scholarly journals Neuroprotective Effect of Schisandra Chinensis on Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Induced Parkinsonian Syndrome in C57BL/6 Mice

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1671 ◽  
Author(s):  
Chi-Lin Li ◽  
Yang-Hwei Tsuang ◽  
Tung-Hu Tsai

Schisandra chinensis (Turcz.) Baill. (S. chinensis) is a well-known botanical medicine and nutritional supplement that has been shown to have potential effects on neurodegeneration. To investigate the potential neuroprotective effect of S. chinensis fruit extract, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was used to induce behavioral disorders and dopaminergic neuronal damage in mice, and biochemical indicators were examined. Male C57BL/6 mice were used to establish the MPTP-induced parkinsonian syndrome model. Open field and rotarod tests were performed to evaluate the overall manifestation of motor deficits and rodent motor coordination. The mice were divided into 8 groups as follows: normal control; MPTP alone (25 mg/kg, i.p.); S. chinensis extract pretreatment (0.5, 1.5, 5 g/kg, p.o.); and S. chinensis extract treatment (0.5, 1.5, 5 g/kg, p.o.). Liquid chromatography coupled to electrochemical detection was used to monitor neurochemicals in the striatum. Tyrosine hydroxylase content was measured by immunohistochemistry, and biochemical antioxidative indicators were used to evaluate the potential neuroprotective effects of S. chinensis fruit extract. The results demonstrated that treatment with S. chinensis fruit extract ameliorated MPTP-induced deficits in behavior, exercise balance, dopamine level, dopaminergic neurons, and tyrosine hydroxylase-positive cells in the striatum of mice. Among the pretreated and treatment groups, a high dose of S. chinensis fruit extract was the most effective treatment. In conclusion, S. chinensis fruit extract is a potential herbal drug candidate for the amelioration and prevention of Parkinson’s disease.

2013 ◽  
pp. 313-321 ◽  
Author(s):  
M. A. FAHIM ◽  
S. SHEHAB ◽  
A. NEMMAR ◽  
A. ADEM ◽  
S. DHANASEKARAN ◽  
...  

The use of the herbicide paraquat (1,1'-dimethyl-4,4'-bipyridylium dichloride; PQ) which is widely used in agriculture is known to cause dopaminergic neurotoxicity. However, the mechanisms underlying this effect are not fully understood. This present study investigated the behavioral manifestations, motor coordination, and dopaminergic neurodegeneration following exposure to PQ. Male rats were injected with PQ (10 mg/kg i.p.) daily for three weeks. Rotarod systems were used for measuring locomotor activity and motor coordination. The effects of PQ on dorsiflexor, electrophysiologically-induced muscle contraction were studied. Dopamine concentrations in the ventral mesencephalon were measured by high performance liquid chromatography and the number of dopaminergic neurons in substantia nigra pars compacta was estimated by tyrosine hydroxylase immunohistochemistry. PQ induced difficulty in movement and significant reduction in motor activity and twitch tension at the dorsiflexor skeletal muscle. The number of tyrosine hydroxylase positive neurons was significantly less in the substantia nigra pars compacta and nigral dopamine level was significantly reduced in PQ treated animals (20.4±3.4 pg/mg) when compared with control animals (55.0±2.4 pg/mg wet tissue). Daily treatment of PQ for three weeks induces selective dopaminergic neuronal loss in the substantia nigra and significant behavioral and peripheral motor deficit effects.


2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Reas S. Khan ◽  
Kimberly Dine ◽  
John G. Geisler ◽  
Kenneth S. Shindler

The ability of novel mitochondrial uncoupler prodrug of 2,4-dinitrophenol (DNP), MP201, to prevent neuronal damage and preserve visual function in an experimental autoimmune encephalomyelitis (EAE) model of optic neuritis was evaluated. Optic nerve inflammation, demyelination, and axonal loss are prominent features of optic neuritis, an inflammatory optic neuropathy often associated with the central nervous system demyelinating disease multiple sclerosis. Currently, optic neuritis is frequently treated with high-dose corticosteroids, but treatment fails to prevent permanent neuronal damage and associated vision changes that occur as optic neuritis resolves, thus suggesting that additional therapies are required. MP201 administered orally, once per day, attenuated visual dysfunction, preserved retinal ganglion cells (RGCs), and reduced RGC axonal loss and demyelination in the optic nerves of EAE mice, with limited effects on inflammation. The prominent mild mitochondrial uncoupling properties of MP201, with slow elimination of DNP, may contribute to the neuroprotective effect by modulating the entire mitochondria’s physiology directly. Results suggest that MP201 is a potential novel treatment for optic neuritis.


