Laine et al.  stated that reactive oxygen species (ROS) generated by neutrophils in gastric mucosa has a critical role in the gastric mucosal injury. Later, Al Rashdi et al.  and Kan et al.  reported that ele- vated production of ROS and depletion of antioxidants are involved in the pathophysiology and development of ethanol-induced gastriculcer. According to Yu et al. , accumulation of ROS leads to lipid peroxidation as a result of their reaction against cell membrane. Our data revealed that, ethanol administration significantly reduced the activity levels of antioxidant enzymes (CAT, SOD and GSH-Px) and increased the concentration of MDA with concomitant depletion in GSH concentration in the gastric tissue of ethanol group, this is in the same line with the previous studies of Sidahmed et al. . On the other hand, pre-treatment of C. ignea extract in ulcerated groups has a great efficacy in preventing free radical mediated oxidative damage by enhancing the ac- tivity of antioxidant enzymes (CAT, SOD and GSH-Px) and restoring the depleted GSH levels together with re- ducing MDA levels. This antioxidant effect of the C. ignea extract could be attributed to its strong free radical scavenging activity due to the presence of a significant amount of, the powerful antioxidants, flavonoids and phenolic compounds. This is consistent with Mei et al.  who established that one of the mechanisms re- sponsible for the healing of ulcer is scavenging of ROS. Our study showed that C. ignea extract had strong anti- oxidant effect, which is comparable to that of ranitidine. Ahmadi et al.  previously reported that therapeutic effect of ranitidine on ulcer could be related to its anti- oxidant capacity through oxidative stress reduction me- diated by scavenging of hydroxyl radical.
long-term inhibition of gastric acid secretion results in mucosal hyperplasia and carcinoid tumor development, due to increase circulating gastrin levels. Ulcer and the preventive indexes were scored, mucin, juice volume, total acidity, luminal haemoglobin, total antioxidant and total peroxide were evaluated. The pro-inflammatory cytokine IL-6 and the major angiogenic growth factor VEGF levels were measured. Conclusion, curcumin and omeprazole are potentially preventing gastric lesions development in the gastric wall during the acute phase of gastriculcer diseases, but curcu- min was more potent in its effect. Curcumin promotes gastriculcer prevention/healing by induction of angiogenesis in the granular tissue of ulcers. That may be via upregulation of VEGF expression as reflected from VEGF level in serum and gastric juice, however, omeprazole might be has no role in this story.
Because of acid peptic secretion in gastric mucosa get degenerate and necrosis is forming which causes peptic/gastriculcer. Generally it can take place at any area of the alimentary canal but normally it can take place in duodenum and stomach due to exposure of HCL and pepsin. Many kind of medicine get used in the gastriculcer but they having limitations and they having major side effects. The anti ulcer or anti secretary drugs are given in table no 7.
This is to certify that the dissertation titled “A STUDY ON CLINICAL OUTCOME OF GASTRICULCER PERFORATION” is the original work done by Dr.S.Venkatesan, post graduate in M.S., General surgery at the department of general surgery, madras medical college, Chennai 600 003 to be submitted to the Tamilnadu Dr.M.G.R Medical university, Chennai 600 032, towards the partial fulfillment of the requirement for the award of M.S.,degree in General Surgery during the academic period from may 2010 – April 2013.
Stomach ulcer is defined as erosion in the lining of the stomach or duodenum and is caused by the disruption of the gastric mucosal defense systems. Ulcer in the stomach is called gastriculcer and in the duodenum is called duodenal ulcer and together it is named as peptic ulcer. Ulcer incidence varies with the type of ulcer, gender and age. Peptic ulcer has initiated as open craters or sores in the inner lining (mucosa) of the stomach or the duodenum. A coating of mucus and other biochemicals normally shield the stomach and duodenum from digesting themselves. When these protective mechanisms are disturbed, powerful digestive acids can erode into the lining of these organs and cause ulcers. Ulceration is an imbalance between the rate of secretion of gastric juice and the degree of protection afforded by the gastro- stomach mucosal barrier as well as the neutralization of the gastric acid by stomach juice. Infection by the bacterial pathogen Helicobacter pylori, frequent usage of Non- Steroidal Antiinflammatory Drugs (NSAIDs) and high acid secretion are main reasons for induction of ulcer. Other causes of peptic ulcer are smoking, alcohol consumption, psychological stress and irregularity in diet. Reduction of gastric acid production as well as re-enforcement of gastric mucosal production has been the major approaches to cure peptic ulcer  . Due to any cause, an increase in aggressive factors or a decrease in defensive factors will lead to loss of mucosal integrity resulting in ulceration  . Gastric ulcers are located in the stomach, characterized by pain and common in older age group. Other symptoms may include nausea, vomiting and weight loss  .
