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Ultra-processed foods (UPFs) are industrial formulations that are ubiquitous in every home and supermarket aisle. This food group includes snacks, soft drinks, ready-to-eat products like pizzas, nuggets, burger till commercial breads. Multiple long cohort studies have shown a relationship between their consumption and the rise in the incidence of obesity, type 2 diabetes, cardiovascular diseases, colorectal cancer and all-cause mortality. In addition, UPFs generate carbon and water footprints with a negative impact in our environment. The intestinal microbiota would play a central role as a trigger of metabolic inflammation (metainflammation). We need to reduce consumption of UPFs and promote healthier and accessible eating habits. Official public policies are needed.

Unlabelled: The immunomodulator effect of Bioflora probiotic on T (CD4+) and B (CD20) lymphocytes in gastrointestinal mucosa and intestinal bacterial translocation was studied using Wistar rats (n = 10 per group). Two experiments were used: (I) stress with immobilization and water immersion at 22 degrees C for 7 h plus the application of indomethacin (Indo) 10 mg/kg SC every 24 h for 3 days (comparator group), and (II) stress experiment I with the addition of 1 mL of Bioflora applied through a orogastric tube every 12 h for 3 days. At the 4th day, in asepsis, a dissection laparotomy of liver, spleen, mesenteric lymphatic nodes, and cecum was performed for microbiological culture, and stomach, ileum, and colon were also dissected for immunohistochemical and quantification of CD4+ and CD20. Findings in experiment I revealed cecum bacterial overdevelopment of 6 x 10(10) +/- 2.3 x 10(9) colony-forming units (CFU) (P < 0.01) and positive cultures in liver, spleen, and all mesenteric lymphatic nodes. On the other hand, in the group treated with Probiotic Bioflora, cecum without overdevelopment (3 x 10(6) +/- 1.3 x 10(5) CFU), negative cultures in liver and spleen, and in lymphatic nodes two positive and eight negative cultures for E. coli and P. vulgaris (P < 0.01) were observed. Immunohistochemistry revealed a relevant increase of T lymphocytes (CD4+) in ileum and colon., Conclusions: Bioflora probiotic was shown to be an intestinal immunomodulator that induced increased T (CD4+) lymphocytes that also offer prophylaxis of intestinal bacterial translocation in a stressed rat model.

Background: The antiinflammatory and gastric cytoprotector effect of angiotensin II AT1 receptor antagonist, such as candesartan, losartan and valsartan was studied., Material and Methods: Wistar rats were ramdomly assigned to receive: (1) 96 degrees ethanol; (2) oral indometacin, (3) solid food (pellets) during two hours and subcutaneous indometacin (production of ulcers in the gastric antrum), (4) Carrageen footpad edema., Results: The three ATI receptor angiotensin antagonists yielded gastric cytoprotection against 96 degrees ethanol, almost total gastrointestinal protection against oral indometacin, prevented gastric ulcers formation in the antrum induced by subcutaneous indometacin, remarkable antiinflammatory response against neutrophil infiltration on the gastrointestinal mucosa, and anti-inflammatory effect in carrageen footpad edema., Conclusions: The AT1 receptor antagonists of angiotensin II are gastric cytiprotectors with a remarkable antiinflammatory effect.

In randomized groups of Wistar rats, the effect inhibitor of selective NASAID over the COX-1, COX-2 and COX-3 the synchronizes inhibition of COX-1 and COX-2, COX-1 and COX-3, COX-2 and COX-3, and COX-1, COX-2 and COX-3 were studied. The conclusions were that the selective inhibition of COX-1, COX-2 and COX-3 no given gastrointestinal damage; the synchronizes inhibition of COX-1 and COX-2 given preferential gastric damage; in contrast the inhibition of COX-2 and COX-3 given massive necrosis preferential in small intestine.

