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 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 The Possible Role of Bifidobacterium longum BB536 and Lactobacillus rhamnosus HN001 on Locomotor Activity and Oxidative Stress in a Rotenone-Induced Zebrafish Model of Parkinson’s Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Ovidiu-Dumitru Ilie ◽  
Emanuela Paduraru ◽  
Madalina-Andreea Robea ◽  
Ioana-Miruna Balmus ◽  
Roxana Jijie ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Locomotor Activity ◽  
Prolonged Exposure ◽  
Bifidobacterium Longum ◽  
The Body ◽  
The Other ◽  
Control Group

Background. As every organ within the body, the brain is also extremely susceptible to a plethora of noxious agents that change its chemistry. One component frequently found in current products against harmful species to crops is rotenone whose effect under prolonged exposure has been demonstrated to cause neurodegenerative disorders such as Parkinson’s disease. The latest reports have indeed revealed that rotenone promotes Parkinson’s in humans, but studies aiming to show congruent effects in zebrafish (Danio rerio) are lacking. Material and Methods. In this context, the aim of the present study was to demonstrate how chronic administration of rotenone for 3 weeks impairs the locomotor activity and sociability and induces oxidative stress in zebrafish. Results. There were no statistically significant differences following the analysis of their social interaction and locomotor tests ( p > 0.05 ). However, several exceptions have been noted in the control, rotenone, and probiotics groups when we compared their locomotor activity during the pretreatment and treatment interval ( p < 0.05 ). We further assessed the role of rotenone in disturbing the detoxifying system as represented by three enzymes known as superoxide dismutase (SOD), glutathione peroxidase (GPx), and malondialdehyde (MDA). Despite the fact that there were no statistically significant changes within SOD and GPx levels between the control group and rotenone, probiotics, and rotenone + probiotics ( p > 0.05 ), relevant changes have been observed between the analyzed groups ( p < 0.05 and p < 0.005 , respectively). On the other hand, significant differences ( p < 0.05 ) have been observed for MDA when we analyzed the data between the control group and the other three groups. Conclusions. Our results suggest that rotenone can be successfully used to trigger Parkinson’s disease-related symptomatology in zebrafish.

scholarly journals An Enriched Environment Ameliorates Oxidative Stress and Olfactory Dysfunction in Parkinson’s Disease with α-Synucleinopathy

2018 ◽  
Vol 27 (5) ◽  
pp. 831-839 ◽  
Author(s):  
Soohyun Wi ◽  
Jang Woo Lee ◽  
MinGi Kim ◽  
Chang-Hwan Park ◽  
Sung-Rae Cho
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Underlying Mechanism ◽  
Olfactory Dysfunction ◽  
Olfactory Function ◽  
Enriched Environment ◽  
Detoxification Enzymes ◽  
Paraoxonase 1 ◽  
Control Group

Parkinson’s disease (PD) features nonmotor symptoms such as olfactory dysfunction referred to as hyposmia, an initial sign of disease progression. Metabolic dysfunction can contribute to neurodegenerative diseases, and various xenobiotics and endogenous compounds are also involved in the pathogenesis of PD. Although aerobic exercise was found to induce preservation or improvement in olfactory function in PD patients in a recent study, the exact underlying mechanism for this effect is not clear. We aimed to investigate the influence of an enriched environment (EE) on olfactory dysfunction especially via metabolic pathways related to detoxification enzymes. Eight-month-old transgenic (Tg) PD mice that overexpress human A53T α-synuclein (α-syn) were randomly allocated to an EE or standard conditions for 2 mo. The buried food test showed that EE group had significantly improved olfactory function compared to the control group. Reverse transcription polymerase chain reaction (PCR) and real-time quantitative PCR showed that expression of the detoxification enzymes–– cytochrome P450 family 1 subfamily A member 2, paraoxonase 1, alcohol dehydrogenase 1, UDP glucuronosyltransferase family 2 member A1 complex locus, aldehyde oxidase homolog 2, and aldehyde glutathione peroxidase 6––was significantly increased in the olfactory bulb (OB) of the PD control group, but these enzymes were normalized in the EE group. Immunohistochemical staining of the OB showed that oxidative stress and nitrated α-syn were significantly increased in the control group but decreased in the EE group. In conclusion, we suggest that exposure to an EE decreases both oxidative stress and nitrated α-syn, resulting in normalized detoxification enzymes and amelioration of olfactory dysfunction.

