Gastric Mucosa Of Guinea Pig Research Articles

Histochemical Assessment of Mucin-Secreting Cells from the Gastric Mucosa of Guinea Pigs

Stomach fragments from 3 guinea pigs were collected from the three regions: cardiac, fundic and pyloric, for histochemical investigations. The anatomical segments were processed by the classical method of inclusion in paraffin and the histological sections were stained with PAS reaction for highlighting the neutral mucins and the Alcian blue method for acid mucins. All the surface cells of the gastric mucosa and in the crypts were positive on the PAS reaction and negative in the case of the alcian blue reaction. This demonstrates that cells on the surface and in the crypts synthetize neutral mucins. In the case of the cardiac region glands, only a small number of cells were positive on the two histochemical reactions, which shows that the cardiac glands in guinea pig synthesize a very small amount of neutral and acidic mucins. There are no positive cells in neither reaction used in the fundic glands case, which shows that these glands do not synthesize mucins, neither neutral nor acidic content. The glands located in the pyloric region have cells in the deep half of the wall which were positive on both histochemical reactions, which shows that they synthesize both neutral mucins and acidic mucins.

Salicylates Promote ROS‐induced Endoplasmic Reticulum Stress Triggering Apoptosis on B16F10 Melanoma

Endoplasmic reticulum stress (ERS) and activation response to this stress have been documented in several types of cancer, suggesting that these cells activate the stress response as a survival strategy. Thus, drugs that cause an imbalance in this response may impair cancer cell viability. Salicylates have proven preventive and anti‐tumor effects in various types of cancer. On regard of ERS, it has been reported to act as potent inhibitor of protein synthesis in rat islets and in the gastric mucosa of guinea pigs. Salicylates also activate ERS through PERK activation in human promonocytic cells. In addition, the treatment with salicylates is correlated to increased reactive oxygen species (ROS) production, probably due to the direct inhibition of catalase activity. Nevertheless, there is still no correlation among salicylates, ERS and cancer. The aim of the present work is to investigate a new mechanism for salicylic acid (SA) and acetylsalicylic acid (ASA) related to their antitumoral effects, which involves the induction of ERS by ROS, and corroborate the new perspectives for the use of these drugs. Melanoma B16F10 cell line was used in all experiments and treated with 10mM SA or ASA. We tested cell viability and apoptosis using Anexin V assay, and ROS production using DCFDA, both by cell sorting. Unfolded protein response (UPR) markers were evaluated by qPCR and Western blot analysis. The treatment of the cells with SA or ASA for 1 or 2 hours promoted an increase in ROS production, as well as in the mRNA levels of the UPR markers ATF4 and CHOP. Increased protein levels of other UPR markers, such as PERK, IRE1, ATF6, cleaved ATF6, BiP and CHOP, are detected within 24 hours of treatment with both drugs. Finally, the treatment triggers apoptosis, which was detected on its early stage after 24 hours. Taken together, our data indicate that treatment of melanoma B16F10 cells with SA or ASA reduces cell viability thought a ROS‐induced ERS mechanism.Support or Funding InformationFinancial support: FAPERJ, CAPES, CNPq

Effect of the flavonoid quercetin on inflammation and lipid peroxidation induced by Helicobacter pylori in gastric mucosa of guinea pig

Helicobacter pylori infection induces an inflammatory response in the gastric mucosa. Activation of polymorphonuclear leukocytes can produce oxidative damage to gastric tissue through intermediary radicals of oxygen and nitrogen. Vegetable extracts containing polyphenols of the flavonoid family have antibacterial activity, and the flavonoid quercetin possesses anti-H. pylori activity in vitro. The aim of this study was to analyze the effect of oral administration of pure quercetin on inflammation and lipid peroxidation induced by H. pylori in the gastric mucosa of the guinea pig. Sixty days after oral infection with H. pylori guinea pigs received 200 mg/kg of quercetin daily by mouth for 15 days. The infiltration index of inflammatory cells and bacterial density in both the pyloric antrum and corpus were histologically determined by myeloperoxidase histochemistry, hematoxylin-eosin, and modified Giemsa stains. The lipid hydroperoxide content was assessed by the orange xylenol spectrophotometric method. Quercetin significantly reduced the infiltration index of mononuclear cell and bacterial colonization in the pyloric antrum and corpus. In the antrum of infected quercetin-treated animals, a significant diminution of neutrophil leukocyte infiltration was observed compared with the infected nonquercetin-treated animals. In the antrum, the lipid hydroperoxide concentration was significantly decreased in infected animals treated with quercetin, whereas in the corpus no significant differences were observed. Our results indicate that in vivo oral quercetin administration decreases H. pylori infection in the gastric mucosa and reduces both the inflammatory response and lipid peroxidation.

Conjugation of 1-naphthol in the gastric mucosa of guinea pigs

1-Naphthol was conjugated in tissue pieces of the gastric wall to naphthol glucuronide (85%) and naphthol sulfate (15%). There was no regioselectivity in different parts of the stomach. In separated gastric mucosal cell populations, the activities of both transferases were highest in the mucous cell fraction (apparent V max of glucuronidation: 0.83 nmol/mg protein/min; apparent V max of sulfation: 0.11) with only little, or no activity in chief cells and parietal cells. Immunohistochemically glucuronosyltransferase 1 was predominantly localized in surface mucous cells. In conclusion, the gastric mucosa is an important organ for phase II biotransformation.

