In vitro cytotoxicity of self-etching primers / 대한치과교정학회지

OBJECTIVE: Several ions and components are released from self-etching primers in the oral cavity. This may cause injury to the periodontal tissues throughout orthodontic treatment. The purpose of this study was to assess the cytotoxicity of self-etching primers to HGF-1, HaCaT, and RHEK cells. METHOD: Transbond XT Primer (3M Unitek, Monrovia, CA, USA), and self-etching primers, Clearfil SE Bond (Kuraray, Osaka, Japan), Transbond Plus SEP (3M Unitek, Monrovia, CA, USA), and Adper Prompt L-Pop (3M Unitek, Monrovia, CA, USA), were evaluated by MTT assay, and cellular changes were also observed. RESULTS: In all cells after 72 hours with all primers, severe morphological changes such as atrophy and necrosis were observed. In the MTT assay using HGF-1, Clearfil SE Bond, Transbond XT Primer, Transbond Plus SEP, and Adper Prompt L-Pop were lined up in order of ascending cytotoxicity.When using HaCaT, Clearfil SE Bond, Adper Prompt L-Pop, Transbond Plus SEP, and Transbond XT Primer were lined up in order of ascending cytotoxicity. When using RHEK, Clearfil SE Bond, Transbond XT Primer, Adper Prompt L-Pop, and Transbond Plus SEP were lined up in order of ascending cytotoxicity. CONCLUSION: The result of this study shows that care is needed because self-etching primers show cytotoxic properties similar to conventional primers.

Apoptotic Effect of Combination Treatment with a Proteasome Inhibitor, Lactacystin, and a Histone Deacetylase Inhibitor, Trichostatin A, on MCF-7 Cells / 대한해부학회지

Although much information has been accumulated about the synergistic interaction of proteasome inhibitors and HDAC inhibitors to induce apoptosis in a certain type of cells, much less is known currently about the underlying mechanism. This study was undertaken to explore the combination effect of a histone deacetylase inhibitor, TSA, and a proteasome inhibitor, lactacystin, on the induction of apoptosis. Pretreatment of TSA and subsequent treatment of lactacystin showed the strong antitumor activity and nuclear condensation. Western blot assay showed that combination treatment of TSA and lactacystin increased Bax/Bcl-2 ratio and decreased level of XIAP. Activation of caspase-7 and cleavage of PARP were demonstrated after the combination treatment. In combination treatment group, cell cycle arrest was induced at G2/M phase and abolished increase in proteasome activity. This study is elucidating the mechanims whereby targeting apoptotic machineries may help in directing therapeutic strategies.

Caspases-dependent Apoptosis in Human Melanoma Cell by Eugenol / 대한해부학회지

Malignant melanoma is a highly metastatic tumor, resistant to chemotherapy and radiotherapy. Recent studies have suggested that many therapeutic agents used against cancer mediate their effects by induction of apoptosis of the cancer cells. Eugenol enhances the generation of tissue-damaging free radicals and inflammation or allergic reactions. In particular, it is more cytotoxic against cancer cells compared with normal fibroblasts. This study was performed to investigate whether the cytotoxic effect of eugenol is associated with the induction of apoptosis and involves activation of caspase in the human melanoma G361 cells. Eugenol-induced apoptosis was confirmed by MTT assay, Hemacolor stain, Hoechst stain, DNA electrophoresis, and Western blot analysis. Eugenol had a significant dose- and time-dependent inhibitory effect on the viability of G361 cells. Eugenol treatment induced caspase-3 and -6 cleavage, and activation. The caspase-3 substrates PARP and DFF45 are cleaved during eugenol-induced apoptosis. It was found that the casapase-6 substrate lamin A was cleaved, whose cleavage has been reported to be necessary for complete condesation of DNA during apoptosis. These results suggest that eugenol may constitute a potential antitumor compound against melanoma occurring in the skin and oral mucosa.

Induction of Apoptosis in Human Oral Squamous Carcinoma Cells by Extracellular Products from Pseudomonas aeruginosa / 대한해부학회지

It was reported that cancer in humans and animals infected with microbial pathogens was regressed about 100 years ago. Bacteria are able to trigger apoptosis by a variety of mechanisms including the secretion of protein synthesis inhibitors, pore forming proteins, molecules activating the endogenous death machinery in the infected cell. This study was conducted in order to investigate whether extracellular products of Psuedomonas aeruginosa (EPPA) induce apoptosis in human oral carcinoma cells (OSC9). The EPPA showed cytotoxic effect on OSC9 cells in dose and time-dependent manner. The cell death was demonstrated to be due to apoptosis characterized by chromatin condensation and nuclear fragment. EPPA treatment induced cleavage of caspase-3 and caspase-6. The caspase substrates, PARP, DFF45 and lamin A were cleaved during EPPA-induced apoptosis. Taken together, EPPA induces apoptosis on human oral squamous carcinoma cells in caspase-dependent manner. Our data therefore provide that EPPA contains a novel antitumor agent for human oral squamous carcinoma.