scholarly journals Protective effect of CoQ10 and Artemisia sieberi combination on PC12 cells model of 6-hydroxydopamine induced toxicity

2020 ◽  
Vol 24 (4) ◽  
pp. 257-267
Author(s):  
Seyed Behnamedin Jameie ◽  
◽  
Mona Farhadi ◽  
Kamelia Gharibzad ◽  
◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Antioxidant Properties ◽  
Combination Method ◽  
Ros Generation ◽  
Therapeutic Effects ◽  
Neuroprotective Effects ◽  
P53 Expression ◽  
Artemisia Sieberi ◽  
Hoechst Staining ◽  
6 Hydroxydopamine

Introduction: Parkinson's disease (PD) is a progressive neurodegenerative disease that affects motor function. The etiology of PD is unknown and routine therapies temporarily relieve the symptoms. Neuroprotective based therapies preserve the remaining neurons and prevent the progression of PD. Artemisia sieberi has anti-cancer and neuroprotective effects. The CoQ10 also is an antioxidant that has proven anti-inflammatory and antioxidant properties. In order to study the effect of Artemisia and CoQ10 on the PD cellular model, the present research was designed. Methods: PC12 cells were treated with different concentrations of 6-hydroxydopamine. Then the cells divided into the control (cells were not treated), DMSO group and experimental groups treated with the different concentrations of Artemisia sieberi extracts, CoQ10 and combination of them for 24h. The viability of the cells, reactive oxygen species (ROS) generation and p53 expression were evaluated. Results: Artemisia at a concentration of 200μg/ml and CoQ10 at a concentration of 75μg/ml significantly increased cell viability in the treated groups after 24h. Their combination showed better and more significant results compared to each alone. Hoechst staining showed significantly reduced apoptosis in treated cells. ROS generation reduced in the treated groups with better results for the combination-treated groups. The same results acquired for the expression of P53 in the treated cells. Conclusion: Regarding the results of both Artemisia and CoQ10, it could be concluded that they act synergistically with possible similar pathways. Although the Artemisia itself showed significant results, it seems that the combination method might have more therapeutic effects.

scholarly journals Echinacoside Protects against 6-Hydroxydopamine-Induced Mitochondrial Dysfunction and Inflammatory Responses in PC12 Cells via Reducing ROS Production

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Yue-Hua Wang ◽  
Zhao-Hong Xuan ◽  
Shuo Tian ◽  
Guan-Hua Du
Keyword(s):  
Mitochondrial Dysfunction ◽  
Pc12 Cells ◽  
Inflammatory Responses ◽  
Neurodegenerative Disorder ◽  
Cell Damage ◽  
Underlying Mechanism ◽  
Ros Production ◽  
Neuroprotective Effects ◽  
Reduction Activity ◽  
6 Hydroxydopamine

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic (DA) neurons at the substantia nigra. Mitochondrial dysfunction and inflammatory responses are involved in the mechanism of cell damage in PD. 6-Hydroxydopamine (6-OHDA), a dopamine analog, specifically damages dopaminergic neurons. Echinacoside (ECH) is a phenylethanoid glycoside isolated from the stems ofCistanche salsa, showing a variety of neuroprotective effects in previous studies. The present study was to investigate its effect against 6-OHDA-induced neurotoxicity and possible mechanisms in PC12 cells. The results showed that 6-OHDA reduced cell viability, decreased oxidation-reduction activity, decreased mitochondrial membrane potential, and induced mitochondria-mediated apoptosis compared with untreated PC12 cells. However, echinacoside treatment significantly attenuated these changes induced by 6-OHDA. In addition, echinacoside also could significantly alleviate the inflammatory responses induced by 6-OHDA. Further research showed that echinacoside could reduce 6-OHDA-induced ROS production in PC12 cells. These results suggest that the underlying mechanism of echinacoside against 6-OHDA-induced neurotoxicity may be involve in attenuating mitochondrial dysfunction and inflammatory responses by reducing ROS production.

scholarly journals Dexmedetomidine exerts neuroprotective effects during high glucose-induced neural injury by inhibiting miR-125b

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Xiaolai Hou ◽  
Fenlan Xu ◽  
Cheng Zhang ◽  
Jianzhong Shuai ◽  
Zhenhua Huang ◽  
...  
Keyword(s):  
Diabetic Neuropathy ◽  
Pc12 Cells ◽  
High Glucose ◽  
Antioxidant Properties ◽  
Protective Role ◽  
Neural Cells ◽  
Dependent Manner ◽  
Neural Injury ◽  
Neuroprotective Effects ◽  
Potential Therapeutic Application

