Helicobacter pylori (H. pylori)
is a major cause of chronic gastritis, gastric ulcers and gastric cancer. Recent studies have identified that probiotics are beneficial to human health due, in part, to their anti-
H. pylori
activities. Therefore, the present study investigated the antagonistic and local immunoregulatory activities of seven commercial probiotic strains and explored their mechanisms of actions. The human gastric epithelial cell line-1 (GES-1) was used to assess the effects of probiotics on the adhesion ability of
H. pylori
. GES-1 cells were infected with
H. pylori
plus lipopolysaccharide (
HP-LPS
) or the drug-resistant
H. pylori
strain (
HP021
) in the presence or absence of live probiotics. Following this, the growth rate and the adhesion ability of GES-1 cells were detected using MTT and urease activity assay. Toll-like receptor 4 (TLR4), NFKB inhibitor-α (IκBα) and nuclear factor (NF)-κB levels were measured by western blot analysis. The amount of interleukin (IL)-8 in the cell culture medium was determined by ELISA. Amongst the seven probiotic strains studied, live
Lactobacillus acidophilus (L. acidophilus)
and
Lactobacillus bulgaricus (L. bulgaricus)
inhibited
H. pylori
adherence to GES-1 cells most significantly.
L. bulgaricus
inhibited IL-8 production by GES-1 cells through modulation of the TLR4/IκBα/NF-κB pathway. Therefore, the present results suggested that consumption of food containing
L. acidophilus
and
L. bulgaricus
may be used as an adjuvant therapy for
H. pylori
-associated gastritis.
Mouthrinse treatment alone or combined with periodontal treatment can, to some extent, reduce the prevalence of oral H. pylori and improve the eradication rate of gastric H. pylori.
With the rising global prevalence of antibiotic resistance, the eradication rate of Helicobacter pylori (HP) is continuing to decrease. Probiotics are beneficial to human health and may be an adjunct therapy to increase the eradication rate of HP, lower treatment-associated side effects, and reduce HP-associated gastric inflammation. However, inconsistent test results have prevented conclusions about the therapeutic prowess of probiotics for HP. The mechanisms of actions of probiotics include the production of substances that inhibit or kill HP or compete with HP for the adhesion site on gastric epithelial cells. Probiotics can also reduce the release of inflammatory factors by regulating the local immune response of the host. We searched the available literature for full-length articles focusing on the role of probiotics in HP management. This review presents the latest advances in this area.
MicroRNAs (miRNAs/miRs) are post-transcriptional regulators that serve important roles in osteoclastogenesis and bone metabolism; however, the roles of miRNAs have not been completely clarified. The present study aimed to investigate the effects of miR-100-5p on the mechanism of liver-bone endocrine metabolism. A miRNA microarray analysis was conducted to evaluate the miRNA expression profile during receptor activator of nuclear factor-κB ligand-stimulated osteoclastogenesis. Hematoxylin and eosin and tartrate-resistant acid phosphatase staining were performed to analyze the trabecular bone microstructure and osteoclast differentiation. The mRNA and protein expression levels were assessed by reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. The results revealed that in vitro osteoclast differentiation and in vivo bone resorption were suppressed by miR-100-5p overexpression. In vivo, a decrease in miR-100-5p and an increase in FGF21 were simultaneously observed in mice following ovariectomy (OVX). Bioinformatics analysis and experimental data confirmed that FGF21 was a direct target of miR-100-5p. Conversely, augmentation of miR-100-5p using a specific agomir in OVX-operated mice decreased the levels of FGF21 in the serum and liver, and prevented osteoclastogenesis and bone loss. The present study revealed that FGF21 may be a signal molecule associated with the mechanism of liver-bone endocrine metabolism and may be targeted by miR-100-5p. In addition, miR-100-5p may serve an important role in protecting against OVX-induced osteoporosis.
Background: Osteoporosis is a worldwide severe bone disease. This study aimed to evaluate the effect of polyphyllin VII on the genesis of osteoclasts from bone marrow macrophages (BMMs) and its potentiality as a therapeutic drug for osteoporosis.Methods: BMMs were induced to differentiate into osteoclasts by RANKL and M-CSF. The cells were then treated with various concentrations of polyphyllin VII. Intracellular reactive oxygen species (ROS) measurement assay, resorption pit formation assay, tartrate-resistant acid phosphatase (TRAP) staining and TRAP activity assessment, cell viability assay, active GTPase pull-down assay, immunofluorescent staining, immunoblotting, and RT-PCR were performed.Results: RANKL + M-CSF significantly increased TRAP activity, number of osteoclasts, number and area of lacunae, intracellular content of ROS, protein levels of Nox1, TRAF6, c-Src and p-PI3K, as well as the content of activated GTP-Rac1, which were significantly blocked by polyphyllin VII in a concentration-dependent manner.Conclusion: These findings suggested that polyphyllin VII inhibited differentiation of BMMs into osteoclasts through suppressing ROS synthesis, which was modulated by TRAF6-cSrc-PI3k signal transduction pathway including GTP-Rac1 and Nox1. Polyphyllin VII could be a therapeutic drug for osteoporosis.
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