Within the limitations of this study, vitamin D3 and K2 alone or in combination did not affect gingival IL-1β and IL-10, serum B-ALP and TRAP-5b levels, or alveolar bone compared with conventional periodontal therapy alone.
The goal of this work was to see how melatonin affected Bax and Bcl‐2 expression, as well as apoptosis and autophagy, in MCF‐7 and MDA‐MB‐231 breast cancer cell lines, which have distinct hormonal sensitivities.
In this study, to investigate the IC50 value of melatonin, varied melatonin concentrations were administered to MCF‐7 and MDA‐MB‐231 breast cancer cell lines. Moreover, cytotoxic activities were analyzed through MTT analysis. Five subgroups were created for both cell lines: control, IC50‐MeL, hIC50‐MeL, DMSO1, and DMSO2. To evaluate the apoptotic effect of melatonin, immunofluorescence staining methods of TUNEL, Bax, and Bcl‐2 were used, and to examine the effects of autophagy, immunofluorescence staining methods of Beclin‐1, LC3, and p62 were used.
In vitro results revealed upregulation of the expression of TUNEL and Bax in both MCF‐7 and MDA‐MB‐231 cell lines regarding dose and time, but downregulation of Bcl‐2 expression. Moreover, autophagy results were consistent with in vitro apoptosis results in both MCF‐7 and MDA‐MB‐231 cell lines. We determined that the expressions of the autophagy markers Beclin‐1, LC3, and p62 were increased. Our findings indicate that treatment of breast cancer cells with melatonin increased the inhibitory effect of melatonin on cell growth through both apoptosis and autophagy in vitro.
Consequently, it was concluded that melatonin might adjust the expression balance of markers that have a role in cell death mechanisms and significantly promote these mechanisms. Therefore, melatonin can inhibit the growth of breast cancer cells by inducing cell death.
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