Novel zinc oxide nanoparticles of Teucrium polium suppress the malignant progression of gastric cancer cells through modulating apoptotic signaling pathways and epithelial to mesenchymal transition.

Management of gastric cancer is still challenging due to resistance to current chemotherapeutics and recurrent disease. Moreover, green- synthesized zinc oxide nanoparticles (ZnO-NPs) using natural resources are one of the most promising therapeutic agents for anticancer therapy. Here we report the facile green synthesis and characterization of ZnO-NPs from Teucrium polium (TP-ZnO-NP) herb extract and the anticancer activities of these nanoparticles on gastric cancer cells. Facile green synthesis of TP-ZnO-NP was achieved using zinc acetate dihydrate. For the characterization of TP-ZnO-NP, UV-vis spectroscopy, FTIR, SEM, XRD and EDX analyses were performed. Antiproliferative and anticancer activities of TP-ZnO-NP were explored using the HGC-27 gastric cancer cell line model. MTT cell viability and colony formation assays were used for the analysis of cell proliferation and migration. Wound healing assay was used to analyze the migration capacities of cells. Annexin V/PI double staining, DNA ladder assay, and Acridine orange/Ethidium bromide staining were performed to analyze the induction of apoptosis. qPCR was used to determine gene expression levels of apoptotic and epithelial to mesenchymal transition marker genes. The aqueous extract of TP served as both a reducing and capping agent for the successful biosynthesis of zinc oxide nanoparticles. Remarkably, synthesized TP-ZnO-NPs were found to have significant antiproliferative and anticancer activities on HGC-27 gastric cancer cells. Collectively, current data suggest that TP-ZnO-NP is a novel and promising anticancer agent for future therapeutic interventions in gastric cancer.

Cinnamic acid decreases periodontal inflammation and alveolar bone loss in experimental periodontitis.

BACKGROUND AND OBJECTIVE: Periodontitis is the chronic destructive disease of the periodontium, which causes severe inflammation in the tissues. Cinnamic acid as an unsaturated carboxylic acid might prevent inflammation and periodontal destruction. The present study aimed to evaluate the effects of cinnamic acid in two different forms as free cinnamic acid and cinnamic acid liposome on experimental periodontitis in Wistar rats. METHODS: Thirty-two female rats were used in the present study. Four main groups were created as follows: C: control group; P: periodontitis group; C-P: free cinnamic acid-administered periodontitis group; and CL-P: cinnamic acid liposome applied group. Periodontitis was induced via ligating 4-0 silk sutures around lower first molar teeth on both right and left mandibles. The study duration was 30 days, and the ligatures were removed from half of the rats in the periodontitis-induced groups. The other half carried the ligatures throughout 30 days, and all rats were euthanized at 30th day. Mandibles were removed and evaluated via stereomicroscope and underwent histological procedures. Inflammatory cell counts, osteoblast, and osteoclast cell counts were determined in hematoxylin-eosin-stained slides, and peroxisome proliferator-activated receptor (PPAR)-γ, cyclooxygenase (COX)-2, receptor activator of nuclear factor κ-B (RANKL), and osteoprotegerin (OPG) expressions were evaluated by immunohistochemistry. RESULTS: Control group had the lowest bone loss, and periodontitis group which kept ligatures had the highest bone loss compared to the other groups. Ligature removal provided significant improvement in bone measurements. Cinnamic acid groups also showed lower bone loss compared to the periodontitis group. The inflammatory cell and osteoclast counts were also higher in the periodontitis group, and both applications of cinnamic acid decreased these values. Osteoblast cells were the lowest in the periodontitis group, and cinnamic acid increased these counts. PPAR-γ and COX-2 levels were higher in the periodontitis group, and cinnamic acid decreased these levels but not to a significant level except for the cinnamic acid liposome ligature removal group, which had significantly lower values in the PPAR-γ and COX-2. OPG levels were lower in the periodontitis group compared to the other groups. Cinnamic acid significantly decreased RANKL and increased OPG levels. CONCLUSION: Periodontitis caused increased inflammation and bone destruction accompanied by increased PPAR-γ, COX-2, and RANKL levels and osteoclast counts. Cinnamic acid decreased osteoclast counts and inflammation and increased osteoblast counts and OPG expression in the present animal model of periodontitis.