The effect of licorice and its active sweet component glycyrrhizin was tested on the growth and adherence to glass of the cariogenic Streptococcus mutans. Neither licorice nor glycyrrhizin promoted growth or induced plaque formation. In the presence of sucrose, glycyrrhizin did not affect bacterial growth, but the adherence (plaque formation) was markedly inhibited. At 0.5-1% glycyrrhizin, inhibition was almost complete. These results support our previous suggestions that glycyrrhizin might serve as an efficient vehicle for topical oral medications.
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http://dx.doi.org/10.1002/jps.2600740121 | DOI Listing |
iScience
January 2025
Department of Orthodontics, Tianjin Medical University School and Hospital of Stomatology & Tianjin Key Laboratory of Oral Soft and Hard Tissues Restoration and Regeneration, No.12 Qixiangtai Road, Heping District, Tianjin 300070, P.R. China.
Dental caries is a common disease resulting from tooth demineralization caused by bacterial plaque. Probiotics have shown great potential against caries by regulating the balance of oral flora. However, obstacles such as poor colonization and lysozyme sensitivity in oral cavity hinder their further application.
View Article and Find Full Text PDFJ Microsc Ultrastruct
December 2022
Department of Oral Pathology, D.Y. Patil Deemed to be University, D.Y. Patil School of Dentistry, Nerul, Navi Mumbai, Maharashtra, India.
Background: The term "peripheral fibro-osseous lesion (PFOL)" is used relatively for common gingival lesions characterized histologically by hypercellular connective tissue showing either new bone-like formations or cementum-like substance and rarely dystrophic calcifications. These lesions are closely related to the other fibro-osseous lesions such as cemental periapical dysplasia, fibrous dysplasia, and other calcifying odontogenic cysts and tumors. The etiology is unknown, but certain authors suggest plaque, dental calculus, and ill-fitting dentures which might be the irritating agents causing irritation to the periodontal ligament which leads to such reactive growth.
View Article and Find Full Text PDFAtherosclerosis
January 2025
State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Department of Cardiology of the Second Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang, China. Electronic address:
Background And Aims: Histologic studies indicated that healed plaque, characterized by a multilayered pattern, is indicative of prior atherothrombosis and subsequent healing. However, longitudinal in vivo data on healed plaque formation in non-culprit plaques are limited. This study aimed to investigate serial changes and clinical significance of new layered pattern formation in non-culprit plaques in patients with acute coronary syndromes (ACS) using serial optical coherence tomography (OCT) imaging.
View Article and Find Full Text PDFIn Vitro Cell Dev Biol Anim
January 2025
College of Traditional Chinese Medicine, Xinjiang Uygur Autonomous Region, Xinjiang Medical University, Urumqi, 830063, China.
The aim of this study is to assess the impact of Tianxiangdan (TXD) on lipophagy in foam cells and its underlying mechanism in treating atherosclerosis, particularly focusing on its efficacy in lowering blood lipids. In vivo, ApoE-/- atherosclerosis mouse models were established for group intervention. Blood lipid levels of the mice were measured, lipid deposition and autophagy levels in atherosclerotic plaques were assessed, and co-localization of lipid droplets and autophagosomes was examined.
View Article and Find Full Text PDFMetab Brain Dis
January 2025
Department of Neurology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, OR, 97239, USA.
Neuroinflammation and mitochondrial dysfunction are early events in Alzheimer's disease (AD) and contribute to neurodegeneration and cognitive impairment. Evidence suggests that the inflammatory axis mediated by macrophage migration inhibitory factor (MIF) binding to its receptor, CD74, plays an important role in many central nervous system (CNS) disorders such as AD. Our group has developed DRhQ, a novel CD74 binding construct which competitively inhibits MIF binding, blocks macrophage activation and migration into the CNS, enhances anti-inflammatory microglia cell numbers and reduces pro-inflammatory gene expression.
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