Effect ofRumex Aquaticus HerbaExtract AgainstHelicobacter pylori-Induced Inflammation in Gastric Epithelial Cells (original) (raw)

Inhibition of Helicobacter pylori-induced inflammation in human gastric epithelial AGS cells by Phyllanthus urinaria extracts

Journal of Ethnopharmacology, 2008

Aim of the study: Helicobacter pylori is linked to a majority of peptic ulcers and to some types of gastric cancer, and its resistance to antibiotic treatment is now found worldwide. This study is aimed at evaluating the antimicrobial activity of Phyllanthus urinaria Linnea (Euphorbiaceae), chloroform (PUC) and methanol (PUM) extracts, and its eight isolates on H. pylori-infected human gastric epithelial AGS cells. Materials and methods: The in vitro anti-bacterial activity of P. urinaria chloroform (PUC) and methanol (PUM) extracts, and its eight isolates were determined. Additional experiments were also performed to know the PUC and PUM ability to inhibit the H. pylori adhesion to and invasion of AGS cells, in addition to the effect of PUC on NF-B activity as well as IL-8 synthesis during H. pylori infection of AGS cells. Results: The results revealed that crude extracts PUC and PUM showed potent antimicrobial activity against H. pylori than pure isolates. On the other hand, in vitro H. pylori-infection model revealed that the inhibition of bacterial adhesion and invasion to AGS cells has dramatically reduced by treatment of extract PUC, while PUM has the same moderate effect. Furthermore, H. pylori-induced nuclear factor (NF)-B activation, and the subsequent release of interleukin (IL)-8 in AGS cells were also inhibited by the extract PUC. Conclusions: These results open the possibility of considering P. urinaria a chemopreventive agent for peptic ulcer or gastric cancer, but this bioactivity should be confirmed in vivo in the future.

Anti-inflammatory and cytoprotective effects of selected Pakistani medicinal plants in< i> Helicobacter pylori-infected gastric epithelial cells

2012

Ethnopharmacological relevance: Helicobacter pylori infection is associated with gastritis, peptic ulcer, and gastric cancer. Due to its high global prevalence and uprising resistance to available antibiotics, efforts are now directed to identify alternative source to treat and prevent associated disorders. In the present study, effect of selected indigenous medicinal plants of Pakistan was evaluated on the secretion of interleukin-8 (IL-8) and generation of reactive oxygen species (ROS) in a bid to rationalize their medicinal use and to examine the anti-inflammatory and cytoprotective effects in gastric epithelial cells. Materials and methods: AGS cells and clinically isolated Helicobacter pylori strain (193C) were employed for co-culture experiments. Anti-Helicobacter pylori activity and cytotoxic effects of the selected plants were determined by serial dilution method and DNA fragmentation assay respectively. ELISA and flow cytometry were performed to evaluate the effect on IL-8 secretion and ROS generation in Helicobacter pylori-infected cells. Results: At 100 g/ml, extracts of Alpinia galangal, Cinnamomum cassia, Cinnamomum tamala, Mentha arvensis, Myrtus communis, Oligochaeta ramose, Polygonum bistorta, Rosa damascena, Ruta graveolens, Syzygium aromaticum, Tamarix dioica, and Terminalia chebula exhibited strong inhibitory activity against IL-8 secretion. Of these, four extracts of Cinnamomum cassia, Myrtus communis, Syzygium aromaticum, and Terminalia chebula markedly inhibited IL-8 secretion at both 50 and 100 g/ml. Cinnamomum cassia was further assessed at different concentrations against Helicobacter pylori and TNF-␣ stimulated IL-8 secretion, which displayed significant suppression of IL-8 in a concentration-dependent-manner. Among the plants examined against ROS generation, Achillea millefolium, Berberis aristata, Coriandrum sativum, Foeniculum vulgare, Matricaria chamomilla and Prunus domestica demonstrated significant suppression of ROS from Helicobacter pylori-infected cells (p < 0.01). Conclusion: Results of the study revealed anti-inflammatory and cytoprotective effects of selected medicinal plants which could partially validate the traditional use of these plants in GI disorders particularly associated with Helicobacter pylori. Furthermore, results obtained may lead to possible future candidates of chemoprevention against peptic ulcer or gastric cancer.

