Effect Of Benzydamine Research Articles

Effects of benzydamine and mouthwashes containing benzydamine on Candida albicans adhesion, biofilm formation, regrowth, and persistence

ObjectivesTo assess the effects of benzydamine and mouthwashes (MoWs) containing benzydamine on different stages of Candida albicans biofilm: adhesion, formation, persistence, and regrowth (if perturbed).Materials and methodsC. albicans CA1398, carrying the bioluminescence ACT1p-gLUC59 fusion product, was employed. Fungal cells were exposed for 1′, 5′, or 15′ to 4 different benzydamine concentrations (0.075 to 0.6%) to 2 mouthwashes (MoWs) containing benzydamine and to a placebo MoW (without benzydamine). Treated cells were tested for adhesion (90 min) and biofilm formation (24-h assay). Next, 24- and 48-h-old biofilms were exposed to benzydamine and MoWs to assess regrowth and persistence, respectively. The effects of benzydamine, MoWs containing benzydamine, and placebo on different biofilm stages were quantified by bioluminescence assay and by the production of quorum sensing (QS) molecules.ResultsBenzydamine and MoWs containing benzydamine impaired C. albicans ability to adhere and form biofilm, counteracted C. albicans persistence and regrowth, and impaired a 48-h-old biofilm. Some of these effects paralleled with alterations in QS molecule secretion.ConclusionsOur results show for the first time that benzydamine and MoWs containing benzydamine impair C. albicans capacity to form biofilm and counteract biofilm persistence and regrowth.Clinical relevanceBenzydamine and MoWs containing benzydamine capacity to affect C. albicans biofilm provides an interesting tool to prevent and treat oral candidiasis. Likely, restraining C. albicans colonization through daily oral hygiene may counteract colonization and persistence by other critical oral pathogens, such as Streptococcus mutans, whose increased virulence has been linked to the presence of C. albicans biofilm.

Effects of Benzydamine and Lidocaine on Cardiovascular and Respiratory Responses to Extubation

Effects of Benzydamine and Lidocaine on Cardiovascular and Respiratory Responses to Extubation

Recreational use of benzydamine as a hallucinogen among street youth in Brazil

To describe the recreational use of benzydamine, an anti-inflammatory drug, among street youth in Brazil. a descriptive, cross sectional survey. 93 welfare services for the street youth in 27 Brazilian capitals. 2807 street youth, 10 to 18 years old. demographic characteristics, drug use pattern (lifetime use, use in the past 30 days, frequency, and characteristics of use in the past month) and effects of benzydamine through the use of a questionnaire. 78 reported lifetime recreational benzydamine use (67 cases identified only in three capitals). Among the 30 respondents reporting drug use in the last month (the month preceding the survey), 66.7% (n = 20) used the drug on 4 or more days (in the month preceding the survey). The most frequently (50%) pleasure effects reported were hallucination and nonspecific sensory changes described as 'trips'. Unwanted effects were reported by 75% of respondents, they were especially nausea and vomiting (21.4%). In the majority of the cases, drug was obtained from drugstores without a medical prescription. This study identifies the recreational use of benzydamine among street youth, mainly in the Northeast of Brazil, and also indicates the need for special controls on the dispensation of this substance.

Effects of benzydamine on mouse muscle type nicotinic acetylcholine receptors expressed in xenopus oocytes

Effects of benzydamine on mouse muscle type nicotinic acetylcholine receptors expressed in xenopus oocytes

Effect of benzydamine, a topically administered NSAID onin vitro prostanoid synthesis by human and rat gastric mucosa and rat kidney, aorta and urinary bladder: Lack of effect on cyclooxygenase but potent inhibition of receptor-linked prostanoid synthesis

