Helicobacter pylori infection and peptic ulcers

Majumdar, Debabrata; Bebb, James R.

doi:10.1016/j.mpmed.2019.02.008

Cited by 14 publications

(16 citation statements)

References 3 publications

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“…However, even when the infection is asymptomatic, H. pylori infection can lead to peptic ulcer and gastric cancer [32]. Chronic gastritis H. pylori is asymptomatic, but the initial onset of the infection causes acute gastritis with hypochlorhydria, which may cause abdominal pain, nausea, and vomiting that resolve within a few days [33]. Epidemiological studies show that 2-3% of H. pylori-infected people develop gastric adenocarcinoma, and 0.1% will develop mucosa-associated lymphoid tissue (MALT) lymphoma [34,35].…”

Section: Helicobacter Pylori and Gastric Cancermentioning

confidence: 99%

Molecular Mechanism of Helicobacter pylori-Induced Gastric Cancer

Alipour

2020

J Gastrointest Canc

154

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Introduction Various types of cancers threaten human life. The role of bacteria in causing cancer is controversial, but it has been determined that the Helicobacter pylori infection is one of the identified risk factors for gastric cancer. Helicobacter pylori infection is highly prevalent, and about half of the world , s population is infected with it. Objective The aim of this study was the role of Helicobacter pylori in the development of gastric cancer. Method We obtained information from previously published articles. Results and Conclusion The bacterium has various virulence factors, including cytotoxin-associated gene A, vacuolating cytotoxin A, and the different outer membrane proteins that cause cancer by different mechanisms. These virulence factors activate cell signaling pathways such as PI3-kinase/Akt, JAK/STAT and Ras, Raf, and ERK signaling that control cell proliferation. Uncontrolled proliferation can lead to cancer.

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Section: Helicobacter Pylori and Gastric Cancermentioning

confidence: 99%

Molecular Mechanism of Helicobacter pylori-Induced Gastric Cancer

Alipour

2020

J Gastrointest Canc

154

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“…On a global scale, more than half of the world's population is infested by this bacteria and this rate reaches about 80% in developing countries [7–9]. The correlation between such infection and digestive diseases such as gastric and/or duodenal ulcers, chronic erosive gastritis, stomach and/or duodenal cancer, and malt lymphomas has been reported [10, 11]. Indeed, infection of the gastric mucosa by HP evolves in several cases into active chronic gastritis which causes in about 50% of the cases an atrophy of the gastric wall, an intestinal metaplasia which is complicated in about 20% of the cases in dysplasia and then in gastric cancer [12].…”

Section: Introductionmentioning

confidence: 99%

Effectiveness ofOpuntia ficus indicaL.inermisSeed Oil in the Protection and the Healing of Experimentally Induced Gastric Mucosa Ulcer

Khémiri

Bitri

2019

Oxidative Medicine and Cellular Longevity

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Gastric ulcer is a painful lesion of the gastric mucosa which can be disabling, or even more very serious in the case of a perforation of the stomach and internal hemorrhage. Traditional pharmacopeias have shown the efficacy of various plant extracts in the treatment of this pathology. Some extracts from Opuntia ficus indica (OFI) have been proven to have medicinal therapeutic benefits. The aim of this study was to investigate the preventive and curative effects of OFI seed oil extracted by cold pressing on an ethanol-induced gastric ulcer model in rats. Gastroprotective activities of the oil were assessed as pretreatments prior to ethanol gavage of Wistar rats compared to reference drugs. Two oil dose effects were tested. Ulcer and gastric parameters were measured (ulcerated areas (mm2), % of ulcer inhibition, gastric juice volume and pH, and mucus weight). Macroscopical and microscopical assessments of the stomachs as well as gastric biopsy histological studies were carried out. OFI oil exhibited a high efficiency in the protection of the cytoarchitecture and function of the gastric mucosa against the severe damages provoked by ethanol intake. Ulcerated areas were very significantly reduced and the % of ulcer inhibition was the highest under OFI oil pretreatment. Mucus production was stimulated, gastric juice volume was reduced, and its pH was increased. Histopathological examination of H&E-stained biopsies collected from gastric mucosae from the different experimental groups confirmed the gastroprotective efficacy of OFI oil against ethanol-induced symptoms such as inflammation and damages like bleeding, erosions, lesions, necrosis, and ulcers. Furthermore, OFI oil treatment speeded-up the reduction of the surface of ethanol-induced ulcerated areas in a dose-dependent manner, leading to a time gain in the healing process. The healing rate reached 91% on day 2 and 99% on day 3, and a complete heal was attained at the fourth day under OFI oil treatment, while ulcer areas were still partially unhealed in all the other groups. The therapeutic effects of OFI oil against gastric ulcer could be mediated by its varied bioactive compounds that we have demonstrated in the analytical study. They could act synergistically or in a delayed manner to optimize the healing process through protective antioxidant properties, as well as an antagonism against histamine H2-receptors, a stimulation of the signaling pathways necessary for mucus and bicarbonate production, and reduction of inflammatory processes in the gastric mucosa. Additionally, OFI oil fatty acids (especially unsaturated) and triacylglycerols contribute to the reconstruction and the repair of the cell membrane lipid bilayer during the gastric ulcer healing process.

