Neuroprotective potential of erucic acid via inhibition of N2a cell lines and rotenone induced Parkinson’s disease rat model

Author:

Sharma Bhawna1,Gupta Pankaj1,Biswas Largee1,Verma Anita Kamra2,Pasha Arif Mohammad3,Thota Prasad4,Medhi Bikash5

Affiliation:

1. Department of Pharmaceutical Sciences, School of Medical and Allied Sciences, K. R. Mangalam University, Sohna Rural, Haryana, India

2. Department of Zoology, Kirori Mal College, University of Delhi, University Enclave, Delhi, India

3. Department of Pharmaceutical Chemistry, Jyothishmathi Institute of Pharmaceutical Sciences, Thimmapur, Telangana, India

4. Indian Pharmacopoeia Commission, Ghaziabad, Uttar Pradesh, India

5. Department of Pharmacology, Post Graduate Institute of Medical Education and Research, Chandigarh, India

Abstract

Abstract: OBJECTIVE: The objective of this study was to investigate the potential for erucic acid (EA), an omega-9 monounsaturated fatty acid, to act as a neuroprotective agent. MATERIALS AND METHODS: In this study, EA was investigated against N2a cell lines and a rotenone (ROT)-induced model of Parkinson’s disease for its neuroprotective potential. The N2a cell line was incubated with fetal bovine serum, penicillin, and streptomycin supplemented with Dulbecco’s Modified Eagle’s Medium, and the following assays were carried out: (i) MTT, (ii) biocompatibility, (iii) DCFDA, and (iv) diphenylamine. A cell morphology study was also performed. Further, ROT 1 mg/kg s.c. and EA 3 and 10 mg/kg p.o. were given to rats on a daily basis for 21 days, and the following parameters were assessed: (i) neurobehavioral studies, (ii) oxidative stress markers, (iii) neuroinflammatory markers, (iv) neurotransmitters, and (v) histopathological study. RESULTS: The cell viability assay revealed that EA showed protection against ROT-induced toxicity in N2a cells, which was confirmed by a cell morphology study. EA decreased oxidative stress and % DNA fragmentation significantly. EA also prevented ROT-induced motor impairment and altered levels of oxidative stress markers, neurotransmitters, and neuroinflammatory markers significantly. When compared to the ROT group, a histological investigation of the EA group showed partial neuronal loss with the existence of intact neurons in between the vacuolated gaps. CONCLUSION: This study revealed that EA possesses profound neuroprotective properties in in vitro and in vivo studies. Additional research can be carried out to study the mechanism of EA with respect to its neuroprotective potential.

Publisher

Medknow

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