Dexketoprofene (De) NSAID was studied as a selective COX-1 inhibitor in comparison with Ketorolac (Ke), a mainly COX-1 inhibitor. De and Ke were administered to different groups of animals in a dose-dependent manner, i.e., 3-15 and 25 mgs/kg. The gastrointestinal mucosa damage was macroscopically and microscopically quantified at 24 hs, as well as leukocyte infiltration (LI) and neosinophilia. Similarly, Indomethacin (Indo) damage (COX-1-COX-2), with 25 mgs/kg. Dose was compared. On the other hand, De and Ke at inhibitory selective COX-1 dose (3 mg/kg) plus Celecoxib, selective COX-2 inhibitor, yielding no gastrointestinal damage, with decreased LI and without neutrophilia, the same as Ke (n.s.). Similarly De at higher dose (2.5 mgs/kg), produced minimal gastrointestinal lesions, showing a preferential COX-1 inhibitor behavior. Ke and Indo produced important gastrointestinal necrotic and erosive lesions with remarkable LI and neutrophilia (p < 0.001). On the other hand, COX-1 De dose plus Celecoxib produced evident gastrointestinal lesions, increased LI and neutrophilia, the same as Indo, pointing out that the gastrointestinal damage is due to COX-1 and COX-2 inhibition.

Five experimental models were developed in different groups of Wistar rats (N = 15) to study selective COX-2-inhibitor NSAIDs such as celecoxib and rofecoxib, as follows: (1) dose-dependent oral Celecoxib and Rofecoxib for 5 days, and 24 hr after oral indomethacin; (2) Same as 1 but subcutaneously; (3) gastric ulcer induced by glacial acetic acid; (4) duodenal ulcer induced by cysteamine; and (5) stress by immobilization and immersion in water at 15 degrees C for 6 hr. Celecoxib and Rofecoxib, either orally or subcutaneously, did not produce necrotic lesions in healthy gastrointestinal mucosa (0%), showing normal histology. In contrast, previously indomethacin-induced lesions were aggravated (90%, P < 0.001). Total necrosis in the small intestine as well as increased ulcers and perforation of gastric and duodenal ulcers induced by acetic acid and cysteamine were observed. There was also aggravation of the necrotic gastric area in stress (60-90%, P < 0.05). Celecoxib and rofecoxib showed neutrophilia (5000/mm3) similar to that with indomethacin. In contrast, there was no leukocyte infiltration in the gastric múcosa; thus, we can consider it a selective COX-2 NSAID. In conclusion, celecoxib and rofecoxib at doses causing COX-2 but not COX-1 inhibition did not produce toxic lesions in healthy gastrointestinal mucosa, yielding a broad therapeutic margin. In contrast, when administered in altered gastrointestinal mucosa, they aggravated and complicated gastric ulcers as well as necrosis in the small intestine, consequently restricting their clinical use.

In 5 random groups of Wistar rats (n = 15 for each group), ulcerogenic doses of NSAIDs COX-1-COX-2 inhibitors such as indomethacin were compared with Celecoxib (COX-2 inhibitor); the production of antrum gastric ulcers and bowel and colon necrotic areas was studied. Celecoxib was given each 12 hs orally and subcutaneously during 5 days and gastrointestinal lesions were not found; in contrast, Celecoxib given after indomethacin aggravated antrum gastric ulcers (p < 0.001); intestinal massive necrosis and death were observed in all the rats. We conclude that Celecoxib does not induce gastrointestinal lesions in healthy mucosa; in contrast, Celecoxib amplifies the gastrointestinal lesions induced by indomethacin.

