Curcumin: A therapeutic strategy for targeting the Helicobacter pylori-related diseases.

Helicobacter pylori is a significant human pathogen of the stomach's epithelial lining. This type of carcinogen is associated with gastric cancer, indigestion, peptic ulcers, and upper digestive diseases. Therefore, successful treatment and eradication of this bacterium are required to reduce the prevalence of these diseases, especially in high-risk individuals. Moreover, some concerns exist regarding the extensive use of elimination therapy, such as anti-microbial resistance and rising H. pylori-associated diseases. Since there is still no effective vaccine, finding alternative therapies would appear to be a worthwhile pursuit. In this regard, curcumin exhibits anti-inflammatory, anti-carcinogenic, anti-oxidant properties and is widely used as a natural product-derived medicine or nutraceutical. Furthermore, curcumin has been reported to have anti-bacterial activity. Therefore, curcumin might be an effective herbal-based medicine for preventing, managing, or treating H. pylori infection. This review discusses the anti-inflammatory, anti-cancer, and anti-bacterial properties of curcumin as it pertains to gastric cancer and H. pylori-associated diseases.

Hepatoprotective effect of the hydroalcoholic extract of Cichorium intybus in a rat model of obstructive cholestasis.

BACKGROUND AND STUDY AIMS: Obstructive cholestasis increases the levels of oxidants and inflammatory mediators, leading to liver damage. Previous studies have found that Cichorium intybus possesses anti-inflammatory effects. In the present study, the effects of the hydroalcoholic extract of C. intybus leaves were assessed in a rat model of obstructive cholestasis. MATERIAL AND METHODS: Male Wistar rats were randomly divided into five groups (n = 6 rats per group): sham-operated, control [bile duct ligation (BDL) + vehicle)] and BDL + extract treatment (100, 200 and 400 mg/kg/day, i.p.) groups. Rats received treatments for 7 consecutive days. On the eighth day, prothrombin time (PT); serum albumin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase and total and direct bilirubin levels and total antioxidant and paraoxonase activities were measured using colorimetric methods. In addition, tumour necrosis factor-α and nitric oxide (NO) levels were measured using enzyme-linked immunosorbent assay. RESULTS: The hydroalcoholic extract of C. intybus significantly decreased PT and the serum levels of AST, ALT, TNF-α and NO compared with the control group (p < 0.05). On the other hand, the serum albumin levels were increased in the extract-treated groups compared with the control group (p < 0.05). CONCLUSION: The hydroalcoholic extract of C. intybus protects the liver against injury induced by obstructive cholestasis.

From genes polymorphisms to mucosal expression of cytokines: evaluating IL-23/IL-17 axis in adult patients with gastritis.

BACKGROUND AND OBJECTIVE: Chronic inflammation is the typical sign of gastritis that may shift into gastric cancer. IL-17A and IL-17F as a novel inflammatory cytokines subset of CD4+Th play the main role in inflammation. A key cytokine receptor in the inflammatory IL-17/IL-23 axis, the interleukin 23 receptor (IL23R), may be related to gastritis. We evaluated the correspondence between IL-17A G197A, IL-17F A7488G and IL23R+2199 A/C polymorphisms with TGF-ß1, IL-6, IL-17, IL-21 and IL-23 mucosal mRNAs expression in uninfected H. Pylori (HP) chronic gastritis patients. MATERIALS AND METHODS: Total RNA and genomic DNA were separated from gastric biopsies of 44 patients with gastritis. Subsequently, mucosal mRNAs expression of TGF-ß1, IL-6, IL-17, IL-21 and IL-23 were assessed by real-time PCR. To polymorphisms determination of IL-17A G197A, IL-17F A7488G and IL-23R +2199A/C the PCR-RFLP was used in gastric biopsies. RESULTS: Results point that IL-17A G197A, IL-17F A7488G and IL23R +2199A/C polymorphisms did not influence the mucosal expression of TGF-ß1, IL-6, IL-17 and IL-21 (p> 0.05). In an opposite result, we don't find a correspondence between IL-17A G197A, IL-17F A7488G polymorphisms and mucosal expression of IL-23 (p> 0.05). In a contrary, we found a correlation between IL23R +2199A/C polymorphism and mucosal expression of IL-23 in patients with chronic gastritis (p< 0.05). CONCLUSION: These findings propose that IL23R +2199A/C polymorphism may change the mucosal expression of IL-23 pattern in patients with gastritis disease in the absence of HP, but to support the conclusion, more research may be required.