Anti-inflammatory and cytoprotective effects of selected Pakistani medicinal plants in Helicobacter pylori-infected gastric epithelial cells

Journal of Ethnopharmacology, 2012

Ethnopharmacological relevance: Helicobacter pylori infection is associated with gastritis, peptic ulcer, and gastric cancer. Due to its high global prevalence and uprising resistance to available antibiotics, efforts are now directed to identify alternative source to treat and prevent associated disorders. In the present study, effect of selected indigenous medicinal plants of Pakistan was evaluated on the secretion of interleukin-8 (IL-8) and generation of reactive oxygen species (ROS) in a bid to rationalize their medicinal use and to examine the anti-inflammatory and cytoprotective effects in gastric epithelial cells. Materials and methods: AGS cells and clinically isolated Helicobacter pylori strain (193C) were employed for co-culture experiments. Anti-Helicobacter pylori activity and cytotoxic effects of the selected plants were determined by serial dilution method and DNA fragmentation assay respectively. ELISA and flow cytometry were performed to evaluate the effect on IL-8 secretion and ROS generation in Helicobacter pylori-infected cells. Results: At 100 g/ml, extracts of Alpinia galangal, Cinnamomum cassia, Cinnamomum tamala, Mentha arvensis, Myrtus communis, Oligochaeta ramose, Polygonum bistorta, Rosa damascena, Ruta graveolens, Syzygium aromaticum, Tamarix dioica, and Terminalia chebula exhibited strong inhibitory activity against IL-8 secretion. Of these, four extracts of Cinnamomum cassia, Myrtus communis, Syzygium aromaticum, and Terminalia chebula markedly inhibited IL-8 secretion at both 50 and 100 g/ml. Cinnamomum cassia was further assessed at different concentrations against Helicobacter pylori and TNF-␣ stimulated IL-8 secretion, which displayed significant suppression of IL-8 in a concentration-dependent-manner. Among the plants examined against ROS generation, Achillea millefolium, Berberis aristata, Coriandrum sativum, Foeniculum vulgare, Matricaria chamomilla and Prunus domestica demonstrated significant suppression of ROS from Helicobacter pylori-infected cells (p < 0.01). Conclusion: Results of the study revealed anti-inflammatory and cytoprotective effects of selected medicinal plants which could partially validate the traditional use of these plants in GI disorders particularly associated with Helicobacter pylori. Furthermore, results obtained may lead to possible future candidates of chemoprevention against peptic ulcer or gastric cancer.

Anti-Helicobacter pylori activity and inhibition of Helicobacter pylori-induced release of IL-8 in AGS cells by plant extracts

Journal of Medicinal Plants Research, 2013

Plants used in popular diet were studied for anti-Helicobacter pylori activity and their effect on the expression of interleukin-8 (IL-8) from H. pylori infected gastric epithelial cells. Extracts were prepared of Allium sativum (A. sativum), Cuminum cyminum (C. cyminum), Piper nigrum (P. nigrum) and their mix in two different dilutions. AGS cell line and H. pylori strains were used for co-culture experiments. Extracts bactericidal activity was determined by a viable colony count. ELISA (Enzyme linked immunosorbent assay) was used to determine IL-8 expression. DNA extracted from bacterial cells was used for polymerase chain reaction (PCR) of cytotoxin-associated gene (cagA) and E (cagE). Results revealed H. pylori strains sensitivity to A. sativum (5.5 mg/ml) was 57% (39/69) (p=0.06), and to 11 mg/ml was 65% (45/69) (p=0.02) compared to amoxicillin, respectively. CagE positive H. pylori, 37% (11/30) (p=0.02) were sensitive to plant mixture (23.5 mg/ml), 60% (18/30) (p<0.001) to plant mix (47 mg/ml), respectively. The expression of IL-8 by AGS cells treated with plant mix, (P=0.0037), C. cyminum (P<0.0001), P. nigrum (P=0.0046) and A. sativum (P=0.0021), respectively compared to positive and negative controls. Thus, dietary plants demonstrated an anti-H. pylori effect. They reduced IL-8 expression from the H. pylori infected AGS cells.

