Effectiveness of mentha extracts against oral microorganisms: an in vitro study / 대한구강보건학회지

Objectives@#Dental caries and periodontal disease are infectious and chronic diseases. The aim of the study was to investigate the antimicrobial effect of mentha extracts against Streptococcus mutans (S. mutans ) and Porphyromonas gingivalis (P. gingivalis ). @*Methods@#This activity of mentha extracts were confirmed by the disk diffusion test and minimum inhibitory concentration (MIC), minimum bactericidal concentration (MBC) and colony forming unit (CFU) assays. @*Results@#S. mutans and P. gingivalis showed the highest antimicrobial activity within the inhibition zones. The antimicrobial activity was interrupted as the MIC and MBC of the herbal extracts against the two bacteria were 1 mg/ml and 10 mg/ml, respectively. The antimicrobial effect was determined by the CFU assay. @*Conclusions@#Mentha herb extract demonstrated potential antimicrobial activity against S. mutans and P. gingivalis that cause dental caries and periodontal disease.

Effect of apoptosis on G361 cells by Cimicifuga rhizoma extract / 대한구강보건학회지

OBJECTIVES: To investigate whether the cytotoxic effect of Cimicifuga rhizoma extract is associated with cell death in the human keratinocyte (HaCaT) and human melanoma cell lines (G361). METHODS: Apoptosis induced by Cimicifuga rhizoma extract was confirmed by water-soluble tetrazolium salts-1 (WST-1) assay, immunocytochemistry, and western blot. Additionally, the release of cytochrome c and apoptosis-inducing factor (AIF) was visualized by confocal laser scanning microscopy. RESULTS: The results showed that Cimicifuga rhizoma extract significantly reduced the viability of G361 cells with half-maximal inhibitory concentration (IC 50) of 200 µg/ml, and the apoptotic process was found to occur via the activation of caspase-3 and caspase-9 pathways. Besides, the release of cytochrome c and AIF was also detected. CONCLUSIONS: This study suggests that Cimicifuga rhizoma extract causes apoptosis of human melanoma cells through the intrinsic apoptotic pathway.

Induction of Melanoma Cell-Selective Apoptosis Using Anti-HER2 Antibody-Conjugated Gold Nanoparticles

PURPOSE: This study was conducted to verify the induction and mechanism of selective apoptosis in G361 melanoma cells using anti-HER2 antibody-conjugated gold nanoparticles (GNP-HER2). MATERIALS AND METHODS: Following GNP-HER2 treatment of G361 cells, cell cycle arrest and apoptosis were measured by WST-1 assay, Hemacolor staining, Hoechst staining, immunofluorescence staining, fluorescence-activated cell sorting analysis, and Western blotting.

Antimicrobial Effect of Low Temperature Atmospheric Plasma against Oral Pathogens

The purpose of this study was to investigate the antibacterial effect of the low temperature atmospheric plasma device with needle tip designed for easy approach to the oral cavity and root canal against Streptococcus mutans, Enterococcus faecalis and Candida albicans. The antibacterial activities evaluated by measuring clear zone of agar plate smeared with each bacteria after plasma treatment. To quantify antibacterial effects, dilution plate method was used. In addition, scanning electron microscope (SEM) was used for observation of changes in bacterial morphology. As treatment time of plasma increased, the clear zone was enlarged. The death rate was more than 99%. The SEM results showed that the globular shape of bacteria was distorted. These results suggest that needle tip plasma could be an innovative device for prevention of dental caries, and treatment of apical infection and soft tissue diseases.

S Phase Cell Cycle Arrest and Apoptosis is Induced by Eugenol in G361 Human Melanoma Cells

Eugenol is an essential oil found in cloves and cinnamon that is used widely in perfumes. However, the significant anesthetic and sedative effects of this compound have led to its use also in dental procedures. Recently, it was reported that eugenol induces apoptosis in several cancer cell types but the mechanism underlying this effect has remained unknown. In our current study, we examined whether the cytotoxic effects of eugenol upon human melanoma G361 cells are associated with cell cycle arrest and apoptosis using a range of methods including an XTT assay, Hoechst staining, immunocytochemistry, western blotting and flow cytometry. Eugenol treatment was found to decrease the viability of the G361 cells in both a time- and dose-dependent manner. The induction of apoptosis in eugenol-treated G361 cells was confirmed by the appearance of nuclear condensation, the release of both cytochrome c and AIF into the cytosol, the cleavage of PARP and DFF45, and the downregulation of procaspase-3 and -9. With regard to cell cycle arrest, a time-dependent decrease in cyclin A, cyclin D3, cyclin E, cdk2, cdk4, and cdc2 expression was observed in the cells after eugenol treatment. Flow cytometry using a FACScan further demonstrated that eugenol induces a cell cycle arrest at S phase. Our results thus suggest that the inhibition of G361 cell proliferation by eugenol is the result of an apoptotic response and an S phase arrest that is linked to the decreased expression of key cell cycle-related molecules.

