Neuroprotective effects of catechins in an experimental Parkinson’s disease model and SK-N-AS cells: evaluation of cell viability, anti-inflammatory and anti-apoptotic effects

2022 ◽  
pp. 1-13
Author(s):  
Gülşen Özduran ◽  
Eda Becer ◽  
Hafize Seda Vatansever ◽  
Sevinç Yücecan
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Viability ◽  
Disease Model ◽  
Neuroprotective Effects ◽  
Anti Inflammatory ◽  
Apoptotic Effects

scholarly journals Chronic Systemic Inflammation Exacerbates Neurotoxicity in a Parkinson’s Disease Model

2020 ◽  
Vol 2020 ◽  
pp. 1-19 ◽  
Author(s):  
Perla Ugalde-Muñiz ◽  
Ingrid Fetter-Pruneda ◽  
Luz Navarro ◽  
Esperanza García ◽  
Anahí Chavarría
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Viability ◽  
Systemic Inflammation ◽  
Disease Model ◽  
Adequate Model ◽  
Mao B ◽  
Mptp Administration ◽  
Inflammatory Profile ◽  
The Impact

Systemic inflammation is a crucial factor for microglial activation and neuroinflammation in neurodegeneration. This work is aimed at assessing whether previous exposure to systemic inflammation potentiates neurotoxic damage by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and how chronic systemic inflammation participates in the physiopathological mechanisms of Parkinson’s disease. Two different models of systemic inflammation were employed to explore this hypothesis: a single administration of lipopolysaccharide (sLPS; 5 mg/kg) and chronic exposure to low doses (mLPS; 100 μg/kg twice a week for three months). After three months, both groups were challenged with MPTP. With the sLPS administration, Iba1 staining increased in the striatum and substantia nigra, and the cell viability lowered in the striatum of these mice. mLPS alone had more impact on the proinflammatory profile of the brain, steadily increasing TNFα levels, activating microglia, reducing BDNF, cell viability, and dopamine levels, leading to a damage profile similar to the MPTP model per se. Interestingly, mLPS increased MAO-B activity possibly conferring susceptibility to MPTP damage. mLPS, along with MPTP administration, exacerbated the neurotoxic effect. This effect seemed to be coordinated by microglia since minocycline administration prevented brain TNFα increase. Coadministration of sLPS with MPTP only facilitated damage induced by MPTP without significant change in the inflammatory profile. These results indicate that chronic systemic inflammation increased susceptibility to MPTP toxic effect and is an adequate model for studying the impact of systemic inflammation in Parkinson’s disease.

scholarly journals Exercise exerts neuroprotective effects on Parkinson's disease model of rats

2010 ◽  
Vol 1310 ◽  
pp. 200-207 ◽  
Author(s):  
Naoki Tajiri ◽  
Takao Yasuhara ◽  
Tetsuro Shingo ◽  
Akihiko Kondo ◽  
Wenji Yuan ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Disease Model ◽  
Neuroprotective Effects

Neuroprotective effects of ginkgetin against neuroinjury in Parkinson's disease model induced by MPTP via chelating iron

2015 ◽  
Vol 49 (9) ◽  
pp. 1069-1080 ◽  
Author(s):  
Y.-Q. Wang ◽  
M.-Y. Wang ◽  
X.-R. Fu ◽  
Peng-Yu ◽  
G.-F. Gao ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Disease Model ◽  
Neuroprotective Effects

scholarly journals Neuroprotective Effects of Bak Foong Pill in 1-Methyl-4-phenyl-1,2,3,6-tetrahyrdropyridine (MPTP)-Induced Parkinson's Disease Model Mice

2004 ◽  
Vol 27 (8) ◽  
pp. 1245-1250 ◽  
Author(s):  
Bin Liu ◽  
Jun Xia Xie ◽  
Dewi Kenneth Rowlands ◽  
Yu Lin Gou ◽  
Ching Cheong Leung ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Disease Model ◽  
Neuroprotective Effects

scholarly journals Pentoxifylline Neuroprotective Effects Are Possibly Related to Its Anti-Inflammatory and TNF-Alpha Inhibitory Properties, in the 6-OHDA Model of Parkinson’s Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-15 ◽  
Author(s):  
Kelly Rose Tavares Neves ◽  
Hélio Vitoriano Nobre ◽  
Luzia Kalyne A. M. Leal ◽  
Geanne Matos de Andrade ◽  
Gerly Anne de Castro Brito ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neuroprotective Effect ◽  
Phosphodiesterase Inhibitor ◽  
Tnf Alpha ◽  
Neuroprotective Effects ◽  
Neuronal Viability ◽  
Male Wistar Rats ◽  
Cox 2 ◽  
Anti Inflammatory