The adjuvant effect of bacitracin on nasal absorption of gonadorelin and buserelin in rats.

Nasal absorption of gonadorelin (luteinizing hormone-releasing hormone; LH-RH) and buserelin, an LH-RH agonist, was studied in anesthetized rats. Administration of peptides was by nasal instillation of aqueous peptide/buffer solutions. Peptide absorption was monitored using different techniques: (a) by specific radioimmunoassays for serum levels of lutropin (LH), (b) by the cumulative urinary excretion of buserelin, and (c) by the ovulatory activity after nasal LH-RH and buserelin, respectively. Without adjuvant the nasal absorption of LH-RH and buserelin was relatively poor compared to subcutaneous or intravenous injection. Using absorption adjuvants of different types, e.g., sodium taurodihydrofusidate (STDHF) and bacitracin, marked increases in nasal absorption and, therefore, significant nasal adjuvant activity were found, as demonstrated by an increase in the biological response after nasal administration of the peptides. The mucosal compatibility of bacitracin at the concentrations used for enhancement of absorption was confirmed by an in vitro investigation using isolated gastric mucosa of guinea pigs as a test model.

Suppression of gastric acid secretion by furosemide in isolated gastric mucosa of guinea pig.

The effect of furosemide on acid secretion and Cl- transport was studied in isolated fundic mucosa of the guinea pig. Furosemide (10(-3) M), applied to the serosal side produced an immediate effect on the short-circuit current (Isc), lowering it by 47 +/- 2%. Potential difference decreased by 29 +/- 3%, electrical conductance by 18 +/- 4%, acid secretion by 38 +/- 1%, and net flux of Cl- from serosal-to-mucosal side by 37%. Application of the drug to the mucosal side produced similar effects on acid secretion and on the electrical parameters. It is suggested that furosemide blocks the entrance of Cl-, by the Na+--Cl- cotransport mechanism, through the basolateral membrane of the secreting cell. The consequent reduction in electrogenic Cl- transport would cause Isc and acid secretion to decrease. A reduction of Cl- conductance of the apical membrane, upon mucosal application of the drug, would cause similar effects on acid secretion and Cl- transport.

Biochemical and cytological alterations in gastric mucosa of guinea pigs under restraint stress

Summary Immobilization of guinea pigs has been found to be a reliable and useful experimental method for the production of gastric and duodenal erosions. The number of animals developing stress erosions increased progressively in time and reached 90% in 40 hr. During the development of the erosions, some animals were likely to develop many lesions, while others developed none. Immobilization caused rapid degranulation of the mast cells of the gastric mucosa. However, there was no correlation between the reduction in mast cells and the occurrence of erosions in individual animals. Acid concentration and volume of gastric juice in the stomach at the time of sacrifice were not significantly different among restrained animals with and without lesions or in fasted controls. Decrease in periodic acid-Schiff positive mucosubstances in surface cells of the gastric mucosa appeared to be present after 18 hr of stress. This occurred together with a progressive decrease in deoxyribonucleic acid synthesis during stress and a loss of ribonucleic acid from the gastric tissue.

Parasitic Development of Obeliscoides cuniculi in Rabbits

Studies on the development of Obeliscoides cuniculi infections in New Zealand white rabbits showed that the second ecdysis was completed within 1 hr of infection and the parasitic third stage larvae penetrated into the gastric mucosa within 24 hr. The third ecdysis occurred in the mucosa and was completed by day 5 while the fourth ecdysis probably occurred as the worms migrated to the stomach surface. Migration from the mucosa started on day 5 and by the 14th day, 35% of the total infection was on the gastric surface. The prepatent periods of two infections were 19 and 25 days. The male to female worm ratio was 1.4:1 at 72 hr and 2.5:1 on day 5 but decreased subsequently to 1:1. Fewer worms were found embedded in the mucosa of the pyloric region of the stomach than in other gastric regions on and after the 14th day of infection. Similarities between the parasitic development of other trichostrongyles and 0. cuniculi are discussed. Alicata (1932) described the development of the preparasitic stages of Obeliscoides cunictli (Graybill), a trichostrongyle which occurs naturally in the stomach of domestic and feral rabbits. He also described the course of infection in the guinea pig which is an unnatural host for this nematode. In the guinea pig the larvae underwent two parasitic ecdyses before becoming adults and segmenting eggs were found in the uteri of most female worms by the 17th day. Alicata found that a smaller percentage of the infective dose reached sexual maturity in the guinea pig than in the rabbit. Worley (1963) concluded that guinea pigs were not particularly suitable hosts for 0. cuniculi since infectivity rates were low and infections were rapidly lost. Alicata (1932) reported adult worms embedded in the gastric mucosa of guinea pigs and Russell et al. (1966) found that as the size of the infective dose given to rabbits was increased, an increasing number of immature larvae appeared during patency. However, no histotropic phase of development has been reported in any host species. Obeliscoides cuniculi was first compared to Ostertagia circumcincta by Threlkeld (1934) on the basis of taxonomic similarities. Worley (1963) suggested the use of 0. cunictli infection as a model for the study of ruminant helminthiasis and Russell et al. (1966) extended this suggestion, noting similar gross pathological changes. Received for publication 23 August 1967. * This investigation was supported by U. S. Public Health Service Training Grant 1 T1 AI 302. t Present address: College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. This report concerns further investigation into the details of the parasitic phase of the life cycle of 0. cJuniculi. MATERIALS AND METHODS