Abstract Diabetic neuropathy (DNP) is the most common complication of diabetes mellitus affecting approximately 50% of diabetes patients. Studying the effect of potential drugs with antioxidant properties and minimal toxicities on neural cells may lead to the development of new and safe pharmacotherapy. Dexmedetomidine (DEX), a highly selective α2-adrenoceptor agonist, is a clinically used sedative also known to have neural protection effect. In the present study, we aimed to investigate the protective role of DEX in high glucose (HG)-induced neural injury and its potential miRNA-related mechanisms. Our results showed that DEX exerted neuroprotective effects during high glucose-induced damage to PC12 cells in a dose-dependent manner. DEX restored cell viability and repressed LDH, Caspase-3 activity, ROS production, and cell apoptosis in HG-treated PC12 cells. MiR-125b-5p was significantly up-regulated in PC12 cells upon HG treatment and it was demonstrated as an target for DEX. The neuroprotective effects of DEX on HG-induced cellular injury were reversed through miR-125b-5p overexpression, and vitamin D receptor (VDR) is a direct targeted of the miR-125b-5p. Together, our results indicate that DEX displays neuroprotective effects on PC-12 cells under high glucose through regulating miR-125b-5p/VDR axis. Our findings might raise the possibility of potential therapeutic application of DEX for managing diabetic neuropathy neural injuries.

scholarly journals Neuroprotective Effects of Cuscutae Semen in a Mouse Model of Parkinson’s Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Minsook Ye ◽  
Seul gi Lee ◽  
Eun Sook Chung ◽  
Su-jin Lim ◽  
Won Seob Kim ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Glutathione Peroxidase ◽  
Pc12 Cells ◽  
Statistical Significance ◽  
Inhibitory Effect ◽  
Ros Generation ◽  
Neuroprotective Effects ◽  
Differentiated Pc12 Cells

Parkinson’s disease (PD) is a neurodegenerative movement disorder that is characterized by the progressive degeneration of the dopaminergic (DA) pathway. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes damage to the DA neurons, and 1-4-methyl-4-phenylpyridinium (MPP+) causes cell death in differentiated PC12 cells that is similar to the degeneration that occurs in PD. Moreover, MPTP treatment increases the activity of the brain’s immune cells, reactive oxygen species- (ROS-) generating processes, and glutathione peroxidase. We recently reported that Cuscutae Semen (CS), a widely used traditional herbal medicine, increases cell viability in a yeast model of PD. In the present study, we examined the inhibitory effect of CS on the neurotoxicity of MPTP in mice and on the MPP+-induced cell death in differentiated PC12 cells. The MPTP-induced loss of nigral DA neurons was partly inhibited by CS-mediated decreases in ROS generation. The activation of microglia was slightly inhibited by CS, although this effect did not reach statistical significance. Furthermore, CS may reduce the MPP+ toxicity in PC12 cells by suppressing glutathione peroxidase activation. These results suggest that CS may be beneficial for the treatment of neurodegenerative diseases such as PD.

scholarly journals Cortex Fraxini (Qingpi) Protects Rat Pheochromocytoma Cells against 6-Hydroxydopamine-Induced Apoptosis

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Jing-Jie Li ◽  
Shi-Ya Zhou ◽  
Huan Zhang ◽  
Kim-Hung Lam ◽  
Simon Ming-Yuen Lee ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Pc12 Cells ◽  
Neurodegenerative Disorder ◽  
Antioxidant Properties ◽  
Radical Scavenging ◽  
Water Extract ◽  
Total Phenolic ◽  
Potential Candidate ◽  
Induced Apoptosis ◽  
6 Hydroxydopamine

