curcumin and Parkinson-Disease--Secondary

Parkinson's disease (PD) is the second common age-related neurodegenerative disease. It is characterized by control loss of voluntary movements control, resting tremor, postural instability, bradykinesia, and rigidity. The aim of the present work is to evaluate curcumin, niacin, dopaminergic and non-dopaminergic drugs in mice model of Parkinson's disease through behavioral, biochemical, genetic and histopathological observations. Mice treated with rotenone rerecorded significant increase in adenosine A

Topics: Adenosine A2 Receptor Antagonists; Animals; Curcumin; Disease Models, Animal; Hippocampus; Humans; Male; Mice; Neuroprotective Agents; Niacin; Parkinson Disease, Secondary; Receptor, Adenosine A2A; Rotenone; Substantia Nigra

Topics: alpha7 Nicotinic Acetylcholine Receptor; Animals; Corpus Striatum; Curcumin; Disease Models, Animal; Dopamine; Dopaminergic Neurons; Humans; Oxidopamine; Parkinson Disease; Parkinson Disease, Secondary; Rats; Substantia Nigra

We aim herein to assess the neurotoxic effects of subchronic Cu-exposition (0125%) for 6 weeks on dopaminergic and astroglial systems then locomotor activity in rats as well as the probable therapeutic efficiency of curcumin-I (30 mg/kg B.W.). We found that intoxicated rats showed a significant impairment of Tyrosine Hydroxylase (TH) within substantia nigra pars compacta (SNc), ventral tegmental area (VTA) and the striatal outputs together with loss expression of GFAP in these structures. This was linked with an evident decrease in locomotor performance. Co-treatment with curcumin-I inverted these damages and exhibited a significant neuroprotective potential, thus, both TH expression and locomotor performance was reinstated in intoxicated rats. These results prove a profound dopaminergic and astroglial damages following subchronic Cu exposition and new beneficial curative potential of curcumin against subchronic Cu-induced astroglial and dopaminergic neurotoxicity. Consequently, we suggest that Cu neurotoxicity may be strengthened in vivo firstly by attacking and weaking the astroglial system, and curcumin could be prized as a powerful and preventive target for the neurodegenerative diseases related metal element, especially Parkinson's disease.

Topics: Animals; Astrocytes; Copper; Curcumin; Male; Parkinson Disease, Secondary; Pars Compacta; Rats; Rats, Wistar; Tyrosine 3-Monooxygenase; Ventral Tegmental Area

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.

Topics: Animals; Behavior, Animal; Curcumin; Electrophysiological Phenomena; Hippocampus; Motor Activity; Neurons; Neuroprotective Agents; Parkinson Disease, Secondary; Rats; Rotenone

Topics: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; Animals; Anti-Inflammatory Agents; Disease Models, Animal; Drug Discovery; Male; Mice, Inbred ICR; Mice, Transgenic; Neuroprotective Agents; Parkinson Disease, Secondary; Phloroglucinol; Serine; Signal Transduction; src-Family Kinases

Curcumin is a plant polyphenolic compound and a major component of spice turmeric (Curcuma longa). It has been reported to possess free radical-scavenging, iron-chelating, and anti-inflammatory properties in different tissues. Our previous study showed that curcumin protects MES23.5 dopaminergic cells from 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in vitro. The present study aimed to explore this neuroprotective effect in the 6-OHDA-lesioned rat model of Parkinson's disease in vivo.. Rats were given intragastric curcumin for 24 days. 6-OHDA lesioning was conducted on day 4 of curcumin treatment. Dopamine content was assessed by high-performance liquid chromatography with electrochemical detection, tyrosine hydroxylase (TH)-containing neurons by immunohistochemistry, and iron-containing cells by Perls' iron staining.. The dopamine content in the striatum and the number of TH-immunoreactive neurons decreased after 6-OHDA treatment. Curcumin pretreatment reversed these changes. Further studies demonstrated that 6-OHDA treatment increased the number of iron-staining cells, which was dramatically decreased by curcumin pretreatment.. The protective effects of curcumin against 6-OHDA may be attributable to the iron-chelating activity of curcumin to suppress the iron-induced degeneration of nigral dopaminergic neurons.

Topics: Animals; Curcumin; Disease Models, Animal; Dopaminergic Neurons; Female; Iron; Iron Chelating Agents; Neuroprotective Agents; Oxidopamine; Parkinson Disease, Secondary; Rats; Rats, Wistar; Substantia Nigra