In Vitro anti-Helicobacter pylori and urease inhibitory effects of polyphenolic extracts of local herbs from Algeria

Background: Gastritis and peptic ulcers are considered as major health problems worldwide with more than 80% of chronic active gastritis are due to the pathogenic bacterium H.pylori. Due to the emergence of antibiotic resistance among clinical strains of H. pylori, alternative approaches are increasingly needed. Methods: Methanolic extracts of Algerian originated Mentha rotundifolia, Eucalyptus globulus, Malva sylvestris, Inula viscosa, Achille aodorata and Utrica dioica and their contents of phenolics and flavonoids were evaluated for the in vitro antimicrobial activity against H. pylori , in addition to its associated urease inhibition. The minimum inhibitory concentrations (MICs) of these extracts was performed using control strain of H. pylori and standard agar diffusion method. Results: The highest phenolic and flavonoid contents were found in M.rotundifolia and E.globulus, while M.sylvestris showed the least phenolic contents. In addition, polyphenolic fractions exhibited anti-H. pylori activity of all of the herbal extracts with highest activity for E.globulus (MIC 0.094mg/ml), I.viscosa, (0.375mg/ml) andU.dioica (0.75 mg/ml), low antimicrobial activity was revealed for A. odorata,M. rotundifolia and Malva sylvestris, respectively (MIC >1mg/ml). For the urease activity, all extracts showed inhibitory effect at concentration of 250mg/ml. However, the range of the urease inhibitory concentrations varied significantly among the extracts with highest activity and widest range found for E.globulus (70-90% at concentrations 8-125 mg/ml).

In vitro anti-inflammatory effect of apigenin in the Helicobacter pylori-infected gastric adenocarcinoma cells

Food and Chemical Toxicology, 2013

Infection with Helicobacter pylori causes extensive gastric epithelial cell inflammation which may progress to atrophic gastritis, intestinal metaplasia, and even gastric adenocarcinoma. Apigenin (4 0 ,5,7-Trihydroxyflavone) is widely distributed in fruits and vegetables, and is a well-known antiinflammatory supplement with low cytotoxicity. In this study, we investigated the anti-inflammatory effects of apigenin in H. pylori-infected MKN45 cells, for which IjBa, cyclooxygenase-2 (COX-2), intercellular adhesion molecule-1 (ICAM-1), reactive oxygen species (ROS), interleukin-8 (IL-8), IL-6, IL-1b, and mucin-2 (MUC-2) expressions were examined. Apigenin treatments (9.3-74 lM) significantly increased the IjBa expression, and thus inhibited nuclear factor kappa B (NF-jB) activation, and the inflammatory factor (COX-2, ICAM-1, ROS, IL-6, and IL-8) expressions decreased. The ROS levels decreased partially based on the intrinsic scavenging property of apigenin. In summary, apigenin treatments effectively inhibited NF-jB activation and the related inflammatory factor expressions, as well as increased MUC-2 expression in the H. pylori-infected MKN45 cells. The compound shows great potential as a candidate agent for the inhibition of H. pylori-induced extensive gastric epithelial cell inflammation.