Parkinson’s disease (PD) is a chronic neurodegenerative disorder having close relationship with oxidative stress induced by reactive oxygen species (ROS). Cortex Fraxini (QP) is a kind of traditional Chinese medicinal herb with antioxidant properties. It may be a potential candidate for preventing the development of chronic neurodegenerative diseases. Thus, the key objective of the current study was to investigate the neuroprotective effect of QP water extract on 6-hydroxydopamine (6-OHDA) induced apoptosis in rat pheochromocytoma (PC12) cells. It was found that QP water extract possesses strong antioxidant property with SC50= 0.15 mg/mL. Total phenolic content of QP water extract was found to be 200.78 ± 2.65 mg GAE/g. QP water extract’s free radical scavenging capacity was demonstrated by reversing the increased level of intracellular ROS induced by 6-OHDA, using 2′,7′-dichlorodihydrofluorescein diacetate. Moreover, QP water extract (0.5 mg/mL) could remarkably increase the viability of PC12 cells treated with 6-OHDA. The protective effect of QP water extract was found to be via inhibiting MEK/ERK pathway and reversing PI3-K/Akt/GSK3βpathway. The current results suggest that QP might be a potential candidate for preventing the development of neurodegenerative diseases, such as PD.

Protective Effect of Schisandrin on Hydrogen Peroxide-Induced Damage in PC12 Cells

2013 ◽  
Vol 750-752 ◽  
pp. 1545-1548
Author(s):  
Kuang Ren ◽  
Yan Chun Wang ◽  
Hong Yan Fan
Keyword(s):  
Protein Expression ◽  
Pc12 Cells ◽  
Antioxidant Properties ◽  
Immunocytochemical Staining ◽  
Potential Candidate ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Pre Treatment ◽  
Vitro Model

In this study, schisandrin was assessed for potential protective effects on pheochromocytoma cell line (PC12 cells). Using PC12 cells damage induced by H2O2(25μmol/L) as in vitro model. After pre-treatment with different concentration of schisandrin (0.3, 0.6, 1.2μM) for 24h, MTT assay was used to detect the cell viability, the supernatant of cells was collected to examine the levels of nitric oxide (NO) in each sample, and immunocytochemical staining was adopted to observe the expression levels of bcl-2. Results showed that schisandrin at different concentrations could increase the viability of PC12 cells and decrease the levels of NO in the culture medium. There were significant differences between schisandrin group and H2O2group (P<0.05,P<0.01). Immunocytochemical staining result revealed that schisandrin could upregulate bcl-2 protein expression. In summary, schisandrin shown significant neuroprotective effects on H2O2-injured PC12 cells through antioxidant properties and upregulate bcl-2 protein expression, and could be a potential candidate for intervention in neurodegenerative diseases.

Cordycepin protects PC12 cells against 6-hydroxydopamine induced neurotoxicity via its antioxidant properties

2016 ◽  
Vol 81 ◽  
pp. 7-14 ◽  
Author(s):  
Opeyemi J. Olatunji ◽  
Yan Feng ◽  
Oyenike O. Olatunji ◽  
Jian Tang ◽  
Zhen Ouyang ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Antioxidant Properties ◽  
6 Hydroxydopamine

scholarly journals Neuroprotective Effects of Glochidion zeylanicum Leaf Extract against H2O2/Glutamate-Induced Toxicity in Cultured Neuronal Cells and Aβ-Induced Toxicity in Caenorhabditis elegans

Biology ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 800
Author(s):  
Chatrawee Duangjan ◽  
Panthakarn Rangsinth ◽  
Shaoxiong Zhang ◽  
Xiaojie Gu ◽  
Michael Wink ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Leaf Extract ◽  
Neuronal Cells ◽  
Antioxidant Properties ◽  
Ros Generation ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Antioxidant Genes ◽  
Age Related

Oxidative stress plays a crucial role in the development of age-related neurodegenerative diseases. Previously, Glochidion zeylanicum methanol (GZM) extract has been reported to have antioxidant and anti-aging properties. However, the effect of GZM on neuroprotection has not been reported yet; furthermore, the mechanism involved in its antioxidant properties remains unresolved. The study is aimed to demonstrate the neuroprotective properties of GZM extract and their underlying mechanisms in cultured neuronal (HT-22 and Neuro-2a) cells and Caenorhabditis elegans models. GZM extract exhibited protective effects against glutamate/H2O2-induced toxicity in cultured neuronal cells by suppressing the intracellular reactive oxygen species (ROS) generation and enhancing the expression of endogenous antioxidant enzymes (SODs, GPx, and GSTs). GZM extract also triggered the expression of SIRT1/Nrf2 proteins and mRNA transcription of antioxidant genes (NQO1, GCLM, and EAAT3) which are the master regulators of cellular defense against oxidative stress. Additionally, GZM extract exhibited protective effects to counteract β-amyloid (Aβ)-induced toxicity in C. elegans and promoted neuritogenesis properties in Neuro-2a cells. Our observations suggest that GZM leaf extract has interesting neuritogenesis and neuroprotective potential and can possibly act as potential contender for the treatment of oxidative stress-induced Alzheimer’s disease (AD) and related neurodegenerative conditions; however, this needs to be studied further in other in vivo systems.

