Document Type : Original Article

Authors

1 Physiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran

2 Endocrinology and Metabolism Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences Kerman, Iran

3 Research Center for Hydatid Disease in Iran, Kerman University of Medical Sciences, Kerman, Iran

4 Department of General Surgery, Faculty of Medicine, Zahedan University of Medicine Sciences, Zahedan, Iran

5 Cardiovascular Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Science, Kerman, Iran

6 Neuroscience Research Center,Institute of Neuropharmacology Kerman University of Medical Sciences,Kerman,Iran

Abstract

Objective: Although numerous pharmacological effects of Shilajit have been explored by extensive experiments, there is no study on the effects of this ayurvedic substance on the mRNA level of NF-κB family members (p50 and RelB) and IKK subunits (IKKα and β), in breast cancers. Accordingly, the objective of the current experiment was the mechanistic evaluation of the anti-tumoral potential of Shilajit against the breast cancer cell line (MCF-7). In this experimental study, the viability% of Shilajit (0, 100, 200, 400, 600, and 800 μg/mL)-treated cells was analyzed after 24, 48, and 72 h. In the following, the apoptotic rate and p50, RelB, and IKKα/β genes expression were assessed using flow cytometry and real-time PCR assays, respectively.
Results: Shilajit had a potent cytotoxic activity in a dose- and time-dependent manner with an IC50 of 280 μg/mL. Based on the Annexin-PI analysis, IC50 concentration of this compound induced significant apoptosis in the cells, possibly through suppression of NF-κB-regulated genes. The expression levels exhibited significant (P≤0.05) downregulation of these genes in the treatment group. The findings of the present experiment clearly indicate that Shilajit possesses promising anti- breast tumor activity through inhibition of IKK/NF-κB signaling pathway.

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