NEUROPROTECTIVE EFFECT OF CASSIA OCCIDENTALIS AGAINST 3-NITROPROPIONIC ACID-INDUCED NEUROTOXICITY IN RATS

Abstract

Huntington's disease (HD) is a neurodegenerative disorder characterized by motor impairment, cognitive decline and
psychiatric symptoms. Systemic administration of 3-nitropropionic acid (3-NP) causes selective striatal degeneration similar to
that seen in HD. Although the precise cause of neuronal cell death in HD is unknown, recent studies clearly demonstrate that
increased oxidative stress is one of the major deleterious events in the 3-NP-induced neurodegenerative process. Cassia
occidentalis (CO) has been studied for its antipyretic, anti-inflammatory and antioxidant properties. In this study was evaluated
the neuroprotective activity of stalks and leaves extracts of CO against behavioral and biochemical parameters induced by
intraperitoneal administration of 3-NP. The in vitro antioxidant activity was determined by the DPPH radical scavenging activity
method. Behavior evaluations were performed using the models of open-field, rotarod and elevated plus maze. The in vivo
antioxidant activity was evaluated in the striatal region after behavioral tests by the lipid peroxidation and the enzymatic activity
of superoxide dismutase. Systemic administration of 3-NP (30 mg/kg, i.p. for 5 days) produced hypolocomotion, muscle
incoordination and memory deficit. CO administration (400 and 800 mg/kg p.o.) improved 3-NP-induced dysfunctional behavior
(locomotor, rotarod and memory retention). Biochemical analysis of the striatum revealed that systemic 3-NP administration
significantly increased lipid peroxidation and decreased superoxide dismutase activity, which was attenuated by daily treatment
with CO. These results suggest that the protective effects of CO against 3-NP-induced rat striatal degeneration are mediated
through its antioxidant activity and suggest a potential therapeutic benefit of this plant in the treatment of HD.