Plaque formation inhibition

Q46 may be used in the treatment of intestinal candidiasis Q47 inhibits plaque formation on teeth Q48 may cause brov/n staining of teeth... 

Chlorhexidine is an antiseptic mouthv/ash that inhibits plaque formation on the teeth. 

Zanamivir (2) is a potent competitive inhibitor of viral neuraminidase glycoprotein, which is essential in the infective cycle of both influenza A and B viruses. It inhibits a wide range of influenza A and B types in vitro as well as in vivo. The concentrations of inhibiting in vitro plaque formation of influenza A and B virus by 50% in Madin-Darby canine kidney (MDCK) cells were 0.004-0.014 p.mol/L in laboratory-passaged strains, and 0.002-16 p.mol/L in assays of clinical isolates. Due to its low bioavailability, it is delivered by inhalation via the Diskhaler , 10 mg twice daily, or intranasally 2-4 times daily for 5 days. After an intravenous dose of 1 -16 mg, the median elimination half-life was ti/2 = 7 h, the volume of distribution at steady state was Vdss = 16 L, and 90% of the dose was excreted unchanged in the urine. After intranasal and inhaled (dry powder) administration, maximum serum concentrations occurred within 2h and the terminal phase half-lives were 3.4 and 2.9 h, respectively. The bioavailabilities were 10 and 25%, respectively, and 20% after inhalation of zanamivir (2) by nebulizer. 

The rate of clearance of chlorhexidine from the mouth after one mouth rinse with 10 mL of a 0.2% aqueous solution follows approximately first-order kinetics, with a half-life of 60 minutes. This means that following application of a single rinse with a 0.2% chlorhexidine solution, the concentration of the compound exceeds the minimum inhibitory concentration (MIC) for oral streptococci (5 mg/mL) for almost 5 hours. The pronounced substantivity, along with the relative susceptibility of oral streptococci, may account for the great effectiveness of chlorhexidine in inhibiting supragingival plaque formation. 

NO also reduces endothelial adhesion of monocytes and leukocytes, key features of the early development of atheromatous plaques. This effect is due to the inhibitory effect of NO on the expression of adhesion molecules on the endothelial surface. In addition, NO may act as an antioxidant, blocking the oxidation of low-density lipoproteins and thus preventing or reducing the formation of foam cells in the vascular wall. Plaque formation is also affected by NO-dependent reduction in endothelial cell permeability to lipoproteins. The importance of eNOS in cardiovascular disease is supported by experiments showing increased atherosclerosis in animals deficient in eNOS by pharmacologic inhibition. Atherosclerosis risk factors, such as smoking, hyperlipidemia, diabetes, and hypertension, are associated with decreased endothelial NO production, and thus enhance atherogenesis. 

Von Itzstein and co-workers [91] have shown that the 4-amino-and 4-guanidino-Neu5Ac2en inhibit influenza strains A/Singapore/1/57 and B/Victoria/102/95 in MDCK cells with IC50 values (the concentration required to inhibit plaque formation in MDCK cells by 50%) of 1.5 mM and 0.065 mM (4-amino) and 0.014 mM and 0.005 mM (4-guanidino) respectively. These IC50 values, in particular for the... 

Pharmaceuticals currently in use to combat Alzheimer s disease are mainly acetylcholine esterase (ACE) inhibitors designed to slow down the removal of acetylcholine so that neurons keep active, however, they do not reverse plaque formation. The only other approach is to inhibit the activities of the secretases, in particular, to favour the formation of AP40 over AP42. 

Mechanism of action A number of mechanisms have been proposed to explain how probucoi lowers serum cholesterol, but its mechanism of action remains uncertain. Recently it has been found that probucoi inhibits the oxidation of cholesterol, resulting in the ingestion of the oxidized cholesterol-laden LDLs by macrophages (Figure 21.7). Loaded with cholesterol, these macrophages become foam cells that adhere to the vascular endothelium and are the basis for plaque formation. Thus prevention of the cholesterol oxidation reaction might slow the development of atherosclerosis. 

Especially the hybrid hamster strain Bio FiB (Bio Breeders Fitchburg, MA, USA) is more susceptible to dietary induced atherosclerosis than other strains (Kowala et al. 1991). Early atherosclerotic lesions can be induced within a 3-months-feeding of a cholesterol/butter-enriched diet. In these animals simvastin dose-dependently inhibited the development of hyperlipidemia and the plaque formation by cholesterol synthesis inhibition The histopathological examination of the aortas showed that the choles-terol/butter fed FiB hamster developed atherosclerotic lesions and functional changes in the aorta which are closely related to man (Schafer et al. 1999). 