2021 ◽  
Vol 10 (4) ◽  
pp. 468-475
Author(s):  
Sradhasini Rout ◽  
Bandana Rath ◽  
Subrat Kumar Bhattamisra ◽  
Anjan Kumar ◽  
Ishani Rath ◽  
...  

Introduction: The pathogenesis of Parkinson’s disease (PD) is multifactorial in which oxidative stress, neuroinflammation, and mitochondrial dysfunction are the leading factors. Currently, the antioxidant and anti-inflammatory agents of natural sources as neuroprotectants have raised much attention. The current study aimed to explore the neuroprotective effect of methanolic extract of Sargassum wightii in male Wistar albino rats against rotenone-induced PD. Methods: The rats were administered with rotenone (10 mg/kg orally) daily for 28 days to induce PD. S. wightii (200 mg/kg and 400 mg/kg) and levodopa+carbidopa combination (10 mg/kg) were administered to different groups of rats one hour prior to rotenone for 28 days. Behavioral parameters (akinesia, tremor, motor coordination, and locomotor activities) and body weight were recorded on days 14th and 28th of drug treatment. On the 28th day, the animals were sacrificed for the neurobiochemical analyses of brain tissue. Results: Rotenone treatment caused a significant reduction in behavioural parameters (P < 0.001), neurochemical deficits (P < 0.001), and elevation of oxidative stress markers (P < 0.001) in the brain. Pre-treatment with S. wightii at 200 mg/kg and 400 mg/kg doses significantly attenuated the rotenone-induced behavioral alterations and restored the mitochondrial NADH dehydrogenase activity and dopamine level in the striatum (P < 0.001). Moreover, 400 mg/kg of S. wightii restored the rotenone-induced increased oxidative stress markers like malondialdehyde (MDA), superoxide dismutase (SOD), and reduced glutathione (GSH) in the striatum (P < 0.01). Conclusion: S. wightii has provided a neuroprotective effect, probably by virtue of its antioxidant and dopamine restoring potential. Hence, it may offer a promising and new therapeutic lead for the treatment of PD but needs further research.


2021 ◽  
Author(s):  
Amandeep Kaur ◽  
Gagandeep Jaiswal ◽  
Jasdeep Brar ◽  
Puneet Kumar

Abstract Traumatic brain injury (TBI) is an insult to the brain from an external mechanical force, leading to temporary/permanent secondary injuries, i.e. impairment of cognitive, physical, and psycho-social functions with altered consciousness. The leading mechanism responsible for neuronal damage following TBI is an increase in oxidative reactions initiated by free radicals generated by the injury along with various other mechanisms. Nerolidol is reported to have potent antioxidant and anti-neuroinflammatory properties. The present study was designed to explore the neuroprotective effect of nerolidol in weight-drop-induced TBI in rats. Animals were injured on the 1st day by dropping a free-falling weight of 200 gm from a height of 1 m through a guide pipe onto the exposed skull. After 14 days of injury, nerolidol (25, 50, and 100 mg/kg, i.p.) treatment was given for the next 14 days. Locomotor activity and motor coordination were evaluated using an actophotometer and rotarod, respectively. Cognitive impairment was observed through the Morris Water Maze and Object Recognition Test. On the 29th day, animals were sacrificed, and their brains were collected for the biochemical estimation. The weight drop model significantly decreased locomotor activity, motor coordination, increased Acetylcholinesterase (AChE) activity, oxidative stress, and induced cognitive deficits in TBI rats. Nerolidol significantly improved locomotor activity, reversed motor incoordination and cognitive impairment, and reduced the AChE activity and oxidative/nitrosative stress. The present study demonstrates the promising neuroprotective effects of nerolidol, which might improve the quality of life of TBI patients.


Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 620
Author(s):  
Dalia M. Kopustinskiene ◽  
Jurga Bernatoniene

Schisandra chinensis Turcz. (Baill.) fruits, their extracts, and bioactive compounds are used in alternative medicine as adaptogens and ergogens protecting against numerous neurological, cardiovascular, gastrointestinal, liver, and skin disorders. S. chinensis fruit extracts and their active compounds are potent antioxidants and mitoprotectors exerting anti-inflammatory, antiviral, anticancer, and anti-aging effects. S. chinensis polyphenolic compounds—flavonoids, phenolic acids and the major constituents dibenzocyclooctadiene lignans are responsible for the S. chinensis antioxidant activities. This review will focus on the direct and indirect antioxidant effects of S. chinensis fruit extract and its bioactive compounds in the cells during normal and pathological conditions.


2009 ◽  
Vol 110 (3) ◽  
pp. 529-537 ◽  
Author(s):  
Irina Lasarzik ◽  
Uta Winkelheide ◽  
Sonja Stallmann ◽  
Christian Orth ◽  
Astrid Schneider ◽  
...  

Background Postischemic endogenous neurogenesis can be dose-dependently modulated by volatile anesthetics. The intravenous anesthetic propofol is used during operations with a risk of cerebral ischemia, such as neurosurgery, cardiac surgery, and vascular surgery. The effects of propofol on neurogenesis are unknown and, therefore, the object of this study. Methods Eighty male Sprague-Dawley rats were randomly assigned to treatment groups with propofol administration for 3 h: 36 mg x kg(-1) x h(-1) propofol with or without cerebral ischemia and 72 mg x kg(-1) x h(-1) propofol with or without cerebral ischemia. In addition, 7 rats with propofol administration for 6 h and 14 treatment-naive rats were investigated. Forebrain ischemia was induced by bilateral carotid artery occlusion and hemorrhagic hypotension. Animals received 5-bromo-2-deoxyuridine for 7 days. 5-Bromo-2-deoxyuridine-positive neurons were counted in the dentate gyrus after 9 and 28 days. Spatial learning in the Barnes maze and histopathologic damage of the hippocampus were analyzed. Results Propofol revealed no impact on basal neurogenesis. Cerebral ischemia increased the amount of new neurons. After 28 days, neurogenesis significantly increased in animals with low-dose propofol administered during cerebral ischemia compared with naive animals, whereas no significant difference was observed in animals with high-dose propofol during ischemia. Neuronal damage in the CA3 region was increased at 28 days with high-dose propofol. Postischemic deficits in spatial learning were not affected by propofol. Conclusions Independent effects of propofol are difficult to ascertain. Peri-ischemic propofol administration may exert secondary effects on neurogenesis by modulating the severity of histopathologic injury and thereby regenerative capacity of the hippocampus.


2017 ◽  
Vol 26 (6) ◽  
pp. 1709-1714
Author(s):  
Su-Jung Cho ◽  
Hye-Jin Kim ◽  
Ji-Young Choi ◽  
Eun-Young Kwon ◽  
Ye Jin Kim ◽  
...  

Toxins ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 708
Author(s):  
Eduardo Rivadeneyra-Domínguez ◽  
José Eduardo Pérez-Pérez ◽  
Alma Vázquez-Luna ◽  
Rafael Díaz-Sobac ◽  
Juan Francisco Rodríguez-Landa

Cassava (Manihot esculenta Crantz) is a plant that contains neurotoxins such as linamarin and lotaustraline. Its long-term consumption is associated with neuronal damage and contributes to the development of motor impairment in humans and rats. We investigated the effects of the consumption of cassava juice on renal and hepatic function and motor impairments in male rats. The rats received the vehicle, non-toxic and toxic doses of cassava juice, or linamarin as a pharmacological control, over 35 consecutive days. The effects were evaluated in an open field test, rotarod, and swim test. The toxic cassava dose and linamarin resulted in motor impairments in the rotarod and swim test from day 7 of treatment. The toxic cassava dose and linamarin increased the parameters that indicate renal and hepatic damage, with the exception of total protein and albumin levels. Behavioral variables that show motor incoordination (i.e., latency to fall in the rotarod) were negatively correlated with biochemical parameters of renal and kidney damage, whereas spin behavior was positively correlated. Our data indicate that chronic oral consumption of cassava juice caused renal and hepatic damage that was correlated with motor coordination impairment in rats, similarly to their principal neurotoxic compound, linamarin.


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