Gastric Antisecretory and Antiulcer Properties of PGE2, 15-Methyl PGE2, and 16,16-Dimethyl PGE2

Robert, André; Schultz, John R.; Nezamis, James E.; Lancaster, C. Roy D.

doi:10.1016/s0016-5085(76)80147-3

Cited by 221 publications

(57 citation statements)

References 42 publications

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“…Prostanoids are produced by a variety of tissues and cell types, and their functions are essential: mice completely lacking COX activity die early during post-partum [89]. Prostanoids regulate cell proliferation, apoptosis and migration [90][91][92][93], gastrointestinal secretion [94], smooth muscle contraction and relaxation, body temperature, pain sensation, and inflammation by signaling through their cognate G-protein coupled receptors [95][96][97][98].…”

Section: Cyclooxygenase-2 and Inflammatory Prostanoidsmentioning

confidence: 99%

Current concepts regarding the pathogenesis of necrotizing enterocolitis

et al. 2009

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Necrotizing enterocolitis (NEC) is a devastating disease that predominantly affects premature neonates. The mortality associated with NEC has not changed appreciably over the past several decades. The underlying etiology of NEC remains elusive, although bacterial colonization of the gut, formula feeding, and perinatal stress have been implicated as putative risk factors. The disease is characterized by massive epithelial destruction, which results in gut barrier failure. The exact molecular and cellular mechanisms involved in this complex disease are poorly understood. Recent studies have provided significant insight into our understanding of the pathogenesis of NEC. Endogenous mediators such as prostanoids, cyclooxygenases, and nitric oxide may play a role in the development of gut barrier failure. Understanding the structural architecture of the gut barrier and the cellular mechanisms that are responsible for gut epithelial damage could lead to the development of novel diagnostic, prophylactic and therapeutic strategies in NEC.

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Section: Cyclooxygenase-2 and Inflammatory Prostanoidsmentioning

confidence: 99%

Current concepts regarding the pathogenesis of necrotizing enterocolitis

et al. 2009

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“…Although it is the methylated prostaglandin analogues that cause the greatest decrease in gastric secretion (26), several of the natural prostaglandins such as PGEl and PGEz inhibit gastric acid secretion in animals and humans when given parenterally but are inactive or weak if given orally (27). PGEz has been shown to lower gastro-esophageal sphincter pressure, but it does not significantly alter gastric motility (28).…”

Section: Discussionmentioning

confidence: 99%

Noninvasive Assessment by Radiotelemetry of Antacid Effect during Labor

O’Sullivan

Bullingham

1985

Anesthesia & Analgesia

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GM, BULLINGHAM RE. Noninvasive assessment by radiotelemetry of antacid effect during labor. Anesth Analg 1985;64:95-100.A noninvasive radiotelemetry technique was used to study the antacid effect of 15 ml of 0.3 M sodium citrate in 26 women in established labor. The subjects swallowed a pH radio pill, whose signal was detected transabdominally by a radio receiver. The median and range of values for the time to return to the preantacid basal pH for all of the women in labor was 84.0 (1 1. 8-195.8) min. However, there was a significant difference ( P < 0.05) in the duration of action of sodium citrate between the women who had received no analgesia and those given intramuscular meperidine. The median and range of values for the time to return to the preantacid basal pH in patients who had received meperidine during iabor was 166.0 (147.7-195.8) min, whilst in those who had received no analgesia the values were 56.7 (1 1.8-143.0) min. There were no significant differences between patients given no analgesia and those given extradural analgesia. Pretreatment with intrauaginal prostaglandins (PGE,) did not influence antacid effect.Numerous preventative and prophylactic measures are practiced in an attempt to reduce the risk of acid pulmonary aspiration (Mendelson's syndrome) (1) during labor and delivery. These include prohibition of solid food during labor, preoperative emptying of the stomach, oral administration of antacids during labor with an additional bolus prior to surgery, and the use of cricoid pressure during the induction of general anesthesia. More recently, the use of H2 receptor antagonists during labor and before cesarean section (2,3) has been suggested.The severity of Mendelson's syndrome is a function of the pH and volume of the aspirated fluid (4,5). In the past, because antacids did not always appear to provide protection against the effect of aspiration (6,7), larger volumes and their more frequent administration during labor were advocated (8,9). The known pulmonary toxicity associated with the aspiration of antacids (lo), the severity of which appears to depend upon the volume aspirated (ll), and the failure to improve maternal mortality despite the use of repeated doses of antacids (12) cast doubt on the validity of administering antacids prophylactically throughout labor.A recent study (13) using a noninvasive radiotelemetry technique demonstrated a wide variation in the efficacy and duration of action of both particulate and nonparticulate antacids. Nor was any difference found in antacid effect between pregnant and nonpregnant women (14). In addition, doubling the volume of the nonparticulate antacid 0.3 M sodium citrate from 15 ml to 30 ml was not found to produce a significantly greater effect (15). These studies did, however, indicate that one of the main factors determining the duration of antacid action was the rate of gastric emptying. During labor, antacid efficacy might differ from that in nonlaboring pregnant women, because of the gastrointestinal effects of labor itself, the asso...