scholarly journals Melatoninergic System in Parkinson’s Disease: From Neuroprotection to the Management of Motor and Nonmotor Symptoms

2016 ◽  
Vol 2016 ◽  
pp. 1-31 ◽  
Author(s):  
Josiel Mileno Mack ◽  
Marissa Giovanna Schamne ◽  
Tuane Bazanella Sampaio ◽  
Renata Aparecida Nedel Pértile ◽  
Pedro Augusto Carlos Magno Fernandes ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neuroprotective Effect ◽  
Antioxidant Properties ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Motor Impairments ◽  
Nonmotor Symptoms ◽  
Neuroprotective Effects ◽  
6 Hydroxydopamine

Melatonin is synthesized by several tissues besides the pineal gland, and beyond its regulatory effects in light-dark cycle, melatonin is a hormone with neuroprotective, anti-inflammatory, and antioxidant properties. Melatonin acts as a free-radical scavenger, reducing reactive species and improving mitochondrial homeostasis. Melatonin also regulates the expression of neurotrophins that are involved in the survival of dopaminergic neurons and reducesα-synuclein aggregation, thus protecting the dopaminergic system against damage. The unbalance of pineal melatonin synthesis can predispose the organism to inflammatory and neurodegenerative diseases such as Parkinson’s disease (PD). The aim of this review is to summarize the knowledge about the potential role of the melatoninergic system in the pathogenesis and treatment of PD. The literature reviewed here indicates that PD is associated with impaired brain expression of melatonin and its receptors MT1and MT2. Exogenous melatonin treatment presented an outstanding neuroprotective effect in animal models of PD induced by different toxins, such as 6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rotenone, paraquat, and maneb. Despite the neuroprotective effects and the improvement of motor impairments, melatonin also presents the potential to improve nonmotor symptoms commonly experienced by PD patients such as sleep and anxiety disorders, depression, and memory dysfunction.

scholarly journals Natural Approaches for Neurological Disorders—The Neuroprotective Potential of Codium tomentosum

Molecules ◽  
2020 ◽  
Vol 25 (22) ◽  
pp. 5478
Author(s):  
Joana Silva ◽  
Alice Martins ◽  
Celso Alves ◽  
Susete Pinteus ◽  
Helena Gaspar ◽  
...  
Keyword(s):  
Dopaminergic Neurons ◽  
Neurodegenerative Disorder ◽  
Ros Generation ◽  
Neuroprotective Effects ◽  
Mitochondrial Dysfunctions ◽  
Chemical Screening ◽  
Cellular Events ◽  
Progressive Degeneration ◽  
Viable Cells ◽  
6 Hydroxydopamine

Parkinson’s disease (PD) is the second most common neurodegenerative disorder, and is characterized by a progressive degeneration of the dopaminergic neurons in the substantianigra. Although not completely understood, several abnormal cellular events are known to be related with PD progression, such as oxidative stress, mitochondrial dysfunction and apoptosis. Accordingly, the aim of this study was to evaluate the neuroprotective effects of Codium tomentosum enriched fractions in a neurotoxicity model mediated by 6-hydroxydopamine (6-OHDA) on SH-SY5Y human cells, and the disclosure of their mechanisms of action. Additionally, a preliminary chemical screening of the most promising bioactive fractions of C. tomentosum was carried out by GC-MS analysis. Among the tested fractions, four samples exhibited the capacity to revert the neurotoxicity induced by 6-OHDA to values higher or similar to the vitamin E (90.11 ± 3.74% of viable cells). The neuroprotective effects were mediated by the mitigation of reactive oxygen species (ROS) generation, mitochondrial dysfunctions and DNA damage, together with the reduction of Caspase-3 activity. Compounds belonging to different chemical classes, such as terpenes, alcohols, carboxylic acids, aldehydes, esters, ketones, saturated and unsaturated hydrocarbons were tentatively identified by GC-MS. The results show that C. tomentosum is a relevant source of neuroprotective agents, with particular interest for preventive therapeutics.

Sign in / Sign up

Export Citation Format

Share Document