In vitro evaluation of the antimicrobial properties of terpinen-4-ol on apical periodontitis-associated bacteria.

Manuka oil and tea tree oil are essential oils with known antibacterial properties that are believed to be caused by one main component: terpinen-4-ol. Terpinen-4-ol has potent antibacterial activity against caries-related microorganisms. However, few studies have investigated the antimicrobial effects of terpinen-4-ol on bacteria in apical periodontitis. Thus, the objective of the present study was to evaluate the antibacterial and antibiofilm potential of terpinen-4-ol against Enterococcus faecalis, Porphyromonas gingivalis, Prevotella intermedia, and Fusobacterium nucleatum, which have all been detected in apical periodontitis. The minimum inhibitory and minimum bactericidal concentrations of terpinen-4-ol were determined to assess its activity against biofilms. The minimum inhibitory concentration of terpinen-4-ol was 0.25% against E. faecalis and F. nucleatum, 0.05% against P. gingivalis, and 0.1% against P. intermedia. The minimum bactericidal concentration of terpinen-4-ol was 1.0% against E. faecalis, 0.2% against P. gingivalis and P. intermedia, and 0.5% against F. nucleatum. In the biofilm evaluations, all terpinen-4-ol-treated bacteria had significant reductions in biofilm viability compared with controls in experiments assessing attachment inhibitory activity. Furthermore, structural alterations and decreased bacterial cell clumping were observed under scanning electron microscopy, and significantly decreased cell survival was noted using fluorescence microscopy. Together, these results suggest that terpinen-4-ol is a potential antibacterial agent with bactericidal properties, and can also act on established biofilms.

MiR-877-5p targets PDK-1 to promote aspirin-induced apoptosis in gastric mucosal cells.

This study aimed to investigate the role of miR-877-5p in aspirin-induced gastric mucosal injury. MiRNA microarray analysis was performed using paired gastric mucosal samples to find differentially expressed miRNAs. miR-877-5p was selected for subsequent analyses. Used as a model system, gastric epithelial cells (GES-1) were transfected with miR-877-5p mimic/inhibitor, then treated with aspirin. The expression of miR-877-5p in GES-1 cells was examined using quantitative real-time PCR (qRT-PCR). Flow cytometry analysis was used to detect cell apoptosis. Western blot assay was used to measure the protein levels of PDK1. The interaction between miR-877-5p and PDK1 was determined by luciferase reporter assay. The expression of miR-877-5p in gastric mucosal injury samples was higher than that in normal samples. Also, depletion of miR-877-5p reduced the apoptosis of GES-1 cells. Luciferase reporting assay confirmed that PDK1 was a target gene of miR-877-5p. PDK1 inhibited the apoptosis of GES-1 cells treated by aspirin. Moreover, this inhibitory effect was abrogated after PDK1 knockdown. Downregulation of miR-877-5p reduced the apoptosis by targeting PDK1 in GES-1 cells treated by aspirin, indicating that miR-877-5p may be a potential therapeutic target for gastric mucosal injury caused by aspirin.

The mechanism of miR-363-3p/DUSP10 signaling pathway involved in the gastric mucosal injury induced by clopidogrel.

Clopidogrel-induced gastric injury is an important clinical problem. However, the exact mechanism is still unclarified. Increasing evidence indicates that miRNAs may be involved in the pathogenesis of gastric mucosal injury. In this study, the aim was to investigate the role of miR-363-3p in the gastric mucosal injury caused by clopidogrel. MiRNA microarray analysis was performed using paired gastric mucosal in order to find differential expression of miRNAs. The levels of miR-363-3p were examined in gastric mucosal injury caused by clopidogrel. The GES-1 cells were used as a model system, miR-363-3p mimic/inhibitor was transfected into GES-1 cells, then GES-1 cells were treated with clopidogrel. The levels of miR-363-3p and DUSP10 were examined in GES-1 cells using quantitative real-time PCR (qRT-PCR). CCK-8 assay and flow cytometry analysis were used to detect cell proliferation and apoptosis, respectively. Western blot assay was used to measure the protein levels of DUSP10. The interaction between miR-363-3p and DUSP10 was determined by luciferase reporter assay. MiR-363-3p was selected as a differentially expressed miRNA. The expression of miR-363-3p in gastric mucosal injury caused by clopidogrel was higher than that in normal samples. Also, depletion of miR-363-3p increased the proliferation of GES-1 cells and reduced the apoptosis. Luciferase-reporting assay results confirmed that DUSP10 was one of the target genes of miR-363-3p. DUSP10 inhibited apoptosis in GES-1 cells treated by clopidogrel. Moreover, DUSP10 knockdown abrogated the inhibitory effects on apoptosis in GES-1 cells mediated by miR-363-3p inhibitor. Knockdown of miR-363-3p increased the proliferation and reduced the apoptosis by targeting DUSP10 in GES-1 cells treated by clopidogrel, indicating that miR-363-3p may be a potential therapeutic target for gastric mucosal injury caused by clopidogrel.