Please use this identifier to cite or link to this item: http://hdl.handle.net/2080/3247
Title: Bacopa monnieri-induced protective autophagy inhibits benzo[a]pyrene-mediated apoptosis
Authors: Bhutia, Sujit Kumar
Keywords: Bacopa monnieri
Beclin-1
Autophagy
Benzo[a]pyrene
Mitochondrial apoptosis
Oxidative stress
Issue Date: Feb-2019
Citation: National Conference on Biodiversity, Biotechnology and Bioinformatics: Innovative and Emerging Trends (NCBBBIET-2019), Berhampur University, Berhampur, Odisha, 22-23 February 2019
Abstract: Benzo[a]pyrene (B[a]P) is capable of inducing oxidative stress and cellular injuries leading to cell death and associates with a significant risk of cancer development. Prevention of B[a]P-induced cellular toxicity with herbal compound through regulation of mitochondrial oxidative stress might protect cell death and have therapeutic benefit to human health. In this study, we demonstrated the cytoprotective role of Bacopa monnieri (BM) against B[a]P-induced apoptosis through autophagy induction. Pretreatment with BM rescued the reduction in cell viability in B[a]P-treated human keratinocytes (HaCaT) cells indicating the cytoprotective potential of BM against B[a]P. Moreover, BM was found to inhibit B[a]P-mediated reactive oxygen species (ROS)-induced apoptosis activation in HaCaT cells. Furthermore, BM was found to preserve mitochondrial membrane potential and inhibited release of cytochrome c in B[a]P-treated HaCaT cells. Bacopa monnieri induced protective autophagy; we knocked down Beclin-1, and data showed that BM was unable to protect from B[a]P-induced mitochondrial ROS-mediated apoptosis in Beclin-1-deficient HaCaT cells. Moreover, we established that B[a]P-induced damaged mitochondria were found to colocalize and degraded within autolysosomes in order to protect HaCaT cells from mitochondrial injury. In conclusion, B[a]P-induced apoptosis was rescued by BM treatment and provided cytoprotection through Beclin-1-dependent autophagy activation.
Description: Copyright of this document belongs to proceedings publisher.
URI: http://hdl.handle.net/2080/3247
Appears in Collections:Conference Papers

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