Gastriculcer is an etiological disease in which several factors such as stress, trauma, sepsis, hemorrhagic shock, burns, Helicobacter pylori, steroidal and non-steroidal drugs [1,2,3,4,5] play significant roles. Regardless of great advances in the field of medical science and understanding of the peptic ulcer illness, gastric ulcers aetiology is still not completely understood. Many of these anti- ulcer drugs in use have been found to have adverse effects and there is recurrent infection after a few weeks . Stress as one of the most commonly used methods to produce ulcer models and an aggressive factor in peptic ulcer formation, underlies other diseases such as depression [7,8]. Depression, accompanied by psychotic and somatic symptoms has been reported to be present in most patients with gastrointestinal ulcers . An increased depression  and anxiety  has been reported to parallel with ulcer development in experimental animals and this holds true in humans [12, 13]. Some anti-psychotic drugs such as perospirone  and risperidone  have already been reported to have anti-ulcer activity. The successful treatment of gastric lesion depends on augmentation of the defensive factors of the gastric mucosa and blockage of acid secretion . This study was carried out to evaluate further the gastroprotection activity of risperidone where information on these areas are still scarty has not been documented in male Wister rats.
The objective of present study is to evaluate the anti ulcer activity of ethanol extract of leaves of Heliotropium indicum. The ethanol extract of H. indicum was investigated for its anti ulcer activity against Aspirin plus pylorus ligation induced gastriculcer in rats, HCl- Ethanol induced ulcer in mice and water immersion stress induced ulcer in rats. The antiulcer activity was assessed by determining and comparing gastric volume, free acidity and ulcer inhibition in aspirin plus pylorus ligation induced gastriculcer model. The number of lesions in HCI-Ethanol induced peptic ulcer model and mean score value of ulcer inhibition in water immersion stress induced ulcer model. A significant antiulcer activity of plant extract was observed in all the models. Pylorus ligation model showed significant reduction in gastric volume, free acidity and ulcer index as compared to control. Also extract showed significant ulcer inhibition in HCl- Ethanol induced ulcer and ulcer protection index in stress induced ulcer. This present study indicates that Heliotropium indicum leaves extract have potential anti ulcer activity in the three models tested.
FIG. 3. Sequence analyses of type A and type C cagA genes. (A) Alignment of the deduced amino acid sequences of type C strains, in the region corresponding to amino acid residues 892 to 969 of the H. pylori ATCC 53726 CagA product (GenBank accession no. L11714). Strain JK14 was from a patient with gastriculcer, and the remaining six strains were from patients with gastric cancer. (B) Comparison of the deduced amino acid sequences of the R1, R2, and R3 regions of type A and type C strains with the same region of the gene product of a reference strain. The reference strains ATCC 43526, G39, ATCC 53726, and CCUG17874 (GenBank accession no. AB003397, X70038, L11714, and X70039, respectively) were used for sequence comparison. Consensus sequences among the cagA genes from H. pylori isolates from patients with chronic gastritis (CG), gastriculcer (GU), duodenal ulcer (DU), and gastric cancer (GC) were separately determined among type A strains.
It is well known that atrophic gastritis is positively associated with both gastriculcer and gastric cancer whereas antral predom- inant gastritis is associated with development of duodenal ulcer. The high-activity and high-producer genotype of H. pylori viru- lence factors and the cagA-positive, vacA s1, m1, and i1 genotypes have been associated with enhanced gastric mucosal inflamma- tion and mucosal atrophy (18). Although the 90.7% of H. pylori isolates with the jhp0947 status in Brazil were reported to be asso- ciated with cagA (23), this relationship was not observed in Indian (19), Dutch (6), or other Brazilian groups (17). In this study, we showed that the jhp0940, jhp0945, jhp0947, and jhp0949 status had no significant associations with vacA s1, m1, and i1 genotypes or with cagA positivity in either Western or East Asian populations. We found that in multivariance analysis jhp0940 and jhp0945 sta- tus was related to peptic ulcer and gastric cancer and to gastric mucosal inflammation and atrophy, suggesting it may be a new virulent marker for H. pylori-related diseases. However, none of the associations were significant.
Parinaam shoola is having similarity to duodenal ulcer according symptoms and annadravya shoola is having similarity to Gastriculcer. In the initial stage it is difficult to distinguish between Gastric and Duodenal ulcer, both are called peptic ulcer. In parinaam shoola pain is produced after digestion of food and in annadrava shoola there is constant severe pain in abdomen.
