scholarly journals Bacoside-A exerts protective effect against Parkinson’s disease-induced functional damage in mice via inhibition of apoptosis and oxidative response

2021 ◽  
Vol 19 (12) ◽  
pp. 2565-2570
Author(s):  
Binbin Zhang ◽  
Jiankuan Shi ◽  
Lei Chang ◽  
Hong Wang ◽  
Yaping Wang ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cytochrome C ◽  
Parkinson Disease ◽  
Protective Effect ◽  
Rat Model ◽  
Neuronal Degeneration ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Bacoside A

Purpose: To determine the effect of bacoside-A on Parkinson's disease (PD) in a rat model, and elucidate its mechanism of action.Methods: A rat model of PD was established by administration of 5 µL of 6-hydroxydopamine in ascorbic acid (0.1 %). Measurement of serum levels of inflammatory factors was carried out using enzyme-linked immunosorbent assay (ELISA) kits. Western blotting was used to assay Bax, cytochrome c and Bcl-2 in rat hippocampus.Results: Bacoside-A treatment significantly reduced PD-induced high turning values in rats (p < 0.05). Treatment with bacoside-A reversed PD-mediated suppression of serum activities of CAT and glutathione peroxidase (GPx). In bacoside-A-treated PD rats, dose-dependent suppression of acetylcholinesterase (AChE) and inducible nitric oxide synthase (iNOS) activities were observed (p < 0.05). Bacoside-A-treated PD rats significantly (p < 0.018) reduced interleukin (IL)-1β and IL-6 levels. Treatment of PD rats with bacoside-A effectively reduced levels of tumor necrosis factor (TNF)-α, NF-κB p65, (COX)-2 and p53 protein, and also reversed up-regulations of Bax, cytochrome C, caspase-3 and caspase-9.Conclusion: Bacoside-A exhibits a protective effect against Parkinson disease-induced oxidative damage and neuronal degeneration in rats through downregulation of iNOS, AChE, inflammatory cytokines and pro-apoptotic proteins. Therefore, bacoside-A has potentials for use in the management of Parkinson disease. Keywords: Parkinson disease, Neuroprotective, Pro-apoptotic, Cytokines, Neurotoxicity

scholarly journals Momordica Charantia Polysaccharides Attenuates MPP+-Induced Injury in Parkinson’s Disease Mice and Cell Models by Regulating TLR4/MyD88/NF-κB Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Dengjun Guo ◽  
Jie Zhou ◽  
Meng Zhang ◽  
Reyisha Taximaimaiti ◽  
Xiaoping Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cytochrome C ◽  
Momordica Charantia ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Cell Models ◽  
Activation Effect

Objective. To investigate the potential role of Momordica charantia polysaccharides (MCPs) in Parkinson’s disease (PD) and reveal the molecular mechanism of its function. Method. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium (1-methyl-4-phenylpyridinium, MPP+) were used to establish PD mice and cell models. The mice and cells were divided into 4 groups: Control group, Control+MCPs group, PD group, and PD+MCPs group. Pole climbing experiment and Rotarod experiment were used to observe the coordination ability of mice. High-performance liquid chromatography and enzyme-linked immunosorbent assay (ELISA) were used to determine neurotransmitters and metabolites, inflammatory factors TNF-α and IL-1β, oxidative stress-related markers SOD, MDA, and GSH in striatum tissues. Western blot was used to determine the protein levels of tyrosine hydroxylase (TH), oxidative stress-related protein Cytochrome C (Cytochrome C), and apoptosis-related proteins Bcl-2, Bax, and cleaved Caspase-3 in tissues and cells. Moreover, flow cytometry, PI staining, and fluorescence were used to observe cell apoptosis. Finally, the activation effect of MCPs on TLR4/MyD88/NF-κB signaling pathway was observed and verified. Results. Compared with the Control group, MPTP treatment can induce brain damage in mice (all P < 0.05 ), change the metabolic state of neurotransmitters (all P < 0.05 ), induce inflammation (all P < 0.05 ), and induce apoptosis and the occurrence of oxidation reaction (all P < 0.05 ); however, MCPs treatment can significantly reverse the above changes (all P < 0.05 ). In cell models, studies have found that MCPs can play a protective role by regulating the activation state of TLR4/MyD88/NF-κB pathway. Conclusion. This study found that the application of MCPs therapy can play anti-inflammatory, antioxidative stress, and antiapoptotic effects in PD by regulating the activation of the TLR4/MyD88/NF-κB pathway.

scholarly journals The Protective Effect of Celecoxib on CA1 Hippocampal Neurons and Oxidative Stress in a Rat Model of Parkinson’s Disease

2019 ◽  
Author(s):  
Maryam Sarbishegi ◽  
Hamidreza Mahmoudzadeh-sagheb ◽  
Zahra Heidari ◽  
Farzaneh Baharvand
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Protective Effect ◽  
Passive Avoidance ◽  
Rat Model ◽  
Hippocampal Neurons ◽  
Wistar Rat ◽  
Tunel Staining ◽  
Model Animal ◽  
Avoidance Memory

