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Influence of autophagy, apoptosis and their interplay in filaricidal activity of C-cinnamoyl glycosides

Published online by Cambridge University Press:  28 June 2019

Priya Roy
Affiliation:
Parasitology Laboratory, Department of Zoology, Centre for Advanced Studies, Visva-Bharati, Santiniketan 731235, West Bengal, India Fishery and Ecotoxicology Revsearch Laboratory, Department of Zoology, The University of Burdwan, Bardhaman 713104, India
Anirban Sengupta
Affiliation:
Immunology Lab, Department of Zoology, University of Calcutta, 35, Ballygunge Circular Road, Kolkata 700019, India
Nikhilesh Joardar
Affiliation:
Parasitology Laboratory, Department of Zoology, Centre for Advanced Studies, Visva-Bharati, Santiniketan 731235, West Bengal, India
Arindam Bhattacharyya
Affiliation:
Immunology Lab, Department of Zoology, University of Calcutta, 35, Ballygunge Circular Road, Kolkata 700019, India
Nimai Chandra Saha
Affiliation:
Fishery and Ecotoxicology Revsearch Laboratory, Department of Zoology, The University of Burdwan, Bardhaman 713104, India
Anup Kumar Misra
Affiliation:
Division of Molecular Medicine, Bose Institute, P-1/12, C.I.T. Scheme VII-M, Kolkata 700054, India
Santi P. Sinha Babu*
Affiliation:
Parasitology Laboratory, Department of Zoology, Centre for Advanced Studies, Visva-Bharati, Santiniketan 731235, West Bengal, India
*
Author for correspondence: Santi P. Sinha Babu, E-mail: [email protected]

Abstract

The present work aims to explore the mechanism of action of C-cinnamoyl glycoside as an antifilarial agent against the bovine filarial nematode Setaria cervi. Both apoptosis and autophagy programmed cell death pathways play a significant role in parasitic death. The generation of reactive oxygen species, alteration of the level of antioxidant components and disruption of mitochondrial membrane potential may be the causative factors that drive the parasitic death. Monitoring of autophagic flux via the formation of autophagosome and autophagolysosome was detected via CYTO ID dye. The expression profiling of both apoptotic and autophagic marker proteins strongly support the initial findings of these two cell death processes. The increased interaction of pro-autophagic protein Beclin1 with BCL-2 may promote apoptotic pathway by suppressing anti-apoptotic protein BCL-2 from its function. This in turn partially restrains the autophagic pathway by engaging Beclin1 in the complex. But overall positive increment in autophagic flux was observed. Dynamic interaction and regulative balance of these two critical cellular pathways play a decisive role in controlling disease pathogenesis. Therefore, the present experimental work may prosper the chance for C-cinnamoyl glycosides to become a potential antifilarial therapeutic in the upcoming day after detail in vivo study and proper clinical trial.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2019 

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Footnotes

*

These authors contributed equally to this work

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