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“…Oxidation or inversion of stereochemistry at this moiety renders these compounds biologically inactive (Collins & Djuric, 1993;Duffy & Guiry, 2010). Inhibition of this process was first achieved by addition of either one C15 methyl (Table 3, entry 1) or two C16 methyl groups (Table 3, entry 2) to PGE 2 (Bundy et al, 1971;Robert et al, 1976). The resulting compounds were orally active and exhibited longer durations of action than the parent.…”

Section: C15-hydroxyl Oxidationmentioning

confidence: 99%

Anti-tumor activities of lipids and lipid analogues and their development as potential anticancer drugs

Murray

Hraiki

Bebawy

et al. 2015

Pharmacology & Therapeutics

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Lipids have the potential for development as anticancer agents. Endogenous membrane lipids, such as ceramides and certain saturated fatty acids, have been found to modulate the viability of tumor cells. In addition, many tumors over-express cyclooxygenase, lipoxygenase or cytochrome P450 enzymes that mediate the biotransformation of ω-6 polyunsaturated fatty acids (PUFAs) to potent eicosanoid regulators of tumor cell proliferation and cell death. In contrast, several analogous products from the biotransformation of ω-3 PUFAs impair particular tumorigenic pathways. For example, the ω-3 17,18-epoxide of eicosapentaenoic acid activates anti-proliferative and proapoptotic signaling cascades in tumor cells and the lipoxygenase-derived resolvins are effective inhibitors of inflammatory pathways that may drive tumor expansion. However, the development of potential anti-cancer drugs based on these molecules is complex, with in vivo stability a major issue. Nevertheless, recent successes with the antitumor alkyl phospholipids, which are synthetic analogues of naturally-occurring membrane phospholipid esters, have provided the impetus for development of further molecules. The alkyl phospholipids have been tested against a range of cancers and show considerable activity against skin cancers and certain leukemias. Very recently, it has been shown that combination strategies, in which alkyl phospholipids are used in conjunction with established anticancer agents, are promising new therapeutic approaches. In future, the evaluation of new lipid-based molecules in single-agent and combination treatments may also be assessed. This could provide a range of important treatment options in the management of advanced and metastatic cancer.

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Gastric Antisecretory and Antiulcer Properties of PGE2, 15-Methyl PGE2, and 16,16-Dimethyl PGE2

Cited by 221 publications

References 42 publications

Current concepts regarding the pathogenesis of necrotizing enterocolitis

Current concepts regarding the pathogenesis of necrotizing enterocolitis

Noninvasive Assessment by Radiotelemetry of Antacid Effect during Labor

Anti-tumor activities of lipids and lipid analogues and their development as potential anticancer drugs

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