scholarly journals Effects of crocin on brain oxidative damage and aversive memory in a 6-OHDA model of Parkinson’s disease

2016 ◽  
Vol 74 (9) ◽  
pp. 723-729 ◽  
Author(s):  
Z Rajaei ◽  
M Hosseini ◽  
H Alaei
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Oxidative Damage ◽  
Medial Forebrain Bundle ◽  
Memory Performance ◽  
Thiobarbituric Acid ◽  
Memory Deficits ◽  
Thiobarbituric Acid Reactive Substances ◽  
Male Wistar Rats ◽  
6 Hydroxydopamine

ABSTRACT The purpose of the present study was to investigate the effect of crocin on brain oxidative damage and memory deficits in a 6-hydroxydopamine (6-OHDA) model of Parkinson’s disease. Male Wistar rats were subjected to unilateral injection of 6-OHDA (16 µg) into the medial forebrain bundle and treated with crocin (30 and 60 mg/kg) for six weeks. The rats were tested for memory performance at six weeks after 6-OHDA infusion, and then were killed for the estimation of biochemical parameters. The increase in thiobarbituric acid reactive substances (TBARS) and nitrite levels in the hippocampus were observed in the 6-OHDA lesioned rats, which was accompanied by memory deficits in a passive avoidance test at the end of week 6. Moreover, treatment with crocin decreased TBARS and nitrite levels in the hippocampus, and improved aversive memory. The present study conclusively demonstrated that crocin acts as an antioxidant and anti-inflammatory agent in the hippocampus of parkinsonian rats and could improve aversive memory through its properties.

scholarly journals Neuroprotective Mechanisms of Three Natural Antioxidants on a Rat Model of Parkinson’s Disease: A Comparative Study

Antioxidants ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 49 ◽  
Author(s):  
Lyubka P. Tancheva ◽  
Maria I. Lazarova ◽  
Albena V. Alexandrova ◽  
Stela T. Dragomanova ◽  
Ferdinando Nicoletti ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neuroprotective Effect ◽  
Memory Performance ◽  
Natural Antioxidants ◽  
Control Group ◽  
Biochemical Assays ◽  
Male Wistar Rats ◽  
Improved Learning ◽  
6 Hydroxydopamine

We compared the neuroprotective action of three natural bio-antioxidants (AOs): ellagic acid (EA), α-lipoic acid (LA), and myrtenal (Myrt) in an experimental model of Parkinson’s disease (PD) that was induced in male Wistar rats through an intrastriatal injection of 6-hydroxydopamine (6-OHDA). The animals were divided into five groups: the sham-operated (SO) control group; striatal 6-OHDA-lesioned control group; and three groups of 6-OHDA-lesioned rats pre-treated for five days with EA, LA, and Myrt (50 mg/kg; intraperitoneally- i.p.), respectively. On the 2nd and the 3rd week post lesion, the animals were subjected to several behavioral tests: apomorphine-induced rotation; rotarod; and the passive avoidance test. Biochemical evaluation included assessment of main oxidative stress parameters as well as dopamine (DA) levels in brain homogenates. The results showed that all three test compounds improved learning and memory performance as well as neuromuscular coordination. Biochemical assays showed that all three compounds substantially decreased lipid peroxidation (LPO) levels, and restored catalase (CAT) activity and DA levels that were impaired by the challenge with 6-OHDA. Based on these results, we can conclude that the studied AOs demonstrate properties that are consistent with significant antiparkinsonian effects. The most powerful neuroprotective effect was observed with Myrt, and this work represents the first demonstration of its anti-Parkinsonian impact.

Resveratrol attenuates 6-hydroxydopamine-induced oxidative damage and dopamine depletion in rat model of Parkinson's disease

2010 ◽  
Vol 1328 ◽  
pp. 139-151 ◽  
Author(s):  
Mohd.Moshahid Khan ◽  
Ajmal Ahmad ◽  
Tauheed Ishrat ◽  
M. Badruzzaman Khan ◽  
Md. Nasrul Hoda ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Oxidative Damage ◽  
Rat Model ◽  
Dopamine Depletion ◽  
6 Hydroxydopamine

scholarly journals Carbohydrate–energy restriction may protect the rat brain against oxidative damage and improve physical performance