Pentoxifylline (PTX) is a phosphodiesterase inhibitor with anti-TNF-alpha activity, associated with its anti-inflammatory action. Considering Parkinson’s disease (PD) as a neuroinflammatory disorder, the objectives were to evaluate PTX neuroprotective properties, in a model of PD. Male Wistar rats, divided into sham-operated (SO), untreated 6-OHDA, and 6-OHDA treated with PTX (10, 25, and 50 mg/kg) groups, received a unilateral 6-OHDA injection, except the SO group administered with saline. Treatments started 24 h after surgery and continued for 15 days when the animals were submitted to apomorphine-induced rotations, open field, and forced swimming tests. At the next day, they were euthanized and their striata processed for neurochemical (DA and DOPAC determinations), histological, and immunohistochemical (Fluoro-Jade, TH, DAT, OX-42, TNF-alpha, COX-2, and iNOS) studies. PTX reversed the behavioral changes observed in the untreated 6-OHDA animals. Furthermore, PTX partially reversed the decrease in DA contents and improved neuronal viability. In addition, decreases in immunostaining for TH and dopamine transporter (DAT) were reversed. The untreated 6-OHDA group showed intense OX-42, TNF-alpha, COX-2, and iNOS immunoreactivities, which were attenuated by PTX. In conclusion, we demonstrated a neuroprotective effect of PTX, possibly related to its anti-inflammatory and antioxidant actions, indicating its potential as an adjunct treatment for PD.

scholarly journals The Neuroprotective Effects of Cannabis-Derived Phytocannabinoids and Resveratrol in Parkinson’s Disease: A Systematic Literature Review of Pre-Clinical Studies

2021 ◽  
Vol 11 (12) ◽  
pp. 1573
Author(s):  
Samay Prakash ◽  
Wayne G. Carter
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Unmet Need ◽  
Neuroprotective Agents ◽  
Eligibility Criteria ◽  
Neuroprotective Effects ◽  
In Vivo Models ◽  
Anti Inflammatory ◽  
Nigral Degeneration

Currently, there are no pharmacological treatments able to reverse nigral degeneration in Parkinson’s disease (PD), hence the unmet need for the provision of neuroprotective agents. Cannabis-derived phytocannabinoids (CDCs) and resveratrol (RSV) may be useful neuroprotective agents for PD due to their anti-oxidative and anti-inflammatory properties. To evaluate this, we undertook a systematic review of the scientific literature to assess the neuroprotective effects of CDCs and RSV treatments in pre-clinical in vivo animal models of PD. The literature databases MEDLINE, EMBASE, PsychINFO, PubMed, and Web of Science core collection were systematically searched to cover relevant studies. A total of 1034 publications were analyzed, of which 18 met the eligibility criteria for this review. Collectively, the majority of PD rodent studies demonstrated that treatment with CDCs or RSV produced a significant improvement in motor function and mitigated the loss of dopaminergic neurons. Biochemical analysis of rodent brain tissue suggested that neuroprotection was mediated by anti-oxidative, anti-inflammatory, and anti-apoptotic mechanisms. This review highlights the neuroprotective potential of CDCs and RSV for in vivo models of PD and therefore suggests their potential translation to human clinical trials to either ameliorate PD progression and/or be implemented as a prophylactic means to reduce the risk of development of PD.

scholarly journals Hesperetin protects SH-SY5Y cells against 6- hydroxydopamine-induced neurotoxicity via activation of NRF2/ARE signaling pathways

2020 ◽  
Vol 19 (6) ◽  
pp. 1197-1201 ◽  
Author(s):  
Jing Li ◽  
Yue Liu ◽  
Li Wang ◽  
Zhaowei Gu ◽  
Zhigang Huan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Viability ◽  
Heme Oxygenase 1 ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Ldh Release ◽  
6 Hydroxydopamine