The Expression of HSP105 in Spitz Nevus and Malignant Melanoma / 대한피부과학회지

BACKGROUND: Spitz nevus and malignant melanoma have common features clinically and histologically, and in some cases it is impossible to distinguish between the two. Heat shock proteins (HSPs) serve to protect cells, and are activated by cell injury. Some HSPs are shown to be elevated in many types of cancers. Previous studies have reported the expression of heat shock protein in association with melanoma; however, a similar relationship with Spitz nevi has never been investigated. OBJECTIVE: This study was designed to measure the expression pattern of HSP 105 in both Spitz nevi and melanomas. METHODS: The specimens of 4 of Spitz nevi and 10 of malignant melanomas were analyzed for heat shock protein 105 expression through immunohistochemical staining. RESULTS: Immunohistochemical examination of HSP 105 showed strong expression in malignant melanoma specimens. On the other hand, weak expression was observed in Spitz nevus specimens. The degree of expression of HSP 105 showed a statistically significant difference (p<0.05). CONCLUSION: These findings provide the possibility of using HSP 105 as a effective marker for differentiating between Spitz nevi and malignant melanomas. In support of this, HSP 105 is considered to be a tumor-associated antigen of malignant melanoma.

Lesional Expression of Heat Shock Protein 70 in Pemphigus / 대한피부과학회지

BACKGROUND: Heat shock proteins (HSP), especially the HSP 70 family, may play certain roles in the immunophysiology of some skin diseases such as psoriasis, pemphigus, and lichen planus. HSPs generally induce down-regulation of the process of apoptosis that is considered to be one of the acantholysis-producing pathways in pemphigus. OBJECTIVE: We planned to examine possible roles of HSPs 70/105 in the blistering process in pemphigus vulgaris (PV) and pemphigus foliaceus (PF), in connection with the detection results of apoptosis in local tissue specimens. METHODS: Immunohistochemical stainings and Western blot analysis were performed for the detection and semiquantitation of HSPs 70/105 in skin specimens from lesional, nonlesional, and normal control sites. Hoechst 33342 staining was simultaneously carried out to examine features of apoptosis in lesional skin specimens. RESULTS: The findings on expression of HSP were as follows. In PV, the expression of HSP 70 was minimum or negative; however, in PF, the expression was obvious and recognizable in lesional and perilesional normal skin. In contrast, HSP 105 was not detected in all cases of PV and PF. The features of apoptosis were evident at the lesional skin of all cases of pemphigus with acantholytic changes. CONCLUSION: PV and PF had different relative intensities of HSPs in lesional tissue stainings, especially in cases with HSP 70. This suggests that there may be subtle differences in the mechanisms causing acantholysis between PV and PF.

Expression of CD133, CD24, CD44 in Cutaneous Malignant Tumors / 대한피부과학회지

BACKGROUND: Based on the unlimited proliferative and self-renewel properties of cancer cells similar to those of stem cells, the idea that cancer may originate from stem cells has been suggested in many different studies and has given rise to cancer stem cell hypothesis. CD133, being normally expressed on the surface of hematopoietic stem cells, has recently been suggested as a marker of cancer stem cells in several malignancies. CD24 and CD44 are membrane proteins reported as markers of various neoplasms. OBJECTIVE: This study was designed to investigate the immunohistochemical expression of the CD24, CD44 and CD133 in squamous cell carcinoma (SCC), basal cell carcinoma (BCC) and malignant melanoma (MM). METHODS: We performed immunohistochemical staining for CD24, CD44 and CD133 using 18 skin cancer tissue samples, including 6 SCCs, 6 BCCs and 6 MMs. The expression of each marker was standardized by the histochemical score (HSCORE). RESULTS: The expression of CD24 showed positive in 1 case of 6 SCCs (mean HSCORE, H; 0.02) and showed negative in 6 BCCs (H; 0.00), 6 MMs (H; 0.00). The expression of CD44 was not observed in 6 SCCs (H; 0.00) but observed in 1 case of 6 BCCs (H; 0.04) and 1 case of 6 MMs (H; 0.03). The expression of CD133 showed positive in 2 cases of 6 SCCs (H; 1.21) and 1 case of 6 BCCs (H; 0.05) and 6 cases of 6 MMs (H; 2.78). CONCLUSION: Our data suggest that CD133 may be a reliable marker of which the higher expression is observed in the more invasive skin cancers and that the existence of cancer stem cells may enhance tumorigenic potential in cutaneous malignant tumors.

Expression of glucocorticoid receptor mRNAs in glucocorticoid-resistant nasal polyps

Glucocorticoids (GCs) are the most effective group of medications available to treat inflammation. Although most patients with inflammation respond to GC, a small group of patients exhibit persistent GC-resistance with prolonged inflammation. Previously, it was proposed that the GC-resistance is caused by low amount of human GC receptor (hGR alpha) and/or excessive presence of a GC receptor isoform, hGR beta that was generated from alternative splicing of the hGR message. We have tested this hypothesis by investigating correlation between the expression pattern of hGR mRNAs in patients with inflammatory nasal polyps and the effectiveness of GC treatment.? We have performed reverse transcription PCR analysis of mRNAs coding each hGR alpha and hGR beta in nasal tissues.? hGR alpha mRNA was more expressed in patients with nasal polyps than in normal subjects. However, the elevated hGR alpha mRNA expression was decreased after GC treatment. Compared with hGR alpha mRNA expression, level of hGR beta mRNA expression was very low in all groups. In patients, hGR beta mRNA was expressed at a similar level regardless of GC efficacy, indicating that there is no correlation between the GC sensitivity and the expression level of hGR beta mRNA. Thus, persistent GC-resistance is not associated with low expression of hGRa or over- expression of hGR beta.