AI Article Synopsis
- HESA-A is a systemic drug with herbal and marine origins that contains various essential minerals and has antioxidant, anti-inflammatory, and immune-modulating effects.
- The study evaluated how HESA-A affects the expression of cyclin D1, EGFR, and E-cadherin in a rat model with induced tongue dysplasia.
- Results showed that HESA-A treatment led to a lower incidence of cyclin D1 and a higher expression of E-cadherin compared to untreated groups, suggesting that HESA-A may have preventive effects against cancer development in dysplastic lesions by regulating these molecular markers.
Article Abstract
HESA-A has herbal and marine bases, containing minerals and rare elements such as Zr, Cr, Ga, Mn, Mg, Ca, Sr, Cu, Ti, etc. Its mechanism of action includes antioxidant, antiinflammatory and adjustment of the immune system. The aim of this study was to evaluate the effects of HESA-A systemic drug on expression of cyclin D1, EGFR and E-cadherin in induced tongue dysplasia in rats. In this experimental study, the effects of the systemic drug HESA-A on the expression of cyclin D1, EGFR, and E-cadherin molecular markers were examined in induced tongue dysplasia in rats. The incidence rate of cyclin D1 in groups receiving HESA-A was lower than the group that did not receive the drug (77.78% in the 0‒5% range versus 77.78% in the 5‒50% range). In the case of expression of E-cadherin in group D, which did not receive HESA-A, a decrease was observed in the expression of this cell adhesion marker as compared to the other two groups. The incidence of E-cadherin was dependent on HESA-A dose, while with 500 mg/kg it was higher than other groups (>75% in 55.55% versus >75% in 11.11%). Concerning the incidence of EGFR in all the three groups most cases were grade 0. The results of the present research indicated that considering changes in the expression of cyclin D1 and E-cadherin markers in groups treated with HESA-A, HESA-A® has preventive effects on development of cancer in dysplastic lesions through regulation of expression of these molecules.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5768951 | PMC |
| http://dx.doi.org/10.15171/joddd.2017.036 | DOI Listing |
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