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General Dentistry 2019-Jan-Feb

Antimicrobial activity of noncytotoxic concentrations of Salvia officinalis extract against bacterial and fungal species from the oral cavity.

Ainult registreeritud kasutajad saavad artikleid tõlkida
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Link salvestatakse lõikelauale
Jonatas de Oliveira
Polyana Vilela
Rosilene Almeida
Felipe de Oliveira
Cláudio Carvalho
Samira Camargo
Antonio Jorge
Luciane de Oliveira

Märksõnad

Abstraktne

The use of medicinal plants can be an alternative method for the control of microorganisms responsible for human infections. This study evaluated the antimicrobial activity of Salvia officinalis Linnaeus (sage) extract on clinical samples isolated from the oral cavity and reference strains of Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus mutans, Candida albicans, Candida tropicalis, and Candida glabrata. In addition, testing assessed the cytotoxic effect of S officinalis on murine macrophages (RAW 264.7). Minimum inhibitory, minimum bactericidal, and minimum fungicidal concentrations of S officinalis extract were determined by broth microdilution method in 60 microbial samples. The cytotoxicity was checked by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The quantities of the proinflammatory cytokines interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) produced by RAW 264.7 were analyzed by an enzyme-linked immunosorbent assay. An S officinalis concentration of 50.0 mg/mL was effective against all microorganisms. Regarding cytotoxicity, the groups treated with 50.0-, 25.0-, and 12.5-mg/mL concentrations of S officinalis presented cell viability statistically similar to that of the control group, which was 100% viable. The production of IL-1β and TNF-α was inhibited at a 50.0-mg/mL concentration of S officinalis. Thus, S officinalis extract presented antimicrobial activity on all isolates of Staphylococcus spp, S mutans, and Candida spp. No cytotoxic effect was observed, as demonstrated by the survival of RAW 264.7 and inhibition of IL-1β and of TNF-α.

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