2003 ◽  
Vol 89 (1) ◽  
pp. 89-96 ◽  
Author(s):  
S. L. de Oliveira ◽  
D. B. Diniz ◽  
J. Amaya-Farfan
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Thiobarbituric Acid ◽  
Energy Restriction ◽  
The Other ◽  
Exhaustive Exercise ◽  
Protein Damage ◽  
Thiobarbituric Acid Reactive Substances ◽  
Male Wistar Rats ◽  
The Brain

Chronic energy restriction, α-tocopherol supplementation and their interaction with exhaustive exercise were investigated. Eleven-week-old male Wistar rats (n 6×10) were fed either a control (C), a 30 % carbohydrate-energy-restricted control (R) or an α-tocopherol-supplemented (S) diet for 5 months. The animals in each diet were divided into exercised (E) and non-exercised (NE) groups. Before killing, the exercised rats were required to run to exhaustion (39 (SE 6), 69 (se 11) and 18 (se 2) min for the C, R and S groups, respectively). Lipid peroxidation (thiobarbituric acid-reactive substances; TBARS), protein damage (reactive carbonyls) and α-tocopherol were determined in gastrocnemius, liver, brain an/r plasma. There was no difference in lipid peroxidation between the R and C groups, but in liver and muscle peroxidation appeared significantly lower in the S than the other two diets. TBARS in the brain were similar in all groups. On the other hand, reactive carbonyls showed that both the R and S diets reduced protein damage in the brain, while exhaustive exercise increased it. For liver and muscle, however, reactive carbonyl levels were similar in all groups. α-Tocopherol supplementation increased the vitamin concentrations in liver, muscle and plasma, but exercise decreased them in plasma and brain. Carbohydrate-energy restriction increased (P=0·0025) resistance to exhaustive exercise considerably without depleting stores of α-tocopherol or exacerbating oxidative damage in monitored tissues. It is concluded that while exhaustive exercise promotes a tissue-specific oxidative damage detectable only in brain proteins, both experimental diets tended to ameliorate this condition.

scholarly journals Propolis as a Potential Disease-Modifying Strategy in Parkinson’s disease: Cardioprotective and Neuroprotective Effects in the 6-OHDA Rat Model

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1551 ◽  
Author(s):  
Valeria C. Gonçalves ◽  
Daniel J. L. L. Pinheiro ◽  
Tomás de la Rosa ◽  
Antônio-Carlos G. de Almeida ◽  
Fúlvio A. Scorza ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Heart Rate ◽  
Parkinson's Disease ◽  
Rat Model ◽  
Autonomic Function ◽  
Neuronal Loss ◽  
Neuroprotective Effects ◽  
Male Wistar Rats ◽  
The Mean ◽  
6 Hydroxydopamine

Patients with Parkinson’s disease (PD) manifest nonmotor and motor symptoms. Autonomic cardiovascular dysregulation is a common nonmotor manifestation associated with increased morbimortality. Conventional clinical treatment alleviates motor signs but does not change disease progression and fails in handling nonmotor features. Nutrition is a key modifiable determinant of chronic disease. This study aimed to assess the effects of propolis on cardiological features, heart rate (HR) and heart rate variability (HRV) and on nigrostriatal dopaminergic damage, detected by tyrosine hydroxylase (TH) immunoreactivity, in the 6-hydroxydopamine (6-OHDA) rat model of PD. Male Wistar rats were injected bilaterally with 6-OHDA or saline into the striatum and were treated with propolis or water for 40 days. Autonomic function was assessed by time domain parameters (standard deviation of all normal-to-normal intervals (SDNN) and square root of the mean of the squared differences between adjacent normal RR intervals (RMSSD)) of HRV calculated from electrocardiogram recordings. Reductions in HR (p = 1.47 × 10−19), SDNN (p = 3.42 × 10−10) and RMSSD (p = 8.2 × 10−6) detected in parkinsonian rats were reverted by propolis. Propolis attenuated neuronal loss in the substantia nigra (p = 5.66 × 10−15) and reduced striatal fiber degeneration (p = 7.4 × 10−5) in 6-OHDA-injured rats, which also showed significant weight gain (p = 1.07 × 10−5) in comparison to 6-OHDA-lesioned counterparts. Propolis confers cardioprotection and neuroprotection in the 6-OHDA rat model of PD.