Unlabelled: Five experimental models were carried out in different groups of Wistar rats (n = 15) in order to study selective (cyclo-oxygenase) COX-2 non-steroid antiinflammatory inhibitors, such as celecoxib and rofecoxib, as follows: 1) Dose-dependent oral celecoxib and rofecoxib for 5 days, and 24 hours after oral indomethacin. 2) Same as 1, but subcutaneously. 3) Gastric ulcer induced by means of glacial acetic acid. 4) Duodenal ulcer induced by means of cysteamine. 5) Stress due to being kept under restraint and immersion in water at 15 degrees C for 6 hours. Celecoxib and rofecoxib, either orally or subcutaneously, did not produce necrotic injuries in healthy gastrointestinal mucosa (0%), showing normal histology. On the other hand, the injuries previously induced by indomethacin worsened (90%, p < 0.001). Total necrosis of small intestine as well as increased ulcer and perforation of gastric and duodenal ulcers induced by acetic acid and cysteamine were observed. There was also worsening of gastric necrotic area with stress (60-90%, p < 0.05). Celecoxib and rofecoxib showed neutrophilia (5,000/mm3) similar to that presented by indomethacin, but there was no leukocyte infiltration in the gastric mucosa; thus we can consider it a COX-2 selective NSAID (non-steroidal anti-inflammatory drug)., Conclusion: Dose-dependent administration of celecoxib and rofecoxib as COX-2 inhibitors and non-COX-1 inhibitors, respectively, did not produce toxic injuries on healthy gastrointestinal mucosa, thus providing a broad therapeutic spectre. On the other hand, when administered in presence of altered gastrointestinal mucosa, they worsened and complicated gastric ulcers, and also induced necrosis in the small intestine, thereby restricting their clinical use.

The role of the autonomic nervous system on gastric stress was studied in different groups of Wistar rats (n = 10). The experimental stress model consisted of immobilization and immersion in 15 degrees C water during 6 hours. The percentage of the gastric mucosa macroscopic lesional area was tabulated, and at the same time cortisol, melatonin, noradrenaline, adrenaline, dopamine and serotonin blood levels were measured. The stress control showed a necrotic area (80%) and in blood there was only and increase in noradrenaline and adrenaline. The following dose dependent drugs were studied: beta adrenergics agonists and antagonists, alpha 1 postsinaptical adrenergic antagonists, anticholinergics and cholinergics, endorphin and GABA receptors. Isoproterenol, prazosim, doxasine, tramadol and vigabatrin yielded a remarkable gastric mucosa protection in stress with an area close to 0% (p < 0.001). In contrast, propanolol, acetylholine, atropine, naloxone and flumazenil showed no difference in control stress (p > 0.5). All the drugs under study yielded similar vasoactive amines than the control stress. It is concluded that the protective gastric mechanism of the autonomic nervous system in stress, could be linked to its receptors with an increase in the splanchnic microcirculation.

Unlabelled: This work was aimed to study COX-1 and COX-2 selectivity in 16 non-steroidal anti-inflammatory drugs (NSAIDs), at ulcerogenic doses in 2 experimental models: 1) provided subcutaneously (sc), after solid food(SF), (antrum ulcers and intestinal erosions); and 2) orally (O) (fundic and intestinal erosions)., Methods: 17 groups of female Wistar rats (n = 7 each group), weighing 200 g, 36 h fasting with water ad libitum, were submitted to the following experiments: 1. SF (Cargill chow) during 1 h, and then sc: 1.1 ml saline; 2. diclofenac (Di); 3. indomethacine (Indo); 4. Ketorolac (Ke); 5. meloxicam (Mel); 6. Pyroxicam (P); 7. tenoxicam (T). The dose for the aforementioned drugs was 60 mg/kg; 8. aceclofenac (Ace); 9. 200 mg/kg nimesulide (Ni); 10. mefenamic acid (Mac); 11. aspirin (A); 12. etodolac (E); 13. ibuprophen (Ibu); 14. nabumetone (Na); 15. naproxene (Nap); 16. ketoprophen (Ket); 17. paracetamol (Pa), 500 mg/kg. II. The drugs where administered by orogastric tubing to the same groups of fasting animals. After 24 h the animals were killed by ether overdose. Laparotomy was performed and the stomach and the small intestine was removed. The percentage of antum ulcer, and fundic and intestinal erosion (mm2) was tabulated by planimetry. Blood and histological samples were obtained., Results: The NSAIDs Indo, Ibu, Ke, Ket, P and Te yielded an antrum ulcer area: 5-29% and intestinal erosion, 101-395 mm2, similar to Indo (p > 0.50). In contrast there were neither ulcers nor intestinal erosions with Mac, A, Di, E and Nap (p > 0.50). While there were absence of ulcers with Ace, Me, Na, Ni and Pa and slight intestinal erosion (0-23 mm2; p < 0.01). II. There were differences in the following oral (NAIDs: Ace, Me, NA, Ni and Pa, yielding 0-5% fundic erosion and 0-22 mm2 intestinal erosion (p < 0.001). The other NSADs yielded 33-90% fundic erosion and 116-550 mm2 intestinal erosion, similarly to Indo (p > 0.50)., Histology: Leukocyte infiltrate in the gastrointestinal mucosa with all the NSADs, except Ibu and Pa. There was also neutrophilia (5000-20,000), but not with Ibu and Pa (700-1200)., Conclusions: COX-2-COX-1 selectivity was demonstrated "in vivo" in aceclofenac, meloxicam, nabumetone, nimesulide and paracetamol.