In aspirin plus pylorus ligation induced gastriculcer model the ethanol extracts of Aegle marmelos reduced the gastric volume, free acidity, total acidity and ulcer index thus showing the anti-secretory mechanism involved in the extracts for their anti-ulcerogenic activity. Ulcer index parameter was used for the evaluation of anti-ulcer activity since ulcer formation is directly related to factors such as gastric volume, free and total acidity. In case of vehicle control, aspirin plus pylorus ligation increased the acid secretion, which in turn caused increase in gastric volume, low pH, increased free and total acidity resulting into increase in ulcer index [12, 52]. Aspirin induced gastriculcer was employed to study the cytoprotective effect of the extracts. Aspirin induced gastric lesion formation may be due to stasis in gastric blood flow which contributes to the development of the haemorrhage and necrotic aspects of tissue injury. Alcohol rapidly penetrates the gastric mucosa apparently causing cell and plasma membrane damage leading to increased intra cellular membrane permeability to sodium and water. The massive intracellular accumulation of calcium represents a major step in the pathogenesis of gastric mucosal injury. This leads to cell death and exfoliation in the surface epithelium . The extract shows protection against characteristic lesions produced by Aspirin administration this antiulcer effect of Aegle marmelos may be due to both reductions in gastric acid secretion and gastric cytoprotection. Ramamurthy and Selvarani  reported that the acid secretary parameters such as pH, gastric volume, free acidity and total acidity were increased significantly in the aspirin administered group. Administration of ethanolic extracts of Azima tetracantha exhibited a significant reduction in all the parameters and the results were comparable with the standard drug Lansoprazole 8 mg/kg. Determination of the concentrations of various muco-proteins such as total protein, total hexoses, hexosamine, fucose and sialic acid revealed a decrease in ulcer induced group. The present study Aegle marmelos showed significant dose-dependent ulcer protective effect against aspirin plus pylorus ligation induced gastric ulcers. Aegle marmelos used in the study have been found to be effective against aspirin pylorus ligation model. It is evident from the results that these drugs produce reduction in the intensity of gastric ulceration as observed from reduced ulcer index in the drug treated groups. However, inconsistent results were obtained as regards to other parameters such as volume of gastric acid secretion, free and total acidity and pepsin activity.
51.Talebi Bezmin Abadi A, Taghvaei T, Wolfram L, Kusters JG. Infection with Helicobacter pylori strains lacking dupA is associated with an increased risk of gastriculcer and gastric cancer development. J Med Microbiol. 2012; 61(Pt 1): 23-30.
The anti ulcer activity of beta vulgaris was evaluated by employing aspirin, alcohol, and pylorus ligation induced ulcer models. These models cause the gastriculcer in humans. Many factors and mechanisms are involved in the ulcerogensis and gastric mucosal damage. Ethanol induced gastriculcer was employed to study the cytoprotective effect of the extracts. The ethanol-induced ulcers is predominant in the glandular part of stomach and was reported to stimulate the formation of leukotriene C4 (LTC4), mast cell secretory products and reactive oxygen species resulting in the damage of rat gastric mucosa. Alcohol rapidly penetrates the gastric mucosa causing cell and plasma membrane damage leading to
Rats pre-treated with either 50 mg/kg cimetidine or the Schiff base TNS and its nickel (II) complex before being given absolute alcohol had significantly reduced areas of gastriculcer formation compared to rats pre-treated with only 10% Tween-20 [Table 1, Figure 1a–c]. Moreover, the compounds significantly suppressed the formation of the ulcers and it was interesting to note the flattening of gastric mucosal folds in rats pretreated with these compounds. It was also observed that protection of gastric mucosa was more prominent in rats pre-treated with both high and low doses of TNS ligand and high dose of the nickel (II) complex (Table 1). The significant inhibition of gastriculcer in pretreatment with the compounds was compared with cimetidine which is a standard drug used for curing gastriculcer.
