Shailasree, S. and Venkataramana, M. and Niranjana, S. R. and Prakash, H. S. (2015) Cytotoxic effect of p-coumaric acid on neuroblastoma, n2a cell via generation of reactive oxygen species leading to dysfunction of mitochondria inducing apoptosis and autophagy. MOLECULAR NEUROBIOLOGY, 51 (1). pp. 119-130. ISSN 1559-1182
Full text not available from this repository. (Request a copy)Abstract
p-Coumaric acid (p-CA), an ubiquitous plant phenolic acid, has been proven to render protection against pathological conditions. In the present study, p-CA was evaluated for its capacity to induce cytotoxic effect to neuroblastoma N2a cells and we report here the possible mechanism of its action. p-CA at a concentration of 150 mu mol/L, upon exposure for 72 h, stimulated 81.23 % of cells to apoptosis, as evidenced by flow cytometer studies mediated through elevated levels of ROS (7.5-fold over control). Excess ROS production activated structural injury to mitochondrial membrane, observed as dissipation of its membrane potential and followed by the release of cytochrome c (8.73-fold). Enhanced generation of intracellular ROS correlated well with the decreased levels (similar to 60 %) of intracellular GSH. Sensitizing neuroblastoma cells for induction of apoptosis by p-CA identified p53-mediated upregulated accumulation of caspase-8 messenger RNA (2.8-fold). Our data report on autophagy, representing an additional mechanism of p-CA to induce growth arrest, detected by immunoblotting and fluorescence, correlated with accumulation of elevated levels (1.2-fold) of the LC3-II protein and acridine orange-stained autophagosomes, both autophagy markers. The present study indicates p-CA was effective in production of ROS-dependent mitochondrial damage-induced cytotoxicity in N2a cells.
Item Type: | Article |
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Subjects: | B Life Science > Biotechnology |
Divisions: | Department of > Biotechnology Department of > Institution of Excellence |
Depositing User: | Users 19 not found. |
Date Deposited: | 17 Jun 2019 04:49 |
Last Modified: | 17 Jun 2019 04:49 |
URI: | http://eprints.uni-mysore.ac.in/id/eprint/2794 |
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