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“…Small or shallow breaches are termed “erosions” while sometimes insignificant, these may herald ulcers. [ 1 ] In the Developed nations, H. pylori incidence has been slowly declining over the past 50 years, and NSAID use has increased. This has resulted in a decline in duodenal ulcers (almost always associated with H. pylori infection) and an increase in gastric ulcers (the main site of ulcers caused by NSAIDs).…”

Section: Introductionmentioning

confidence: 99%

Gastroprotective and ulcer healing effects of camel milk and urine in HCl/EtOH, non-steroidal anti-inflammatory drugs (indomethacin), and water-restraint stress-induced ulcer in rats

Hu¹,

Chang²,

Qing³

et al. 2017

Phcog Mag

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Background:Camel milk has been reportedly used to treat dropsy, jaundice, tuberculosis, and diabetes while camel urine is used to treat diarrhea and cancer. However, there is no scientific evidence on the antiulcer activity of camel milk and urine. Thus, the present is designed to investigate the gastroprotective and ulcer healing effect of camel milk and urine on experimentally induced gastric ulcer models in rats.Materials and Methods:The gastroprotective effect was investigated in HCl/EtOH, water-restraint stress (WRS) and non-steroidal anti-inflammatory drugs (indomethacin)-induced ulcer models while ulcer healing activity was investigated in indomethacin-induced ulcer model. Cimetidine (100 mg/kg) was used as a standard antiulcer drug.Results:Acute toxicity study done up to a dosage of 10 ml/kg of camel milk and urine showed no signs of toxicity and mortality among the rats, indicating the present dosage of 5 ml/kg is safe to be administered to the rats. In the HCl/EtOH model, oral administration of cimetidine (100 mg/kg), camel urine (5 ml/kg), and camel milk (5 ml/kg) significantly (P < 0.05) inhibited gastric lesions by 83.7, 60.5 and 100%, respectively. In the WRS-induced model, cimetidine, and camel urine showed an ulcer inhibition of 100% while camel milk showed an inhibition of 50%. Similarly, in the indomethacin-induced ulcer model, cimetidine, camel milk, and urine showed an ulcer inhibition of 100, 33.3, and 66.7%, respectively. In addition, camel milk and urine also showed a significant (P < 0.05) ulcer healing effect of 100% in indomethacin-induced ulcer model, with no ulcers observed as compared to that of cimetidine, which offers a healing effect of 60.5%.Conclusion:The antiulcer activity of camel milk and urine may be attributed to its cytoprotective mechanism and antioxidant properties.SUMMARY Acute toxicity findings revealed the dosage of 10 ml/kg of camel milk and urine seems no toxic and indicating the dosage of 5 ml/kg is safe to be administered to the ratsOral administration of cimetidine (100 mg/kg), camel urine (5 ml/kg), and camel milk (5 ml/kg) significantly inhibited gastric lesions by 83.7, 60.5 and 100% in the HCl/EtOH experimental modelThe results of this investigation have proven that camel milk and urine showed strong ulcer healing effect in indomethacin-induced gastric damage. Abbreviations used: NSAIDs: Non-steroidal anti-inflammatory drugs, UI: Ulcer index, ANOVA: One-way analysis of variance, WRS: Water-restraint stress, ROS: Reactive oxygen species

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Helicobacter pylori infection and peptic ulcers

Cited by 14 publications

References 3 publications

Molecular Mechanism of Helicobacter pylori-Induced Gastric Cancer

Molecular Mechanism of Helicobacter pylori-Induced Gastric Cancer

Effectiveness ofOpuntia ficus indicaL.inermisSeed Oil in the Protection and the Healing of Experimentally Induced Gastric Mucosa Ulcer

Gastroprotective and ulcer healing effects of camel milk and urine in HCl/EtOH, non-steroidal anti-inflammatory drugs (indomethacin), and water-restraint stress-induced ulcer in rats

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