different types of biochemical parameters or oxidative health biomarkers were also determined in the present study including total oxidant status, malondialdehyde, total antioxidant capacity and CAT were also determined in the current study. It has been concluded from the results that when indomethacin was given at a dose rate of 20 mg/kg, total oxidant status and malondialdehyde were enhanced significantly while total antioxidant capacity and CAT activity were reduced significantly. Indomethacin encourages the reactive oxygen metabolites that may play a role in gastric damage. These reactive species cause damage to the biochemical markers e.g. lipid and increased the production of free radicals that increased MDA production and decreased CAT and these free radicals production also because of impairment of cellular enzyme that involve in defensive mechanism of gastriculcer such as total antioxidant capacity and CAT activity 36 . On the other hand,
Date, is a large, broad-leaved, tropical tree found in Haryana and other parts of India and Asia. The word Tamarind is from Arabic 'tamar-ul-Hind', meaning, "the date palm of India". The tree can grow up to 25 meters with a spread of 12 m, and stays evergreen in regions without a dry season. Tamarind are many and it is used extensively in the Indian system of medicine, Ayurveda Tamarind preparations are universally recognized as refrigerants in fevers and as laxatives and carminatives. Tamarind leaves and flowers, dried or boiled, are used as poultices for swollen joints, sprains and boils. Extracts made from them are used in treating conjunctivitis, as antiseptics, as vermifuges, treatments for dysentery, jaundice, erysipelas and hemorrhoids and various other ailments. The aim of the present study was to evaluate the pharmacological activity of Tamarindus indica in experimental models of gastriculcer .
samples into three main groups and correlated to the disease. One main group contained most of the gastric cancer tissues and gastriculcer tissues based on their low CD8/Foxp3 and CD8/PD-L1 expression, as shown in Fig. 5h. Other normal tissues and gastric disease tissues, which exhibited relatively high expression of CD8/Foxp3 and CD8/PD-L1, were clustered into another group. The hierarchical clustering was also supported by additional Pearson correlation analysis in gastric cancer tissues. As shown in Fig. 6a–c, the correlation coefficient between the expression of CD8 and Foxp3 in gastric cancer tissues was 0.479 (p < 0.01). Moreover, the expression of Foxp3 was also high correlated with PD-L1 with the coefficient of 0.473 (p < 0.05). However, no significant relationship was found between the expression of CD8 and PD-L1 in gastric cancer tissues. Then we applied hierarchical clus- tering analysis in gastric cancer tissues (Fig. 6d). Based on the ratio of CD8:PD-L1, gastric cancer tissues were divided into three groups. However, after adding the ratio of CD8/Foxp3 for the further clustering analysis, more
Ulcers are deep lesions penetrating through the entire thickness of the gastrointestinal tract (g.i.t) mucosa and muscularis mucosa. Peptic ulcer has unquestionably been a disease of the twentieth century. Epidemiological data for this disease and its complications have shown striking geographical variations in incidence and prevalence. There are different types of ulcers most common are peptic ulcer: gastriculcer, which appeared to be due to damage to the lining of the stomach, and duodenal ulcer, which was associated with excessive acid secretion by the stomach. The aetiology of peptic ulcer was fiercely debated. It is believed that peptic ulcers develop due to an imbalance between aggressive factors (Helicobacter pylori, NSAIDs, gastric acid) and protective factors (mucin, bicarbonate, prostaglandins), leading to an interruption in the mucosal integrity. Various factors are implicated that play a pivotal role in the pathogenesis of ulcertions like, sedentary life style, alcohol intake, spicy food, drugs and various bacterial infections. Moreover, several endogenous substances have been identified and are reported to be involved in the production of gastrointestinal lesions in animals. The more important ones include some of the bacterial infection, various drugs and chemicals, gastric secretion, lipid metabolites, neuropeptides, inflammatory mediators and reactive free radicals. Oxidative stress has emerged as one of the major pathogenic factors in progression of ulcer that directly impaired the cellular functions and promotes cellular organelles damage in the cells, including mitochondria, lysosomes, and nucleus. Also, NO is accepted as vital mediator of GIT mucosal defense as decreased NO generation or synthesis contribute to the pathogenesis of ulceration. The present study summarizes the ulcerogenic mechanisms of these substances and the enable us to understand better the etiology of peptic ulcer.
Indomethacin is a cyclooxygenase inhibitor which suppresses gastroduodenal bicarbonate secretion reduces endogenous prostaglandin biosynthesis and disrupts the mucosal barrier as well as mucosal blood flow in animals. It is also well known that prostaglandin synthesized in large quantities by the gastrointestinal mucosa can prevent experimentally induced ulcers by ulcerogens. Thus when the gastriculcer is induced by indomethacin, the cytoprotective effect of the anti-ulcer agent can be mediated through endogenous prostaglandins (Brestel 1994).Further, several studies also evidenced that the gastriculcer is mainly due to damage of gastric mucosa by free radicals and reactive oxygen species (Bandyapadhyay et al., 2002). In both ethanol and indomethacin induced ulcer models, Ficus talboti treatment significantly reduced the severity of the ulcers.