In groups of female Wistar rats, someted to stress by immobilization and immersion in 18 degrees C water during 6 hrs, the role of nitric oxide (NO) in its pathophysiologic was studied. Agonist and antagonist of the isoforms Constitutive NO Synthase (cNOS) and of the inducible NO Synthase (iNOS) were used. Was found that the overdose of L-arginine aggravated of stress acute gastric lesions. The agonist of iNOS the NMDA and the antagonists dexamethasone and aminoguanidine were used. The NMDA aggravated the stress acute gastric lesions; in contrast, dexamethasone and aminoguanidine given a evident protection of the gastric mucosa in stress. Was concluded that the production of NO given by iNOS, play a role important in the pathophysiologic in stress acute gastric lesions.

Aim: To search in retrospectively and prospectively from the efficacy of biofeedback training in patients with fecal incontinence and to investigate the determinant factors of improvement of the patients., Methods: The incontinent patients were evaluated in phases: I: In 37 subjects, 14 men and 23 women, aged between 13 and 82 years, biofeedback training was done, and the efficacy was determined retrospective form. II: In 14 patients, 2 men and 12 women, aged between 19 and 79 years, biofeedback training was done, and rectal balloon sensitivity, force of contraction and motor/sensitivity index were evaluated in prospective form before and after biofeedback training., Results: In the group of the patients studied in phase I, findings were: 21 patients (60%) complete continence, 12 (34%) improvement, and 2 (5.7%) without change. In the group of the patients studied in phase II, findings were: 8 patients (57%) complete continence, 4 (29%) improvement and 2 (14%) without change. In patients with complete continence there was a decrease in rectal balloon sensitivity (P < 0.05) and an increase of the motor/sensitivity index (P < 0.05), before and after biofeedback training., Conclusion: Biofeedback is a simple, painless and effective treatment for patients with fecal incontinence. It allows to improve rectal sensitivity and to increase the motor/sensitivity index, determinant for patients continence.

The aim of this study was to compare the serum-ascites albumin gradient (GS-A) to the transudate-exudate concept in the classification of ascites. The second objective was to analyze the predictive value and efficacy of GS-A, ascites total protein, LDH, Ratio and ascites cholesterol in patients with liver disease and malignant ascites. For this purpose we studied prospectively 98 patients (in prospective form). The transudate-exudate concept classified correctly the causes of ascites only in 65.6% of the patients. In contrast, the GS-A did it 95.7% of the patients. In differentiating ascites caused either by chronic liver disease or by malignancy, the tests with best efficacy were cholesterol (98%), (predictive value 97%) and GS-A efficacy 94% (predictive value 94%). We conclude that GS-A was better than the traditional transudate-exudate concept in classification of ascites. The test with the best efficcacy separating ascites caused by chronic liver disease or by malignancy was the ascites cholesterol.