Orally administered NSAIDs are notorious for their frequent and severe side-effects in the gastrointestinal tract and kidney, whereas topically administered NSAIDs may avoid these untoward effects. Since NSAID-induced side-effects are largely prostaglandin (PG)-mediated, the effects of the topically administered NSAID, benzydamine, onin vitro PGI2 and PGE2 synthesis by the rat and human gastric mucosa and rat kidney slices was investigated. The effect on receptor-linked PG synthesis in the isolated rat aorta (adrenergic) and urinary bladder (cholinergic) was also investigated since NSAIDs may disrupt mobilization of calcium therein. Benzydamine was a very weak inhibitor of spontaneous PGI2 and PGE2 synthesis by human and rat gastric mucosa and rat kidney. In contrast, benzydamine was a potent inhibitor of noradrenaline- and carbachol-stimulated (but not arachidonate- or trauma-stimulated) PGI2 synthesis. It is concluded that: a) benzydamine is unlikely to elicit cyclooxygenase-mediated side-effects on the gastrointestinal tract or kidney, b) the anti-inflammatory action of benzydamine is mediated by disruption of calcium linked to receptor-PG synthesis coupling, and c) calcium-dependent inflammatory processes may also be affected by benzydamine.

Effect of benzydamine on exocytosis and respiratory burst in human neutrophils and mononuclear phagocytes.

The effect of benzydamine on stimulus-dependent respiratory burst activity and enzyme release was tested in human neutrophils, monocytes and monocyte-derived macrophages. Established anti-inflammatory compounds, indomethacin, phenylbutazone and bufexamac, were tested for comparison. Care was taken to avoid cytotoxic or cytolytic concentrations of the test compounds, and their effect on release of lactate dehydrogenase was also tested. Release of specific and azurophil granules contents were induced in human neutrophils by A23187, PMA and fMLP with and without cytochalasin B pretreatment. Benzydamine inhibited stimulus-dependent release of vitamin B12-binding proteins, a marker for the specific granules, in a concentration-dependent fashion. By contrast, phenylbutazone and bufexamac were practically inactive. The effect of benzydamine on exocytosis of azurophil granules was tested in cytochalasin B-pretreated neutrophils. Benzydamine, again in contrast to the two reference anti-inflammatory compounds, inhibited release concentration-dependently also under these conditions. The concentration of the compound which inhibited exocytosis by 50% was 30-100 microM in normal and 3-10 microM in cytochalasin B-treated neutrophils. The effect of benzydamine and reference compounds on the respiratory burst was tested by assaying for superoxide formation in neutrophils and H2O2 formation in mononuclear phagocytes. Benzydamine was inactive on neutrophils and inhibited slightly the burst response of monocytes and macrophages. Two reference compounds, bufexamac and phenylbutazone, were generally more active. The strongest inhibitory effect was that of phenylbutazone on fMLP-stimulated cells. Benzydamine lacked activity under these conditions, indicating that it does not bind to the receptor of formylated chemotactic peptides.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of benzydamine on the lipolytic system of fat cells

Benzydamine dose-dependently increased cyclic 3',5'-AMP levels in isolated fat cells and competitively inhibited phosphodiesterase activity ( K i = 1.1 mM). ATP levels of isolated cells and cyclic 3',5'-AMP-dependent protein kinase activity were not affected. However, benzydamine caused a dose-dependent inhibition of lipolysis in isolated fat cells stimulated by norepinephrine or dibutyryl cyclic 3',5'-AMP. The enhancement of cyclic 3',5'-AMP formation may be due to the local anaesthetic properties of benzydamine. The antilipolytic effect appears to result from the direct inhibition of hormone sensitive triglyceride lipase.

Effects of benzydamine on experimental gastric ulcers produced by indomethacin and reserpine

Experiments conducted in rats confirm that benzydamine does not produce gastric lesions. Moreover, the drug statistically inhibits indomethacin and reserpine-induced ulcers. This provides further evidence for the dissociability of antinflammatory and ulcerogenic properties in a non-steroidal antinflammatory agent.

Effects of ulcerogenic and antiulcer drugs on gastric secretion in rats

Summary Effects of benzydamine, proxazole, banthine, indomethacin and reserpine on gastric secretion in rats are reported. Among the tested compounds displaying anti-ulcer activity, benzydam i ne depressed acid secretion and increased mucin production; pr o xazole selectively increased mucin production; banthine exerted a non specific inhibition on gastric secretion. Among compounds displaying ulcerogenic effects indomethacin did not affect gastric secretion, whereas reserpine increased acid secretion. On the basis of the results obtained, the mechanisms of antiulcer and ulcerogenic effects are discussed.