In vitro susceptibility of Helicobacter pylori to urease inhibitory effects of polyphenolic extracts of local herbs from Algeria

Background: Gastritis and peptic ulcers are considered as major health problems worldwide with more than 80% of chronic active gastritis are due to the pathogenic bacterium H.pylori. Due to the emergence of antibiotic resistance among clinical strains of H. pylori, alternative approaches are increasingly needed. Methods: Methanolic extracts of Algerian originated Mentha rotundifolia, Eucalyptus globulus, Malva sylvestris, Inula viscosa, Achille aodorata and Utrica dioica and their contents of phenolics and flavonoids were evaluated for the in vitro antimicrobial activity against H. pylori , in addition to its associated urease inhibition. The minimum inhibitory concentrations (MICs) of these extracts was performed using control strain of H. pylori and standard agar diffusion method. Results: The highest phenolic and flavonoid contents were found in M.rotundifolia and E.globulus, while M.sylvestris showed the least phenolic contents. In addition, polyphenolic fractions exhibited anti...

Effect of methanolic extract of Terminalia arjuna against Helicobacter pylori 26695 lipopolysaccharide-induced gastric ulcer in rats

Journal of Pharmacy and Pharmacology, 2008

Helicobacter pylori lipopolysaccharide (HP-LPS) is a potent virulence factor in the causation of gastric ulcer and gastritis. H. pylori-induced gastric pathology is prevalent throughout the world. Herbal medicines are attracting attention because of their traditional values, popularity and belief, as well as for their advantages such as less toxicity, affordability and medicinal value. The present study aimed to evaluate the anti-ulcer effect of a methanolic extract of Terminalia arjuna (TA) against HP-LPS-induced gastric damage in rats. Ulcers were induced with HP-LPS (50 mg per animal) administered orally daily for 3 days. The efficacy of TA on gastric secretory parameters such as volume of gastric juice, pH, free and total acidity, pepsin concentration, and the cytoprotective parameters such as protein-bound carbohydrate complexes in gastric juice and gastric mucosa was assessed. The protective effect of TA was also confirmed by histopathological examination of gastric mucosa. HP-LPS-induced alterations in gastric secretory parameters were altered favourably in rats treated with TA, suggesting that TA has an anti-secretory role. Furthermore, HP-LPS-induced impairments in gastric defence factors were also prevented by treatment with TA. These results suggest that the severe cellular damage and pathological changes caused by HP-LPS are mitigated by TA; these effects are comparable with those of sucralfate. The anti-ulcer effect of TA may reflect its ability to combat factors that damage the gastric mucosa, and to protect the mucosal defensive factors. Helicobacter pylori was first isolated in human biopsies by Warren and Marshall in 1983, and is now considered to be a major cause of gastric ulcers, duodenal ulcers and gastritis. H. pylori infection is also reported to be an important cause of ulcer relapse (Parmar & Desai 1994). Approximately 40% and 80% of individuals in developed and developing countries, respectively, are infected before adulthood, making H. pylori one of the most common bacterial infections in humans (Mitchell 1993). The factors implicated in the virulent actions of H. pylori against mucosal integrity include CagA and VacA cytotoxins, which are capable of inducing the release of pro-inflammatory cytokines, excessive production of ammonia, known for its strong toxic effect on the gastric epithelium, and the impairment of feedback inhibition of gastrin release by somatostatin (Piotrowski et al 1995; Konturek et al 1999). Cell wall lipopolysaccharide (LPS) of H. pylori is also involved in its virulent actions (Slomiany et al 1997, 2000). H. pylori LPS (HP-LPS) elicits acute mucosal inflammatory responses within 2 days, accompanied by a massive epithelial cell apoptosis, increase in mucosal expression of endothelin-1, stimulation of tumour necrosis factor a, increase in nitric oxide (NO) synthase (NOS)-2, decrease in constitutive NOS (cNOS) activity (Slomiany et al 2000), excessive nitric oxide generation, apoptotic caspase activation and a marked enhancement in gastric epithelial cell apoptosis (Slomiany et al 1997, 1998a, 1998b, 1999). Other pathogenic effects of HP-LPS relevant to the progression of the mucosal inflammatory process involve stimulation of nuclear factor (NF)-kB nuclear translocation, disturbances in mitogen-activated protein kinase cascades, and a marked up-regulation in gastric mucosal level of endothelin-1 (Slomiany et al 1999; Gupta et al 2001a; Slomiany & Slomiany 2001).