Effects of Oleanolic Acid Derived from Wine Pomace on Periodontopathic Bacterial Growth in Healthy Individuals: A Randomized Placebo-Controlled Study.

Periodontal disease is caused by oral pathogenic bacteria and is associated with systemic disease and frailty. Therefore, its prevention is crucial in extending healthy life expectancy. This study aimed to evaluate the effect of orally administered oleanolic acid, extracted from wine pomace, on periodontopathic bacterial growth in healthy individuals. In this randomized, placebo-controlled, double-blind, parallel-group comparison study, 84 healthy adults were assigned to a placebo (n = 29), low-dose (n = 29, 9 mg oleanolic acid), or high-dose (n = 26, 27 mg oleanolic acid) groups. The number of oral bacteria in their saliva, collected before and 5 h after administration, was determined using the polymerase chain reaction-invader technique. The proportion of periodontopathic bacteria among the total oral bacteria in the saliva was calculated. Oleanolic acid significantly decreased the proportion of Porphyromonas gingivalis among the total oral bacteria in a dose-dependent manner (p = 0.005 (low-dose) and p = 0.003 (high-dose) vs. placebo, Williams' test). Moreover, high-dose oleanolic acid decreased the proportion of Tannerella forsythia (p = 0.064 vs. placebo, Williams' test). Periodontopathic bacteria are closely associated with the development and progression of periodontal disease; thus, the continuous daily intake of oleanolic acid derived from pomace may be helpful in maintaining a healthy oral microbiome by controlling the proportion of periodontopathic bacteria.

The Anti-Arthritis Effect of Olive-Derived Maslinic Acid in Mice is Due to its Promotion of Tissue Formation and its Anti-Inflammatory Effects.

SCOPE: A previous study demonstrated that intake of olive pomace extract containing maslinic acid (MA), a triterpene, effectively prevents and alleviates arthritis in animals and humans. Here, the molecular mechanisms involved in the anti-arthritis effect of MA have been elucidated by determining gene expression changes induced by olive-derived MA intake in collagen antibody-induced arthritis (CAIA) mice. METHODS AND RESULTS: Mice are divided into the untreated (CT), CAIA (CA), and CAIA administered MA (CA + MA) groups. The CA + MA mice are fed MA at a daily dose of 200 mg kg-1 of body weight from day 1. CAIA is then induced on day 8 and evaluated on day 12. Arthritis symptoms are alleviated, and the gene expression of inflammatory cytokines is reduced in the CA + MA group compared with the CA group. A DNA microarray analysis of synovial membranes reveals that MA alters the expression levels of genes related to inflammation, including glucocorticoid responses, immune responses, and the extracellular matrix. CONCLUSIONS: The preventive effect of MA on arthritis is attributable to the promotion of tissue formation as well as suppression of inflammation in the synovium via inactivation of Toll-like receptor signaling and downregulation of leukotrienes through the glucocorticoid receptor.

Ribosome biogenesis factors bind a nuclear envelope SUN domain protein to cluster yeast telomeres.

Two interacting ribosome biogenesis factors, Ebp2 and Rrs1, associate with Mps3, an essential inner nuclear membrane protein. Both are found in foci along the nuclear periphery, like Mps3, as well as in the nucleolus. Temperature-sensitive ebp2 and rrs1 mutations that compromise ribosome biogenesis displace the mutant proteins from the nuclear rim and lead to a distorted nuclear shape. Mps3 is known to contribute to the S-phase anchoring of telomeres through its interaction with the silent information regulator Sir4 and yKu. Intriguingly, we find that both Ebp2 and Rrs1 interact with the C-terminal domain of Sir4, and that conditional inactivation of either ebp2 or rrs1 interferes with both the clustering and silencing of yeast telomeres, while telomere tethering to the nuclear periphery remains intact. Importantly, expression of an Ebp2-Mps3 fusion protein in the ebp2 mutant suppresses the defect in telomere clustering, but not its defects in growth or ribosome biogenesis. Our results suggest that the ribosome biogenesis factors Ebp2 and Rrs1 cooperate with Mps3 to mediate telomere clustering, but not telomere tethering, by binding Sir4.