scholarly journals Therapeutic effect of TO901317 on 6-OHDA-induced Parkinson rats in vitro and in vivo

2020 ◽  
Author(s):  
Miaomiao Li ◽  
Junqing Yang ◽  
Oumei Cheng ◽  
Zhe Peng ◽  
Yin Luo ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Stem Cells ◽  
Parkinson's Disease ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Dopamine Neurons ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Fibroblast Growth ◽  
Fibroblast Growth Factor 8

Abstract Background: Stem cells from different sources could differentiate into dopamine-producing cells and ameliorate behavioral deficits in Parkinsonian models. Especially, human bone marrow mesenchymal stem cells (hBMSCs) have many advantages without ethical dispute. Liver X receptor s (LXRs) are involved in the maintenance of the normal function of the central nervous system myelin. We have reported the induction of cocktail-induced da phenotypes from adult rat BMSCs by using sonic hedgehog (SHH), fibroblast growth factor 8 (FGF8), basic fibroblast growth factor (bFGF) and TO901317 (agonist of LXRs) with 87.42% of efficiency in 6 days of period of induction. But the previous work did not verify whether the induced cells had the corresponding neural function. Methods: In this study, we demonstrated that TO901317 could promote the differentiation of hBMSCs into dopaminergic neurons. Neuronal markers (Tuj1, Neun and Nestin), dopamine neuron markers (tyrosine hydroxylase, TH), LXRa and LXRb were detected by immunofluorescence. RT-qPCR was used to measure the mRNA expressions of adenosine triphosphate-binding cassette transporter A1 (ABCA1). Western Blotting detected the changes of LXRa, LXRb and TH expression. Results: TO901317 significantly enhanced the differentiation from hBMSCs to DA neurons. Only the LXR+GF group released dopamine by the result of enzyme linked immunosorbent assay (ELISA). Compared with the control group and GF group, the optimal time for differentiation of hBMSCs treated by 0.5mM TO901317 combined with GF was six days. And the maximum induction efficiency was 91.67%. After transplanting induced-cells into Parkinson's disease rats, the symptoms of Parkinson's rats decreased, and the number of dopamine neurons increased in the substantia nigra and striatum. Conclusions: TO901317 promoted differentiation of hBMSCs into dopamine neurons may be related to activation of LXR-ABCA1 signaling pathway. These data suggest that TO901317 may serve as a potential therapeutic methods for Parkinson's disease.

scholarly journals Neuroprotective Effects of Thymol, a Dietary Monoterpene Against Dopaminergic Neurodegeneration in Rotenone-Induced Rat Model of Parkinson’s Disease

2019 ◽  
Vol 20 (7) ◽  
pp. 1538 ◽  
Author(s):  
Hayate Javed ◽  
Sheikh Azimullah ◽  
MF Meeran ◽  
Suraiya Ansari ◽  
Shreesh Ojha
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Body Weight ◽  
Therapeutic Potential ◽  
Nigrostriatal System ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Dopaminergic Neurodegeneration

Parkinson’s disease (PD), a multifactorial movement disorder that involves progressive degeneration of the nigrostriatal system affecting the movement ability of the patient. Oxidative stress and neuroinflammation both are shown to be involved in the etiopathogenesis of PD. The aim of this study was to evaluate the therapeutic potential of thymol, a dietary monoterpene phenol in rotenone (ROT)-induced neurodegeneration in rats that precisely mimics PD in humans. Male Wistar rats were injected ROT at a dose of 2.5 mg/kg body weight for 4 weeks, to induce PD. Thymol was co-administered for 4 weeks at a dose of 50 mg/kg body weight, 30 min prior to ROT injection. The markers of dopaminergic neurodegeneration, oxidative stress and inflammation were estimated using biochemical assays, enzyme-linked immunosorbent assay, western blotting and immunocytochemistry. ROT challenge increased the oxidative stress markers, inflammatory enzymes and cytokines as well as caused significant damage to nigrostriatal dopaminergic system of the brain. Thymol treatment in ROT challenged rats appears to significantly attenuate dopaminergic neuronal loss, oxidative stress and inflammation. The present study showed protective effects of thymol in ROT-induced neurotoxicity and neurodegeneration mediated by preservation of endogenous antioxidant defense networks and attenuation of inflammatory mediators including cytokines and enzymes.