Purpose: To investigation the protective effects of hesperetin against 6-hydroxydopamine (6-OHDA)- induced neurotoxicity. Methods: SH-SY5Y cells were incubated with 6-OHDA to create an in vitro model of neurotoxicity. This model was used to test the neuroprotective effects of hesperetin. Cell viability was assessed by MTT and lactate dehydrogenase (LDH) release assays. Flow cytometry and western blot were used to quantify apoptosis. Oxidative stress was evaluated by determining intracellular glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), and reactive oxygen species (ROS). Results: In SH-SY5Y cells, treatment with 6-OHDA decreased cell viability and promoted LDH release. However, exogenous hesperetin protected against 6-OHDA-mediated toxicity. Similarly, although incubation with 6-OHDA induced apoptosis and increased cleaved caspase-3 and -9 levels, treatment with hesperetin protected against these effects. Treatment with 6-OHDA also led to significant oxidative stress, as indicated by reduced GSH and SOD levels and increased MDA and ROS levels in SH-SY5Y cells. However, these changes were reversed by pre-treatment with hesperetin. Of interest, hesperetin led to changes in 6-OHDA-induced expression of NRF2, heme oxygenase-1 (HO-1), glutamate-cysteine ligase (GCL) catalytic subunit (GCLC), and GCL modulatory (GCLM). Conclusion: Hesperetin protects against cell toxicity, apoptosis, and oxidative stress via activation of NRF2 pathway in a 6-OHDA-induced model of neurotoxicity. Future studies should investigate the use of hesperetin as a potential therapeutic approach for prevention or management of Parkinson’s disease. Keywords: Hesperetin, 6-OHDA, Neurotoxicity, NRF2, Parkinson’s disease

Aspidosperma pyrifoliumMart: neuroprotective, antioxidant and anti-inflammatory effects in a Parkinson's disease model in rats

2018 ◽  
Vol 70 (6) ◽  
pp. 787-796 ◽  
Author(s):  
Dayane P. de Araújo ◽  
Patrícia C.N. Nogueira ◽  
Alan Diego C. Santos ◽  
Roberta de Oliveira Costa ◽  
Jalles D. de Lucena ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Disease Model ◽  
Anti Inflammatory

scholarly journals Gastrodin Protects Apoptotic Dopaminergic Neurons in a Toxin-Induced Parkinson’s Disease Model

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Hemant Kumar ◽  
In-Su Kim ◽  
Sandeep Vasant More ◽  
Byung-Wook Kim ◽  
Young-Yil Bahk ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopaminergic Neurons ◽  
Disease Model ◽  
Motor Impairment ◽  
Protective Effects ◽  
Dopamine Depletion ◽  
Active Constituent ◽  
Neuroprotective Effects ◽  
Phenolic Glucoside

Gastrodia elata(GE) Blume is one of the most important traditional plants in Oriental countries and has been used for centuries to improve various conditions. The phenolic glucoside gastrodin is an active constituent of GE. The aim of this study was to investigate the neuroprotective role of gastrodin in 1-methyl-4-phenylpyridinium (MPP+)/1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine- (MPTP) induced human dopaminergic SH-SY5Y cells and mouse model of Parkinson’s disease (PD), respectively. Gastrodin significantly and dose dependently protected dopaminergic neurons against neurotoxicity through regulating free radicals, Bax/Bcl-2 mRNA, caspase-3, and cleaved poly(ADP-ribose) polymerase (PARP) in SH-SY5Y cells stressed with MPP+. Gastrodin also showed neuroprotective effects in the subchronic MPTP mouse PD model by ameliorating bradykinesia and motor impairment in the pole and rotarod tests, respectively. Consistent with this finding, gastrodin prevented dopamine depletion and reduced reactive astrogliosis caused by MPTP as assessed by immunohistochemistry and immunoblotting in the substantiae nigrae and striatata of mice. Moreover, gastrodin was also effective in preventing neuronal apoptosis by attenuating antioxidant and antiapoptotic activities in these brain areas. These results strongly suggest that gastrodin has protective effects in experimental PD models and that it may be developed as a clinical candidate to ameliorate PD symptoms.

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