ABSTRACT
Parkinson disease (PD) is a chronic progressive neurodegenerative disease characterized by both motor and non-motor features. Numerous risk factors (oxidative stress, free radical formation, and several environmental toxins) have been associated with PD. The experimental studies were carried out under in vivo conditions. Biochemical data analysis indicated that compared with the parameters of control (C) rats, rotenone-induced PD rats showed a significant decrease in the specific content of the total fraction of isoforms of O2--producing, heat-stable, NADPH-containing associates (NLP-Nox) from membrane formations of tissues (brain, liver, lung, and small intestine). Compared with the C group indices, in the PD and PD + curcumin (PD + CU) groups there is some change in the shape of the optical absorption spectra of isoforms associated with a change in the amount of Nox in the isoform composition of the total fraction of the NLP-Nox associate. Thus, daily administration of CU (200 mg/kg, i.p.) to PD rats for 63 days had a regulatory effect, bringing the specific content and O2--producing activity of the total fraction of NLP-Nox isoforms closer to the norm. CU has membrane-stabilizing effects in rotenone-induced PD.
Subject(s)
Curcumin , Neurodegenerative Diseases , Neuroprotective Agents , Parkinson Disease , Rats , Animals , Parkinson Disease/drug therapy , Rotenone/pharmacology , Curcumin/pharmacology , Curcumin/therapeutic use , Neuroprotective Agents/pharmacology , Oxidative Stress , Disease Models, AnimalABSTRACT
Rotenone is involved in the degeneration of dopaminergic neurons, and curcumin may prevent or effectively slow the progression of Parkinson's disease (PD). Previous research has shown that the naturally occurring phenolic compound curcumin can reduce inflammation and oxidation, making it a potential therapeutic agent for neurodegenerative diseases. The present study involves investigation of rotenone-induced histological changes in the brain area, hippocampus using Nissl staining after 35 day of subcutaneous injection of rotenone in adult male rats. We sought to determine whether curcumin could protect against rotenone-induced dopaminergic neurotoxicity in a rat model by in vivo electrical recording from Substantia nigra pars compacta (SNc). Curcumin treatment significantly improved electrical activity of neurons in the SNc of rotenone-induced PD model rats. The pattern of histological alterations corresponds with electrophysiological manifestations.
Subject(s)
Curcumin , Parkinson Disease , Animals , Curcumin/pharmacology , Curcumin/therapeutic use , Dopaminergic Neurons , Male , Parkinson Disease/drug therapy , Pars Compacta , Rats , Rotenone/toxicity , Substantia NigraABSTRACT
Curcumin is a naturally occurring phenolic yellow chemical isolated from the rhizomes of the plant Curcuma longa (turmeric), and is a major component of the spice turmeric. Curcumin has protective effects against rotenone-induced neural damage in Parkinson's disease (PD). The present study aims at providing new evidence for the validity of the rotenone rat model of PD by examining whether neuronal activity in the hippocampus is altered. Male albino rats were treated with rotenone injections (2.5 mg/ml intraperitoneally) for 21 days. We examined the effects of curcumin (200 mg/kg) on behavior and electrophysiology in a rat model of PD induced by rotenone. Motor activity was assessed by cylinder test. The electrical activity of neurons was measured in hippocampus. Rotenone causes significant reduction of neuronal activity. The results show that curcumin can improve the motor impairments and electrophysiological parameters and may be beneficial in the treatment of PD.
Subject(s)
Curcumin/pharmacology , Electrophysiological Phenomena/drug effects , Hippocampus/drug effects , Motor Activity/drug effects , Neuroprotective Agents/pharmacology , Parkinson Disease, Secondary/drug therapy , Animals , Behavior, Animal/drug effects , Behavior, Animal/physiology , Curcumin/therapeutic use , Electrophysiological Phenomena/physiology , Hippocampus/physiopathology , Motor Activity/physiology , Neurons/drug effects , Neurons/physiology , Neuroprotective Agents/therapeutic use , Parkinson Disease, Secondary/chemically induced , Parkinson Disease, Secondary/physiopathology , Rats , RotenoneABSTRACT
Parkinson's disease (PD) is the most common neurodegenerative disease of unknown etiology and characterized by motor symptoms of tremor, rigidity, bradykinesia, and postural instability. Interactions between the dopaminergic systems and the hippocampus in synaptic plasticity and behavior are found. The rotenone-induced animal model is commonly used in research studies involved in PD. Administration of rotenone causes alterations of electrical neuronal activity. Rotenone (2.5 mg/kg/day) was administered intraperitoneally for 21 days to adult rats, and rotenone effects on rearing activity and electrophysiology were examined. Dose-dependent reduction of evoked neural activity and a reduction in firing strength were found in the hippocampus. Behaviorally, Rotenone rats showed a more consistent decrease in rearing across the 3 weeks, compared with animals in the control group. Thus, rotenone causes changes in hippocampal electrical activity and behavioral changes.