Objective: To verify wether a cytoprotective or a antisecretant drug is effective on stress acute gastric., Method: Female Wistar rats (n=7), 200 g, 24 h fasted, water ad lib. were used. Experiment I. Stress (s) by immobilization and immersion in 181/3 C water, 6 h (control). 30 min pretreatment with 2 ml 800 mg/Kg in OG bolus Sucralfate. 800 mg/Kg OG Magaldrate. 800 mg/Kg OG AIMgOH. 800 mg/Kg OH Hydrotalcite. 100 aeg/Kg OG Misoprostol (antisecretant). 125 mg/Kg s.c. Somatostatine (Octeotride). 30 mg/Kg i.p. Ranitidine. 30 mg/Kg i.p. Omeprazole and 30 mg/Kg i.p. Lanzoprazole. The rats were sacrificed by ether overdose, and laparotomy was performed to remove stomach and to assess the percentage gastric lesional area by computerized planimetry and histological examination. Experiment II. With the same scheme above described and previous anesthesia, laparatomy and pylorus ligature, the acid gastric secretion was studied. Results Exp. I. Percentage of gastric lesional area: C: 80.5 +/- 5.1; Sucralfate: 25.6 +/- 4.1 (p < 0.05). Magaldrate: 51.6 +/- 7.1 (NS). AIMgOH 78.6 +/- 7.1. Hydrotalcite; 85.6 +/- 5.1. Misoprostol (cytoprotector) 59.5 +/- 6.1 (NS). Misoprostol (antisecretant) 1 +/- 0.1 (p < 0.001). Somatostatine: 20.3 +/- 5.1 (p < 0.01). Ranitidine: 46.5 +/- 7.8 (NS). Omeprazole: 1 +/- 0.1 and Lanzoprazole: 1 +/- 0.1 (p < 0.001). Histological examination demonstrated gastric cytoprotection in the groups pretreated with Omeprazole and Lanzoprazole. Exp. II. 6 h m/Mol HCl output: C: 0.22 +/- 0.09. Sucralfate: 0.2 +2- 0.07 (NS). Magaldrate: 0.19 +/- 0.08. AIMgOH: 0.18 +/- 0.07. Hydrotalcite: 0.19 +/- +/- 0.10. Misoprostol (cytoprotector): 0.23 +/- 0.07. Misoprostol (anti-secretor): 0.11 +2- 0.05 (p < 0.05). Somatostatin: 0.09 +/- 0.04. Ranitidine: 0.08 +/- 0.05. Omeprazole: 0.02 +/- 0.01 (p < 0.001) and Lanzoprazole: 0.02 +/- 0.01., Conclusion: In the prevention of stress acute gastric lesions Sucralfate might be indicated as a partial cytoprotector and Omeprazole or Lanzoprazole as antisecretant and lesion preventive drugs.

The effect of Molsidomine as a gastric mucosa protector against absolute ethanol was studied in Wistar rats. It was found that Molsidomine provided an important gastric cytoprotection and it behaved in a similar way as the nitric oxide (NO), the latter verified by specific NO antagonist, namely the NG-monomethyl-L arginine. It was also demonstrated that the cytoprotector mechanism of Molsidomine, as well as of other nitroderivates was sulfhydryl and HEM dependent regarding the guanylate-cyclase enzyme. It can be concluded that both Molsidomine and the NO behaved as modulator of the gastric microcirculation, venous and arterial vasodilator and that their gastric cytoprotective mechanism was endogenous prostaglandin dependent.

The role of sucralphate in prevention of acute gastric injuries and its comparison with free radical blockers such as allopurinol, soybean trypsin inhibitor and superoxidase dismutase in the ischemia-reperfusion model by total occlusion of the coeliac artery in Wistar rats, was studied. The gross gastric mucosal necrotic area was 80%. In contrast with the antioxidant drugs the necrotic area attained was between 7 to 15%, while with sucralphate, an antioxidant-cytoprotective drug that enhances the gastric defensive barrier, the prevention of the secondary aggression induced by free radicals was more important.