T-bet+ Cells Polarization in Patients Infected with Helicobacter pylori Increase the Risk of Peptic Ulcer Development.

BACKGROUND: Peptic ulcer disease (PUD) is a common disease worldwide moreover known as stomach ulcer or peptic ulcer. Increased the number of T CD4+ helper cells in response to gastric infection by Helicobacter pylori (H. pylori) play an important role in the development of PUD. The aim of this study was to determine the frequency of T-bet+ cells in H. pylori-infection, its interaction with Th17/Treg cells and its association with the clinical consequences of the infection. METHODS: A total of 63 patients with PUD, 89 patients with gastritis and 48 H. pylori-negative subjects were enrolled in this study. The number of T-bet+ cells were determined by immunohistochemistry. RESULTS: The numbers of T-bet+ cells and INF-γ expression in infected patients were significantly higher than uninfected. Moreover, the number of T-bet+ cells and INF-γ expression in infected patients with PUD were significantly higher than infected patients with gastritis. Additionally, the number of T-bet+ cells and INF-γ expression were found to be inversely correlated with degree of H. pylori density and chronic inflammation score (CIS) in infected patients with gastritis disease, but this correlation was positive in the infected patients with PUD. The number of T-bet+ cells was found to be positively correlated with the number of Th17 cells and inversely correlated with the number of Treg cells in infected patients with gastritis and PUD. CONCLUSION: Abnormal hyper-activation of T-bet+ cells during H. pylori-infection may lead to tissue damage caused by immunopathologic reactions.

Study of VSX1 mutations in patients with keratoconus in southwest Iran using PCR-single-strand conformation polymorphism/heteroduplex analysis and sequencing method.

OBJECTIVE: Keratoconus (KC) is an eye disorder in which the cornea is swollen, thinned and deformed. Despite extensive studies, the pathophysiological processes and genetic etiology of KC are unknown. The disease incidence is approximately 1 in 2,000, and it is the most common cause of corneal transplantation in the USA. Many genes are involved in the disease, but evidence suggests a major role for VSX1 in the etiology of KC. This study aimed to determine the frequency of mutations in exons 2, 3 and 4 of the VSX1 gene in Chaharmahal va Bakhtiari province in the southwest of Iran. STUDY DESIGN: In this experimental study, mutations in 3 exons, namely exons 2, 3 and 4, of VSX1 were investigated in 50 patients with KC and 50 healthy control subjects. DNA was extracted using a standard phenol-chloroform method. PCR-single-strand conformational polymorphism/heteroduplex analysis was performed, followed by DNA sequencing to confirm the identified motility shifts. RESULTS: H244R mutations were found in 1 patient and also in 1 healthy control subject. Furthermore, 12 polymorphisms were identified in patients with KC and 7 in healthy control subjects [rs6138482 and c.546A>G (rs12480307)]. CONCLUSION: Our investigation showed that KC-related VSX1 mutations were found in a very small proportion of the studied patients from Iran. Further investigations on other genes are needed to clarify their roles in KC pathogenesis.

Association between virulence factors of helicobacter pylori and gastric mucosal interleukin-18 mRNA expression in dyspeptic patients.

BACKGROUND: Helicobacter pylori (Hp) infection is associated with gastritis and marked infiltration of the gastric mucosa by several cytokines secreting inflammatory cells that contribute to sustain and expand the local inflammation. Different clinical expressions of the infection may reflect distinctive patterns of cytokine expression. IL-1ß, TNF-α, IL-17 and IL-23 have been reported to be involved in Hp-induced gastric mucosal inflammation, but the details and association to different patterns of inflammation and virulence factors remain unclear. METHODS: Total RNA was extracted from gastric biopsies of 51 Hp-infected patients and 44 Hp-negative patients. Mucosal IL-18 mRNA expression in gastric biopsies was determined by Real-Time PCR. Presence of virulence factors was evaluated using PCR. RESULTS: IL-18 mRNA expression was significantly increased in biopsies of Hp-infected patients compared to Hp-uninfected individuals. There was no association between virulence factors and IL-18 mRNA expression. Also severity of mononuclear infiltration was significantly higher in gastritis patients with vacA (m1)-positive compare patients with vacA (m2)-positive. CONCLUSIONS: IL-18 may play an important role in the inflammatory response and promote the chronic and persistent inflammatory changes in the stomach. This may ultimately influence the outcome of Hp-associated diseases that arise within the context of gastritis.