MATERIALS AND METHODS: Saliva was collected from 4- to 6-year-old kindergarten students. Salivary neutrophils were obtained by instructing the subjects to rinse their mouth with 1 mL of sterile 1.5% NaCl for 30 seconds before expectorating it into a sterile glass. The expression of CFSE+CD35+ and CFSE+CD89+was measured and analyzed using flow cytometry.
RESULTS: The expression of CFSE+CD89+ in the caries-free group (2.46 ± 0.39) was significantly lower than that in the S-ECC group (3.41 ± 1.11), with a p-value of 0.0001, while the expression of CFSE+CD35+ in the caries-free group was (2.35 ± 0.56) compared with (1.54 ± 0.35) (p = 0.0001) in the S-ECC group.
CONCLUSIONS: The expression ratio of CFSE+CD89+ and CFSE+CD35+constitutes a marker for S-ECC.
Methods: An in vitro cell model for tamoxifen-resistant HER2 overexpressed UACC732 cells was created using the pulse method. Cells were exposed to oxidized LDL (oxLDL) and very low density lipoprotein (VLDL) separately. Effects on cell morphology was studied using phase contrast microscopic changes. Percentage of cell viability was measured using proliferation assay kit. Development of tamoxifen resistance was determined based on P-gp expression with flow cytometry. Further analysis includedcell death measurement with flow cytometry method.
Results: UACC732 cells exposed to VLDL exhibited fibroblast-like morphology. This was further supported by proliferation assay, where the percentage of cell viability achieved more than 100% with 100 μg/ml of VLDL exposure, indicating cell proliferation. Findings also showed that VLDL caused reduction in expression of Pgp in resistant cells compared to resistant cells alone (p = 0.02).
Conclusion: Results of this study suggest that VLDL may play a role in growth of drug-resistant HER2-overexpressing cells. Lower expression of P-gp in presence of VLDL need to be investigated further.
Methods: The cytotoxicity of FD extract was assessed by MTS solution. BV2 cells were divided into 5 experimental groups, intervened, respectively, by FD (4 mg/mL) and LPS + FD (0, 1, 2, and 4 mg/mL). Besides, a blank control group was set up without any intervention. TNF-α release was assessed by enzyme linked immunosorbent assay (ELISA). The expression of CD40 was examined by flow cytometry. Immunocytochemical staining was used to show the morphology of BV2 cells.
Results: FD extract of different concentrations (1, 2, and 4 mg/mL) had no significant toxic effects on the BV2 cells. FD suppressed the activation of microglia in morphology and reduced TNF-α production and expression of CD40 induced by LPS.
Conclusion: FD extract has a therapeutic potential against neuroinflammatory diseases.