In Wistar rats, four experiments were carried out, studying specific inhibitors for ACE (angiotensin-converting enzyme), such as captopril, enalapril, lisinopril, ramipril and cilazapril, in presence of 20% and 95% ethanol induced gastric lesions. The effect of lisinopril and angiotensin I on the same injury was also studied. Subsequently, drugs with known role in gastric mucosa cytoprotection, such as enprostil, paracetamol, ketotiphen, levamisole, diazepam, bromocriptine, dopamine and clonidine, before and after absolute ethanol gastric injury were also studied. Finally, to examine the potential role of ACE in gastric cytoprotection, pretreatment with enalapril, followed by cytoprotective drugs, was carried out. We conclude that all ACE blockers aggravate the gastric lesion induced by 20% and 95% ethanol and are similar to the findings with angiotensin I. The gastric ACE probably plays an important role in the gastric mucosa defense. On the other hand, gastric ACE, as a physiologic regulator of microcirculation, acts by a double mechanism. a) converting the vasopressor amine, angiotensin I in angiotensin II. b) activating vasoactive peripheric receptors such as DA 2 dopaminergic and alfa 2 adrenoreceptors.

The role of Sucralfate in prevention of acute gastric injuries and its comparison with free radicals blockers as Allopurinol, Soybean Trypsin Inhibitor and Superoxide Dismutase was studied in the ischemia-reperfusion model by total occlusion of the celiac axis in Wistar rats. In control rats, the gross gastric mucosal necrotic area was of 80%; in contrast, the antioxidant drugs resulted in a necrotic area of 7%-15% and Sucralfate resulted in a necrotic area of only a 4%. It was concluded that Sucralfate, as antioxidant-cytoprotective drug, by enhancing the gastric defensive barrier was more important than the secondary aggression induced by free radicals.

eSS rats exhibit a non-insulin-dependent diabetic syndrome, significantly influenced by diet. Long-term effects of intermittent dietary restriction were studied in male eSS rats. Experimental animals were fed ad libitum during 48 h and food-deprived the next 24 h (R) while controls (L) of the same strain were freely fed every day. This schedule was maintained from 21 days of age until all rats were sacrificed. R animals were leaner than L rats at 5, 8 and 13 months of age. Moreover, an improved metabolic profile (i.e., lower levels in blood triglycerides, total blood cholesterol, basal blood glucose and blood glucose after an oral glucose load) was found. Histological examination of nuchal skin specimens showed a significant increase of dermal thickness and epidermal hypotrophy in free-fed animals. Collagenous fibers closely packed were found just beneath the dermo-epidermal junction in L rats. This finding was less pronounced in R rats. The above mentioned results suggest that eSS rats would draw advantage from living in environments where food availability is uncertain. The importance of early dietary restrictions in predisposed genotypes appears to be a valuable preventive measure against diabetic evolution and complications.

Six percent hydrogen peroxide (H2O2) was used as a generator of the *OH free radical, and as an aggressor of gastric mucosa, in 100 Wistar rats. The mucosal cytoprotector effect of sucralfate, misoprostol, enprostil, cimetidine, ranitidine, famotidine and 10% aluminum sulphate yielded almost complete macroscopic and histological protection to the gastric mucosa. Misoprostol or enprostil gave partial protection whereas the H2 blockers aggravated the gastric necrotic lesions produced by the H2O2. We conclude that sucralfate is a true anti-oxidant that protects the gastric mucosa through its aluminum and sulphydril components, the increment of gastric mucins and endogenous PGs.

The unknown mechanism of adaptative gastric cytoprotection (AGC) induced by 20% ethanol and subsequent injury with 70% ethanol was studied in wistar rats. Pretreatment with indomethacin or HgII2 did not prevent the AGC, there suggesting that neither endogenous PGS nor gastric mucus take part in its mechanism. On the other hand, ranitidine pretreatment blocked and even aggravated the damage induced by ethanol-ethanol. In contrast, the latter phenomenon was reverted by 20% acidified ethanol. It is concluded that a back diffusion of H+ and bicarbonate play important roles in the AGC mechanism.