The beneficial effect of vanillin on 6-hydroxydopamine rat model of Parkinson’s disease

2020 ◽  
Vol 38 (5) ◽  
pp. 369-373
Author(s):  
Rasha Abuthawabeh ◽  
Amjad N. Abuirmeileh ◽  
Karem H. Alzoubi
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Beneficial Effect ◽  
Wistar Rats ◽  
Neurodegenerative Disorder ◽  
Striatal Dopamine ◽  
Intracerebral Injection ◽  
Protective Properties ◽  
Male Wistar Rats ◽  
6 Hydroxydopamine

Background: Parkinson’s disease (PD) is a progressive neurodegenerative disorder that is related to neuroinflammation. Vanillin, which possesses both antioxidant, and anti-inflammatory properties, can be a candidate for neuroprotection in PD. Objective: This study was aimed to investigate the effects of vanillin on the 6-hydroxydopamine (6-OHDA) rodent model of PD. Methods: Male Wistar rats were administrated intraperitoneal (i.p) or oral vanillin at a dose of 20 mg/kg/day for 7 days that was started at three days before or seven days after intracerebral injection of 6-OHDA. The 6-OHDA-induced lesions were assessed behaviorally using the apomorphine rotation test, neurochemically via measuring striatal dopamine concentrations, and through immunohistochemistry. Results: Both oral and IP vanillin at three days before or seven days after 6-OHDA lesioning exhbited significantly lower tight contralateral rotations upon apomorphine challenge, and higher striatal dopamine concentrations. Conclusions: Vanillin seems to offer protective properties against 6-OHDA lesion via preserving striatal dopamine levels.

scholarly journals Astrocytes and retrograde degeneration of nigrostriatal dopaminergic neurons in Parkinson’s disease: removing axonal debris

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Ingrid Morales ◽  
Ricardo Puertas-Avendaño ◽  
Alberto Sanchez ◽  
Adrian Perez-Barreto ◽  
Clara Rodriguez-Sabate ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Medial Forebrain Bundle ◽  
Physiological Role ◽  
Cell Degeneration ◽  
Retrograde Degeneration ◽  
Microglial Phagocytosis ◽  
Transporter Protein ◽  
Cellular Debris ◽  
6 Hydroxydopamine

Abstract Objective The dopaminergic nigrostriatal neurons (DA cells) in healthy people present a slow degeneration with aging, which produces cellular debris throughout life. About 2%–5% of people present rapid cell degeneration of more than 50% of DA cells, which produces Parkinson’s disease (PD). Neuroinflammation accelerates the cell degeneration and may be critical for the transition between the slow physiological and the rapid pathological degeneration of DA cells, particularly when it activates microglial cells of the medial forebrain bundle near dopaminergic axons. As synaptic debris produced by DA cell degeneration may trigger the parkinsonian neuroinflammation, this study investigated the removal of axonal debris produced by retrograde degeneration of DA cells, paying particular attention to the relative roles of astrocytes and microglia. Methods Rats and mice were injected in the lateral ventricles with 6-hydroxydopamine, inducing a degeneration of dopaminergic synapses in the striatum which was not accompanied by non-selective tissue damage, microgliosis or neuroinflammation. The possible retrograde degeneration of dopaminergic axons, and the production and metabolization of DA-cell debris were studied with immunohistochemical methods and analyzed in confocal and electron microscopy images. Results The selective degeneration of dopaminergic synapses in the striatum was followed by a retrograde degeneration of dopaminergic axons whose debris was found within spheroids of the medial forebrain bundle. These spheroids retained mitochondria and most (e.g., tyrosine hydroxylase, the dopamine transporter protein, and amyloid precursor protein) but not all (e.g., α-synuclein) proteins of the degenerating dopaminergic axons. Spheroids showed initial (autophagosomes) but not late (lysosomes) components of autophagy (incomplete autophagy). These spheroids were penetrated by astrocytic processes of the medial forebrain bundle, which provided the lysosomes needed to continue the degradation of dopaminergic debris. Finally, dopaminergic proteins were observed in the cell somata of astrocytes. No microgliosis or microglial phagocytosis of debris was observed in the medial forebrain bundle during the retrograde degeneration of dopaminergic axons. Conclusions The present data suggest a physiological role of astrocytic phagocytosis of axonal debris for the medial forebrain bundle astrocytes, which may prevent the activation of microglia and the spread of retrograde axonal degeneration in PD.

