Piperine mitigates behavioral impairments and provides neuroprotection against 3-nitropropinoic acid-induced Huntington disease-like symptoms

ABSTRACT

Background: Piperine (PIP) is a powerful anti-oxidant and anti-inflammatory alkaloid which has been widely used in the treatment of various pathological conditions. However, few studies have clearly discussed the protective effects and potential mechanism of PIP in different neurological diseases. The aim of this study was to investigate the neuroprotective effect of PIP against 3-nitropropioninc acid (3-NP) induced neurobehavioral, biochemical and histopathological alterations in animals.

Methods: Adult male Wistar rats were randomly divided into three groups. Group 1, the vehicle administered control group, received normal saline (p.o.). Group 2 received 3-NP (20 mg/kg.b.wt., i.p.) for 4 consecutive days. Group 3 received PIP (10 mg/kg.b.wt., p.o.) twice daily for a period of 4 days, 30 min before and 6 h after the 3-NP injection. Upon termination of treatment schedule, behavioral experiments were performed to access the behavioral outcomes. The brain striatal tissue was used for the estimation of monoamine oxidase activity and serotonin level. In addition, astrocytes activation was observed by GFAP immunostaining.

Results: Our results showed that 3-NP induced behavioral impairments are attenuated by PIP co-treatment. Next, the extent of neuronal loss and astrocytes activation was reduced in the striatal brain region in PIP treated rats. Finally, it was observed that PIP alleviated the behavioral, biochemical, immunohistochemical and histological alterations.

Conclusion: The results of the current study reveal the neuroprotective competency of PIP against Huntington disease like symptoms in rats.

KEYWORDS:

• Huntington’s disease
• 3-nitropropioninc acid
• piperine
• behavioural impairments
• neuroprotection

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by Department of Science and Technology: [Grant Number DST/CSRI/2017/150]; Department of Science and Technology: [Grant Number SR/PURSE Phase 2/39[C]]; University Grants Commission: [Grant Number 25-1/2014-15(BSR)/7-91-2007(BSR)].

Notes on contributors

Mohd Salman

Mohd Salman, is presently pursing his doctoral prorgam in the field of Toxicology at Jamia Hamdard. His research focuses on molecular mechanisms involved in neurodegeneration. His expertise in surgical models of rodents provides an excellent platform for developing neurotherapeutics.

Heena Tabassum

Heena Tabassum, Ph.D., is a Scientist in Biomedical Sciences Division at Headquarters of Indian Council of Medical Research, New Delhi, India. Her research interests are nanomedicine, neuroscience, pharmacology and toxicology.

Suhel Parvez

Suhel Parvez, Ph.D., is Professor and current Head in the Department of Toxicology, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi, India. His current research interest focusses on deciphering cellular and molecular mechanisms involved in traumatic brain injury, ischemic stroke and neurodegenerative diseases. He is exploring the avenue of drug repurposing with pre-clinical studies.