In groups of white Wistar rats, the cytoprotective effect induced by TDB on the gastric mucosa against the ethanol injury, was studied; where macroscopic protection and histologic cytoprotection in gastric corpus was found, and no in antrum mucosa. The cytoprotective mechanism give by TDB, were studied by the test of Indomethacin, Cl2Hg, Domperidone, Chlorpromazine and Acetazolamide, where each drug was given as pretreatment. Was conclude that TDB give gastric cytoprotection by the mechanism of the nonprotein sulfhydryl, by to be one peripheral agonist of the neuronal dopamine receptors, by increase of endogenous prostaglandin, by little increment of cAMP and no participate the gastric bicarbonate secretion.

In Wistar rats, the acid factor, the peripheral dopaminergic mechanism and the role of Brunner gland (BG), in the prevention of the Cysteamine duodenal ulcer (CDU) were studied. It was found that Bromocriptine; a peripheral dopaminergic neuronal receptor agonist (DA2), produced prevention of the CDU and blocked of PAS depletion of the BG; in contrast, SCH23390, a peripheral dopaminergic vascular receptor antagonist (DA1), and SAMe, a peripheral and central antidopaminergic; induced aggravation of CDU and total depletion of the BG. In conclusion, the HCl factor, a peripheral dopaminergic mechanism and impaired Brunners gland secretion of PAS mucus, in the pathogenesis of the CDU was postulated.

The administration of oral S-adenosylmethionine (SAMe) (100 mg/kg body weight) was well tolerated by the rat gastroduodenal tract. Moreover, rats given SAMe exhibited a significant increase in non-protein sulfhydryl groups of gastroduodenal mucosa as compared with control animals. The abilities of SAMe and misoprostol, a prostaglandin E1 analogue, to protect the gastric mucosa against necrosis induced by various noxious stimuli (ethanol, aspirin, stress) were also compared in standardized, experimental rat models. Pretreatment with SAMe or misoprostol significantly and to the same extent reduced gastric mucosal injury. The experiments described herein indicate that SAMe, a molecule used for the treatment of osteoarthritis, can exert a gastric cytoprotective effect in animals. As preliminary data have shown that this effect may also be reproduced in humans, SAMe seems to provide a therapeutic advantage, in contrast to currently available nonsteroidal anti-inflammatory agents.

The cytoprotective effects on the gastric mucosa of the Bromocriptine, a peripheral dopaminergic receptor agonist compared with Misoprostol against ethanol-induced injury were studied. Pretreatment with SCH 23390 (a DA1 receptor antagonist) and Domperidone (a DA2 receptor antagonist), showed that Misoprostol was peripheral dopaminergic receptor dependent in the gastric cytoprotective mechanism, and that Bromocriptine was a selective peripheral DA2 receptor agonist in the gastric cytoprotection mechanism; as well as, indomethacin pretreatment, showed that peripheral DA2 receptors were endogenous prostaglandin dependent. In conclusion, a prostaglandin-dopaminergic mechanism was postulated in gastric cytoprotection.

On 58 healthy subjects, it was evaluated in endoscopic and histopathologic form, the cytoprotective effect on the gastroduodenal mucosa, such of T.G.E 1 (misoprostol) as of SAMe, in the present of acute bleeding gastritis induced by 1300 mg aspirin in a single dose and during 2 hours. SAMe was given in progressive doses up to 500 mg, which were ingested simultaneously with aspirin, and so with Misoprostol in doses of 50 mg, showed an endoscopic score of 0 without microscopic lesion of the gastroduodenal mucosa, this was confirmed by the histopathology, where both drugs give a cytoprotection of the gastroduodenal mucosa by about 95% of total biopsies gastrointestinal mucosa. It is suggest that T.G.E.1 (misoprostol) and SAMe are choice drugs in the treatment of hemorrhagic gastritis.