Wyss-Coray T, Yan E, Lin AH, Lambris JD, Alexander JJ, Quigg RJ, Masliah E (2002) Prominent neurodegeneration and increased plaque formation in complement-inhibited Alzheimer s mice. Proc Natl Acad Sci USA 99 10837-10842. 

The oxidation of LDL cholesterol is now recognized as a key event in atherosclerosis. Macrophages take up oxidized LDL cholesterol more readily, and this contributes to plaque formation. Soy isoflavones have been reported to inhibit oxidation by macrophages. Clinical trials have reported that consumption of 56-57 mg/day of isoflavones causes a significant increase (8-15%) in the lag time for cholesterol oxidation, and consequently decreased levels of oxidized LDL cholesterol. ... 

Fish is the most important source of the n-3-PUFAs Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and populations consuming fish have lower heart rates. Other important parameters reported were lower blood pressure and higher HDL cholesterol. The strongest evidence for an effect of n-3-fatty acids on disease is the inverse relationship between diet, blood, and tissue levels and coronary heart disease. n-3-PUFAs prevent heart disease by preventing arrhythmias, generating prostanoids and leukotrienes with anti-inflammatory actions, and inhibiting synthesis of cytokines and mitogens that provoke inflammation and promote plaque formation. ... 

Benzoxonium is a quaternary ammonium compound with antibacterial, antiviral, and antimycotic activity. It can be used in topical disinfection, disinfection of surgical instruments, inhibition of plaque formation, and in veterinary products. 

Mouthwashes containing cetylpyridinium chloride have been shown to inhibit plaque formation, although efficacy is variable owing to limited published data. ... 

Friedman M, Harrari D, Rimer A, Stabholz A. Inhibition of plaque formation by a sustained release delivery system for cetylpyridi-nium chloride. Int J Pharm 1988 44 243-247. 

The cytotoxicity of distamycin derivatives was estimated on the basis of the morphological modifications induced in HeLa cell cultures, after incubation for 40 h in Hanks saline solution + 0.5 % lactalbumin hydrolysate + 5 % calf serum (HLS). Assay on vaccinia virus Cultures of HeLa cells (grown in HLS medium) or mouseembryo cells (grown in HLS medium plus 0.1 % yeastolate) infected with vaccinia virus (Strain WR/ATCC) were used. Preliminary assays were made according to Herrmann et al.° Subsequent studies were carried out by assessing the inhibition of plaque formation (ECP) as well as the inhibition of infectious virus production in test tube cultures treated with the compounds for 40 h after the absorption of the virus. 

Express the minimal antiviral inhibitory concentration as the IC50, or the concentration required to inhibit virus-induced CPE or plaque formation by 50%. IC50s are estimated from (semilogarithmic) graphic plots of the number of plaques (percentage of control) or percentage of CPE as a function of the concentration of the test compound. 

M. oleifera extracts inhibits plaque formation of anti-herpes simplex vims type 1 (HSV-1) more than 50% at 100 ag/ml in a plaque reduction assay (55). M. oleifera extracts are also effective against thymidine kinase-deficient HSV-1 and phosphonoacetate-resistant HSV-1 vims strains. The extract ofM. oleifera at a dose of 750 mg/kg body weight per day significantly delays the development of skin lesions, prolongs the mean survival times and reduces the mortality of HSV-1 infected mice. Compared to the synthetic compound acyclovir, M. oleifera extracts delay the development of skin lesions and has mean survival times as acyclovir. A polysaccharide from hot aqueous extract of mature pods (fruits) of M oleifera with a structural repeating unit [->4)-a-D-GlCp(l->] has immunoenhancing properties (76). 

Thus, atorvastatin may have effects on inflammatory endpoints independent of cholesterol lowering. Activity on serum amyloid P could result in the lowering of plaque formation and inhibition of complement activation. 

Inhibition of adenovirus 11 by methisazone> t ame as a surprise however, the virus dose used was extremely small and it was found, by other test methodsthat methlsazone did not affect plaque formation of adenoviruses 1, 2, and 5 These same methods did reveal that methlsazone produced considerable toxicity in HeLa cells, the type of cell used in the original study. It is possible that the antiviral action observed was due to a toxic reaction not readily observed in the test system used. 

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