Carvacrol Induces Apoptosis via Caspase Activation in HL-60 human leukemia cells.

Authors

Akash-Samuel
Department of Biotechnology, School of Bioengineering, SRM Institute of Science and Technology, Kattankulathur, Tamil Nadu, India.
Prem-Santhosh
Department of Biotechnology, School of Bioengineering, SRM Institute of Science and Technology, Kattankulathur, Tamil Nadu, India.
Ravichandran Jayasuriya
Department of Biotechnology, School of Bioengineering, SRM Institute of Science and Technology, Kattankulathur, Tamil Nadu, India
Amin Karan
Department of Biotechnology, School of Bioengineering, SRM Institute of Science and Technology, Kattankulathur, Tamil Nadu, India.
Gautham V Ganesh
Department of Biotechnology, School of Bioengineering, SRM Institute of Science and Technology, Kattankulathur, Tamil Nadu, India.
Kunka Mohanram Ramkumar
SRM Research Institute, SRM Institute of Science and Technology, Kattankulathur, Tamil Nadu, India.

Synopsis

MTT assay was performed to analyze the cytotoxic effect of carvacrol and was found to be toxic in the range of 20-100mM/ml. The main cytotoxic effect appears to be attributable to its induction of apoptotic cell death as assessed by TUNEL assay. Exposure of the cultured cells to carvacrol (100 mM/ml) led to an increase in malonyldialdehyde (MDA) production, an indicator of free radical formation, and reduction in the level of different antioxidant enzymes including reduced glutathione (GSH) and superoxide dismutase (SOD) (p < 0.05). Further studies revealed that the dissipation of mitochondrial membrane potential of intact cells is accompanied by the activation of caspase-3. Conclusion: Our findings indicate that carvacrol-induced cellular apoptosis by collapsing mitochondrial membrane potential, generating free radicals, and depleting intracellular antioxidant enzyme levels, thereby indicating its potential for cancer treatment.

NCB4EBT-2021
Published
March 16, 2021