METHODOLOGY: Three sodium-fluoride(NaF) concentration(0.01%w/v,0.1%w/v and 0.5%w/v respectively)and two poly-γ-glutamic acid(PGGA)concentration(1%w/v and 2%w/v respectively)were prepared in 0.1 M acetic acid(pH4.0)and deionized distilled water.For de/re-mineralisation study, tooth samples (18 teeth varnished, leaving a 2 mm2 window on the mid-buccal surfaces) were immersed in respective acidified NaF and PGGA solutions. The Ca2+ release/uptake was monitored with ISE over 72-hr with increasing pH every 24-h from 4.0 to 6.0.These teeth were later subjected to cross-sectional microhardness to determine integrated mineral recovery of enamel on increasing pH of respective acidified solution.In order to determine mechanism of PGGA,two concentrations of PGGA in deionized-water-solutions were used for tooth samples immersion followed by overnight drying then later subjected to Fourier Transform Infra-Red(FT-IR) analysis.The FT-IR analysis was also carried out on PGGA powder.For control,the experiment was repeated using hydroxyapatite(HAp)pellets.The density of PGGA solutions(1%and2%)was also measured to determine their dynamic viscosities.
RESULTS: The ISE and microhardness testing revealed statistically significant (ρ ≤ 0.05) dissolution inhibition and remineralisation potential for tooth sample treated with acidified 2%PGGA. From the FT-IR spectra, it was observed that the profiles of the enamel and HAp surfaces treated with 1%-and 2%-PGGA solutions were similar to those of PGGA powder.It was found that the viscosity of PGGA increases with increasing concentration.
CONCLUSION: The study implies that 2% PGGA is more effective than NaF as forms a coating layer to protect from demineralisation and promote remineralisation of the tooth surface.
Materials and Methods: SF1 was produced by optimized methodology for bioassay-guided fractionation. Fourier transform infrared (FTIR) spectroscopy and liquid chromatography-mass spectrometry (LC-MS) were carried out to characterize the SF1. SF1 was screened for cytotoxicity activity toward HeLa, SiHa, and normal cells (NIH) cells by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay. The anticancer mechanism of SF1 was evaluated toward SiHa cells, which showed highest cytotoxicity toward SF1 treatment. The mechanism includes cell cycle progression and protein expression, which was detected using specific antibody-conjugated fluorescent dye, p53-FITC, by flow cytometry.
Results: Major constituents of SF1 were alkaloids with amines as functional group. SF1 showed highest cytotoxic activity against SiHa (half-maximal inhibitory concentration [IC50] < 10 µg/mL) compared to HeLa cells. Cytoselectivity of SF1 was observed with no IC50 detected on normal NIH cells. On flow cytometry analysis, SF1 was able to induce apoptosis on SiHa cells by arresting cell cycle at G1/S and upregulation of p53 protein.
Conclusion: SF1 showed anticancer activity by inducing apoptosis through arrested G1/S cell cycle checkpoint-mediated mitochondrial pathway.