The United Arab Emirates (UAE) has been under continuous populational influences from Asia, Europe, and Africa, making it an ideal site for epidemiological studies on Helicobacter pylori. However, there has been a paucity of well-designed prevalence studies on H. pylori from UAE. The aim of this study was to determine the prevalence of H. pylori and its associated risk factors in the UAE. A prospective cross-sectional study was conducted on healthy asymptomatic residents of UAE. Socio-demographic, lifestyle, and gastrointestinal characteristics of participants were obtained through a questionnaire in parallel within the stool sample collection. A total of 350 participants were included in this study and were tested for H. pylori using the stool antigen test (Premier Platinum HpSAT). Out of the total tested study participants, 41% were found to be H. pylori-infected. Logistic regression analysis has shown a significant association between H. pylori infection and gender, age, ethnicity, profession, domestic overcrowding, source of drinking water, and gastrointestinal characteristics of participants. Based on the results from this study, we suggest that preventive measures against H. pylori infection should be considered worthy by public health authorities.

Gastric cancer is ranked fifth in cancer list and has the third highest mortality rate. Helicobacter pylori is a class I carcinogen and a predominant etiological factor of gastric cancer. H. pylori infection may induce carcinogenesis via epigenetic alterations in the promoter region of various genes. H. pylori is known to induce hypermethylation-silencing of several tumor suppressor genes in H. pylori-infected cancerous and H. pylori-infected non-cancerous gastric mucosae. This article presents a review of the published literature mainly from the last year 15 years. The topic focuses on H. pylori-induced DNA methylation linked to gastric cancer development. The authors have used MeSH terms “Helicobacter pylori” with “epigenetic,” “DNA methylation,” in combination with “gastric inflammation”, gastritis” and “gastric cancer” to search SCOPUS, PubMed, Ovid, and Web of Science databases. The success of epigenetic drugs such as de-methylating agents in the treatment of certain cancers has led towards new prospects that similar approaches could also be applied against gastric cancer. However, it is very important to understand the role of all the genes that have already been linked to H. pylori-induced DNA methylation in order to in order to evaluate the potential benefits of epigenetic drugs.

Cinnamomum cassia is widely employed for gastrointestinal complaints such as dyspepsia, flatulence, diarrhea, and vomiting. Studies report cinnamaldehyde (CM) as a major active constituent of cinnamon. The aim of this study was to evaluate the anti-inflammatory mechanism of CM on Helicobacter (H.) pylori-infected gastric epithelial cells in order to validate cinnamon traditional use in gastrointestinal (GI)-related disorders. AGS/MKN-45 cells and H. pylori (193C) were employed for co-culture experiments. Anti-H. pylori cytotoxic and anti-adhesion activity of CM were determined. Enzyme linked immunosorbent assay, real time polymerase chain reaction analysis and immunoblotting were used to measure the effect on interleukin-8 (IL-8) secretion/expression. The effect on activation of nuclear factor kappa B (NF-κB) was determined by immunoblot analysis. The non-cytotoxic CM (≤125 µM) was also non-bactericidal at the given time, suggesting the effect in H. pylori/cell co-culture system was not due to alteration in H. pylori viability or the toxicity to the cells. Also, CM did not show any anti-adhesion effect against H. pylori/cell co-culture. However, pre-incubation of the cells with CM significantly inhibited the IL-8 secretion/expression from H. pylori-infected cells (p<0.01). In addition, CM suppressed H. pylori-induced NF-κB activation and prevented degradation of inhibitor (I)-κB This study provides evidence that the anti-inflammatory effect of C. cassia on H. pylori-infected gastric cells is due to blockage of the NF-κB pathway by cinnamaldehyde. This agent can be considered as a potential candidate for in vivo and clinical studies against various H. pylori related gastric pathogenic processes.

Cadmium (Cd) is a heavy metal and a highly toxic pollutant that is released into the environment as a byproduct of most modern factories and industries. Cd enters our body in significant quantities from contaminated water, cigarette smoke, or food product to many detrimental health hazards. Based on causal association all the Cd-related or derived compounds have been classified as carcinogens. In this study, we present an overview of the published literature to understand the molecular mechanisms for Cd-induced carcinogenesis and its prevention. In acute Cd poisoning production of reactive oxygen species is a key factor. However, chronic Cd exposure can transform cells to become more resistant to oxidative stress. Also, as an epigenetic mechanism Cd acts indirectly on DNA repair mechanisms via alteration of reactions upstream. Those transformed cells acquire resistance to apoptosis and deregulation of calcium homeostasis. Leading to uncontrolled carcinogenic cell proliferation and inherent DNA lesions. Flavonoids commonly found in plant foods have been shown to have a protective effect against Cd-induced carcinogenicity. A wide variety of tumorigenic mechanisms involved in chronic Cd exposure and the beneficial effects of flavonoids against Cd-induced carcinogenicity necessitate further investigations.