Abstract- Several studies point to an important role of neuroinflammation in Parkinson's disease (PD). Cognitive and memory impairments have been known in the early stages of PD. In the present study, we examined the effects of celecoxib (CLX), a selective inhibitor of cyclooxygenase-2 (COX-2), on hippocampus cell loss, passive avoidance memory and antioxidant status in a rat model of PD. We used the subcutaneous injection of 2.5 mg/kg/48h rotenone (ROT) for 4 weeks for induction of PD in a male Wistar rat. Animals were randomized to 4 groups (n=12): Control, sham, PD and PD+CLX group that receive celecoxib (20 mg/kg/day) for 4 weeks. Passive avoidance memory evaluated. We also determined the protective effect of CLX on a number of CA1 neurons in Nissl and TUNEL staining. Total antioxidant capacity (TAC) and malondialdehyde (MDA) a marker of lipid peroxidation in hippocampus assessed. Our findings indicated administration of CLX increase the passive avoidance memory (P<0.05), and by a decrease in apoptosis caused an increase in viable pyramidal neurons in CA1 hippocampus (P<0.01). On the other hand, CLX markedly reduced MDA level and increased TAC in the hippocampus of the PD model animal (P<0.05). It seems CLX with anti-inflammatory and antiapoptotic effect could prevent neurons loss and memory impairment which induced in PD.

Protective effect of adenosine in rat model of Parkinson's disease: neurobehavioral and neurochemical evidences

2003 ◽  
Vol 26 (2) ◽  
pp. 143-151 ◽  
Author(s):  
Khan Shoeb Zafar ◽  
Almas Siddiqui ◽  
Iqbal Sayeed ◽  
Muzamil Ahmad ◽  
Sofiyan Saleem ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Protective Effect ◽  
Rat Model

Protective effect of alpha mangostin on rotenone induced toxicity in rat model of Parkinson’s disease

2020 ◽  
Vol 716 ◽  
pp. 134652 ◽  
Author(s):  
Abhijeet Parkhe ◽  
Pathik Parekh ◽  
Lakshmi Vineela Nalla ◽  
Nishant Sharma ◽  
Monika Sharma ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Protective Effect ◽  
Rat Model

scholarly journals Dose-dependent protective effect of selenium in rat model of Parkinson's disease: neurobehavioral and neurochemical evidences

2003 ◽  
Vol 84 (3) ◽  
pp. 438-446 ◽  
Author(s):  
Khan Shoeb Zafar ◽  
Almas Siddiqui ◽  
Iqbal Sayeed ◽  
Muzamil Ahmad ◽  
Sofian Salim ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Protective Effect ◽  
Rat Model ◽  
Dose Dependent

Protective effect of a novel herbmedicine, Hepad, on apoptosis of SH-SY5Y cells and a rat model of Parkinson’s disease

2015 ◽  
Vol 11 (2) ◽  
pp. 223-230 ◽  
Author(s):  
Seung Yeop Baek ◽  
Na Rae Lee ◽  
Da Hye Kim ◽  
Ayoung Gu ◽  
Seong Yeol Kim ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Protective Effect ◽  
Rat Model

scholarly journals Levels of serum IL6, TNF-α and sLAG3 are changed and correlated with clinical characteristics in Parkinson’s disease patients: A case-control study

2021 ◽  
Vol 26 (4) ◽  
pp. 709-714
Author(s):  
Yuting Zhu ◽  
Xiaoming Guo ◽  
Yong Zhou ◽  
Dongmei Zhang ◽  
Xiaoyi Yi ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Clinical Characteristics ◽  
Disease Assessment ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Immune Disorder ◽  
Tnf Α ◽  
Previous Hypothesis ◽  
And Gender

Objective: An increasing body of studies have proved that inflammation plays a crucial role in Parkinson’s disease (PD) pathogenesis. IL-6, TNF-α and sLAG3 are associated with immune disorder. This study aimed to examine the expression of serum IL-6, TNF-α and sLAG3 in PD patients from China. Methods: Forty six PD patients and 42 age and gender-matched healthy controls (HC) were recruited. clinical data, disease assessment scale and serum IL-6, TNF-α and sLAG3 were assessed in PD patients. The levels of inflammatory factors were determined by enzyme-linked immunosorbent assay (ELISA). Results: The levels of serum IL-6 and TNF-α were significantly higher in PD patients compared to HC. Serum IL-6 and TNF-α were independent risk factors for PD. The levels of serum sLAG3 and TNF-α were higher in female patients than those of male patients. Significant positive correlation was found between serum TNF-α and H-Y, UPDRS III and HAMA in PD patients. Serum sLAG3 positively correlated with HAMA. Conclusion: Changes in serum inflammatory factors were observed in PD patients, which were correlated with the clinical characteristics. The study supports the previous hypothesis that inflammation is involved in the pathogenesis of PD.

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