimethyl-prostaglandin E2 potently attenuates the intestinal atrophy associated with parenteral feeding but does not prevent bacterial translocation [9].
• The effects of absolute ethanol (EtOH) and 16,16-dimethyl-prostaglandin E2 (PGE2) on the ultrastructure of rat gastric mucosa were assessed using standard electron microscopic techniques [18].
• These studies were done to determine the effects of fluoride (F) on the structure and function of the canine gastric mucosa and the possible protective effects of 16,16-dimethyl-prostaglandin E2 (dmPGE2) [19].
• We studied the effect of either placebo, 16,16-dimethyl-prostaglandin E2 (16,16-dimethyl-PGE2), or cimetidine on spontaneous degeneration of isolated rat gastric glands maintained in vitro in a basic oxygenated medium for 24 h [20].

Gene context of 16,16-dimethylprostaglandin E2

• It was found that both EGF and polyamines significantly and dose-dependently prevented the formation of gastric lesions induced by absolute ethanol, the effect being similar to that obtained with 16,16-dimethylprostaglandin E2 [21].
• Half-maximal inhibition of glucagon-stimulated cAMP accumulation occurred at approx. 10(-7) M 16,16-dimethylprostaglandin E2 [22].
• The effects of 16,16-dimethyl-prostaglandin E2 and the thiaprostaglandin E2 EMD 33 290 were tested on basal acid secretion as well as on the aspirin- and bile salt-induced fall of gastric transmucosal potential difference in man [23].
• The effect of 16,16-dimethylprostaglandin E2 (dmPGE2) and corticotropin-releasing factor (CRF) on duodenal blood flow, alkaline secretion, and acid-induced deep duodenal villous injury was studied [24].

Analytical, diagnostic and therapeutic context of 16,16-dimethylprostaglandin E2

• 3. Topical administration of 16,16-dimethylprostaglandin E2 by oral intubation caused a significant increase in thickness in both rat and frog at doses of 5 microgram/ml and 0.5 microgram/ml respectively [25].
• Subjects received pretreatment with saline or 16,16-dimethyl-prostaglandin E2 1 micrograms/kg b.w. and 15 min later 40 ml of 60% alcohol were sprayed on the gastric mucosa through an endoscope [26].

References