This study was conducted to examine the activity of alpha-mangostin against Candida albicans, the most important microorganism implicated in oral candidiasis. Its activity was compared to Clotrimazole and Nystatin. Results showed that alphamangostin was effective against C. albicans, the minimum inhibitory concentration (MIC) and minimum fungicidal concentration (MFC) were 1,000 and 2,000 µg/ml, respectively. The C. albicans killing activity of alpha-mangostin was more effective than Clotrimazole and Nystatin. The cytotoxicity of alphamangostin was determined and it was found that alphamangostin at 4,000 µg/ml was not toxic to human gingival fibroblast for 480 min. The strong antifungal activity and low toxicity of alpha-mangostin make it a promising agent for treatment of oral candidiasis. (J Oral Sci 51, [401][402][403][404][405][406] 2009)

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Background:Periodontitis, a chronic inflammatory disease, is the leading cause of tooth loss in adults. Evidence for the anti inflammatory activity of M. alba Stem Extract (MSE) in periodontal disease is limited.Objective:The study aimed to investigate the inhibitory effect of MSE on the growth of periodontopathic bacteria and expression of interleukin (IL)-6 and IL-8 in Porphyromonas gingivalis Lipopolysaccharide (LPS)-stimulated human Periodontal Ligament (hPDL) fibroblasts.Methods:The antimicrobial activities of MSE were tested against P. gingivalis and Aggregatibacter actinomycetemcomitans by the disk diffusion, the minimum inhibitory concentration and the minimal bactericidal concentration methods. Cytotoxicity of P. gingivalis LPS and MSE on hPDL fibroblasts was determined by MTS assay. The expression of cytokines (IL-6 and IL-8) mRNA and proteins in hPDL fibroblasts was measured using the reverse transcription-qPCR and enzyme-linked immunosorbent assay, respectively.Results: MSE exhibited antibacterial activities against P. gingivalis and A. actinomycetemcomitans with the zones of inhibition of 10.00 ± 0.33 mm and 17.33 ± 0.58 mm, respectively. MIC and MBC values for MSE against P. gingivalis were 62.5 μg/ml. The MIC and MBC values against A. actinomycetemcomitans were 250 μg/mL and 500 μg/ml, respectively. P. gingivalis LPS was shown to mediate the expression of pro-inflammatory cytokines in hPDL fibroblasts. However, treatment with MSE concentrations of 2.5 and 5.0 μg/ml significantly suppressed P. gingivalis LPS-induced IL-6 and IL-8 mRNA and protein expression (p< 0.05).Conclusion: The present study demonstrates that MSE has antibacterial activity against two putative periodontal pathogens. MSE suppressed IL-6 and IL-8 expression in P. gingivalis LPS-stimulated hPDL fibroblasts, indicating a possible anti-inflammatory effect. Thus, it is a potential adjunctive agent for the treatment of periodontitis.

Objectives The aim of this study is to evaluate the inhibitory effects of M. alba stem extract (MSE) on the expression of matrix metalloproteinases (MMP)-1, MMP-9, and tissue inhibitors of metalloproteinase (TIMP)-1 in Porphyromonas gingivalis lipopolysaccharide (LPS)-activated-acute monocytic leukemia cell line (THP-1). Materials and Methods THP-1 cells were treated with noncytotoxic concentrations of MSE combined with 1 µg/mL of P. gingivalis LPS. The mRNA levels of MMP-1, MMP-9, and TIMP-1 were evaluated via quantitative real-time polymerase chain reaction. The secreted proteins in the culture media were detected by enzyme-linked immunosorbent assay. The degradation of inhibitor of kappa B-alpha (IκBα) protein was tracked by Western blotting. Statistical Analysis Comparisons in experiments were analyzed with analysis of variance followed by Tukey honestly significant difference comparison test. ResultsTwenty and 40 µg/mL of MSE significantly downregulated MMP-1 and MMP-9 genes and protein expression but upregulated the gene expression of TIMP-1 (p < 0.05). P. gingivalis LPS induced degradation of IκBα, while addition of MSE (20 and 40 µg/mL) increased IκBα cytosolic levels. MSE was able to suppress the P. gingivalis LPS-induced MMPs expression and also increased the gene expression of TIMP-1 via the inhibition of the cytoplasmic IκBα degradation in THP-1 cells. Conclusions The present observations suggest that MSE exerted a positive effect on the regulatory mechanism between MMPs and TIMP, which is an important implication for the therapeutic potential of MSE in periodontitis.

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