scholarly journals Cognitive-Enhancing Effect of Quercetin in a Rat Model of Parkinson's Disease Induced by 6-Hydroxydopamine

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Napatr Sriraksa ◽  
Jintanaporn Wattanathorn ◽  
Supaporn Muchimapura ◽  
Somsak Tiamkao ◽  
Kamoltip Brown ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Spatial Memory ◽  
Rat Model ◽  
Wistar Rats ◽  
Once Daily ◽  
Enhancing Effect ◽  
Neuron Density ◽  
Male Wistar Rats ◽  
6 Hydroxydopamine

Oxidative stress has been reported to induce cognitive impairment in Parkinson's disease. This paper aimed to determine the effect of quercetin, a substance possessing antioxidant activity, on the cognitive function in a rat model of Parkinson's disease. Male Wistar rats, weighing 200–250 g, were orally given quercetin at doses of 100, 200, 300 mg/kg BW once daily for a period of 14 days before and 14 days after the unilateral lesion of right substantia nigra induced by 6-hydroxydopamine (6-OHDA). Their spatial memory was assessed at 7 and 14 days of treatment and neuron density was determined, malondialdehyde (MDA) level, the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were evaluated at the end of the experiment. In addition, the activity of acetylcholinesterase (AChE) was also measured. It was found that all doses of quercetin enhanced spatial memory. Therefore, it is suggested that the cognitive-enhancing effect of quercetin occurs partly because of decreased oxidative damage resulting in increased neuron density.

Methanolic extract of Hibiscus asper leaves improves spatial memory deficits in the 6-hydroxydopamine-lesion rodent model of Parkinson's disease

2011 ◽  
Vol 133 (2) ◽  
pp. 773-779 ◽  
Author(s):  
Harquin Simplice Foyet ◽  
Lucian Hritcu ◽  
Alin Ciobica ◽  
Marius Stefan ◽  
Pierre Kamtchouing ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Spatial Memory ◽  
Methanolic Extract ◽  
Memory Deficits ◽  
Rodent Model ◽  
6 Hydroxydopamine

scholarly journals Neuroprotective Effect of Intrastriatal Caffeic Acid Phenethyl Ester Treatment in 6-OH Dopamine Model of Parkinson’s Disease in Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Burak Cem Soner ◽  
Eda Acikgoz ◽  
Salim Yalcin Inan ◽  
Sule Ayla ◽  
Ayse Saide Sahin ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Caffeic Acid ◽  
Neurodegenerative Disorder ◽  
Neuroprotective Effect ◽  
Caffeic Acid Phenethyl Ester ◽  
Adhesive Tape ◽  
Behavioral Studies ◽  
Male Wistar Rats ◽  
6 Hydroxydopamine

Parkinson’s disease (PD) is the second most common neurodegenerative disorder, and the main cause of PD is still not known. Until now, no cure for Parkinson’s disease is yet in sight. Caffeic acid phenethyl ester (CAPE) is a polyphenolic component of the propolis, which can be derived from honeybee hive propolis. We aimed to determine the effect of intrastriatal CAPE administration as a neuroprotective agent on 6-hydroxydopamine (6-OHDA)-induced PD model. Adult male Wistar rats weighing 280–320 g were used. The PD model was induced with unilateral intrastriatal 6-OHDA injection. Treatment groups received 20 μmol/5 μL/4 day and 80 μmol/5 μL/4 day CAPE 24 h after 6-OHDA injection. Eight days after 6-OHDA application, behavioral studies (adhesive tape removal test, open-field test, cylinder test, and apomorphine-induced asymmetric rotational behavior) were performed once more to compare the effects of CAPE on behavior tests. Striatal histological verifications, immunohistochemistry, and stereological quantitation were performed. Our results for the first time showed that, besides improving the motor performance, CAPE treatment also prevents 6-OHDA-induced loss of TH-positive neurons. From our results, CAPE may be a promising clinical agent in the treatment of PD.

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