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    Article

    Naringin Ameliorates Doxorubicin‑induced Neurotoxicity In vitro and Cognitive Dysfunction In vivo

    Grandhi Venkata Ramalingayya2,3, Pawan G. Nayak2, Rekha R. Shenoy2, Sanchari Basu Mallik2, Karthik Gourishetti2, Shalam M. Hussain4, Chamallamudi Mallikarjuna Rao2, Krishnadas Nandakumar2★★ Corresponding author

    1. 1Department of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education, Manipal, Karnataka.
    2. 2Discovery Biology, Suven Life Sciences Ltd., Hyderabad, Telangana, India.
    3. 3Department of Pharmacology and Toxicology, Unaizah College of Pharmacy, Qassim University, Al Malida, KSA.

    CORRESPONDENCE

    Krishnadas Nandakumar

    Discovery Biology, Suven Life Sciences Ltd., Hyderabad, Telangana, India.

    nandakumar.k@manipal.edu

    Received: 17-08-2017; Revised: 19-10-2017.

    Volume 14, Issue 55s · pp. S197–S207 · PUBLISHED 28 June 2018 · DOI: 10.4103/pm.pm_364_17

    View on Pharmacogn. Mag. original site ↗

    ABSTRACT

    Objectives: The primary objective of the study was to study the neuroprotective potential of naringin (NAR) against doxorubicin (DOX)‑induced neurotoxicity in vitro and DOX‑induced cognitive deficits (chemobrain) in vivo. Materials and Methods: In vitro methods, viz., 3‑[4,5dimethylthiazol‑2‑yl]‑2,5‑diphenyl tetrazolium bromide assay, flow cytometry, acridine orange/ethidium bromide staining, and neuritogenic and reactive oxygen species (ROS) assays, assessed neuroprotective potential of NAR and its aglycone naringenin (NGN) in IMR‑32 cells. Chemobrain was developed in Wistar rats on chronic administration of ten cycles of DOX, and episodic memory was assessed using novel object recognition task. Serum cortisol, locomotor activity, and hematological biochemical and histological analysis were carried out. Results: A protective effect of NAR or NGN was observed upon pretreatment with the respective compounds in IMR‑32 cells challenged with DOX. Flow cytometry revealed that flavonoids reduced cell cycle changes produced by DOX. In addition, an increase in apoptosis, intracellular ROS generation, and inhibition of neurite growth was noticed in IMR‑32 cells with DOX treatment, which was significantly prevented by NAR or NGN pretreatment. Interestingly, NAR (50 mg/kg, p.o.) significantly ameliorated episodic memory deficit associated with DOX without influencing locomotion, upon chronic treatment. NAR also prevented histological changes to major organs observed with DOX. Conclusion: NAR showed neuroprotective potential and may be used as an adjuvant therapy for amelioration of neurocognitive complications associated with chemotherapy in cancer survivors.

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      Ramalingayya, G. V., Nayak, P. G., Shenoy, R. R., Mallik, S. B., Gourishetti, K., Hussain, S. M., Rao, C. M., & Nandakumar, K. (2018). Naringin Ameliorates Doxorubicin‑induced Neurotoxicity In vitro and Cognitive Dysfunction In vivo. Pharmacognosy Magazine, 14(55s), S197–S207. https://doi.org/10.4103/pm.pm_364_17