Parkinsonism-like disease induced by rotenone in rats: Treatment role of curcumin, dopamine agonist and adenosine A2A receptor antagonist

2021 ◽  
Vol 14 ◽  
Author(s):  
Asmaa Fathy Aboul Naser ◽  
Wessam Magdi Aziz ◽  
Yomna Rashad Ahmed ◽  
Wagdy Khalil Bassaly Khalil ◽  
Manal Abdel Aziz Hamed
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Inflammatory Mediator ◽  
Adenosine A2a Receptor ◽  
Control Group ◽  
A2a Receptor ◽  
Adenosine A2a

Background: Parkinsonism is a neurodegenerative disorder that affects elderly people worldwide. Methods: Curcumin, adenosine A2AR antagonist (ZM241385) and Sinemet® (L-dopa) were evaluated against Parkinson’s disease (PD) induced by rotenone in rats and comparativelyrelatively compared with our previous study on mice model. Results: Rats injected with rotenone showed severe alterations in adenosine A2A receptor gene expression, oxidative stress markers, inflammatory mediator, energetic indices, apoptotic marker and DNA fragmentation levels as compare with the control group. Treatments with curcumin, ZM241385, and Sinemet® restored all the selected parameters. The brain histopathological features of cerebellum regions confirmed our results. By comparing our results with the previous results on mice, we noticed that mice respond to rotenone toxicity and treatments more than rats regarding to behavioral observation, A2AR gene expression, neurotransmitter levels, inflammatory mediator and apoptotic markers, while rats showed higher response to treatments regarding to oxidative stress and energetic indices. Conclusion: Curcumin succeeded to attenuate the severe effects of Parkinson’s disease in rat model and can be consider as a potential dietary supplement. Adenosine A2AR antagonist has almost the same pattern of improvement as Sinemet® and may be considered as a promising therapy against PD. By comparing the role of animal species in response to PD symptoms and treatments, our previous report on mice explore the response of mice to rotenone toxicity than rats, while rats showed higher response to treatments. Therefore, no animal model can perfectly recapitulate all the pathologies of PD.

The role of «hunger hormone» in the regulation of eating behavior in patients with Parkinson’s disease

2021 ◽  
Author(s):  
K. A. Tarianyk
Keyword(s):  
Parkinson’S Disease ◽  
Body Mass Index ◽  
Parkinson's Disease ◽  
Body Mass ◽  
Eating Behavior ◽  
Disease Duration ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Clear Correlation ◽  
Group 2

Objective — to evaluate the correlation between ghrelin levels, body mass index and the course of the disease in patients with Parkinson’s disease Methods and subjects. We examined 40 patients with Parkinson’s disease and 20 patients without signs of neurodegenerative disease (control group), who were examined and admitted to the neurological department. Patients were distributed into groups: 1 group — 20 patients with a disease duration of 12.1 ± 2.3 years, group 2 — 20 patients with a disease duration of 7.3 ± 1.6 years, group 3 — control, 20 patients without signs of morbidity. The diagnosis was made according to the criteria of the World Brain Bank of Great Britain. The severity of the disease was determined by the Hen and Yar scale. All patients, after signing the consent agreement, underwent a general clinical, neurological examination with assessment of anthropometric parameters: height, weight, body mass index. Also, patients underwent laboratory determination of serum ghrelin levels using the method of enzyme‑linked immunosorbent assay (ELISA) on the basis of the Research Institute of Genetic, Immunological Basis of Pathology and Pharmacogenetics of the Ukrainian Medical Dental Academy. Results. Studies indicate that in the group of patients with a longer course of the disease (group 1) there was an increase in BMI, which can be interpreted as obesity or overweight, compared with group 2 and control, where the rate was normal. In group 2, where the duration of the disease was shorter, there was a decrease in BMI, accompanied by weight loss of patients. In each group of examined patients there were patients with different forms of the disease, but in the second group patients with akinetic‑rigid form of the disease prevailed, so these patients in neurological status suffered more from stiffness, immobility. Normally, ghrelin level rises in the morning during hunger and decreases after eating. A similar picture was observed in the control group of patients, where the rate of morning ghrelin was elevated. When assessing fasting plasma ghrelin levels in groups of patients, there is a slight decrease in the indicator compared with the control group. Conclusions. There is a clear correlation between the duration of the disease, body mass index and hunger hormone levels in patients with Parkinson’s disease. In patients with the initial stages of the disease there is a decrease in body mass index, which is a prognostically unfavorable sign. Fluctuations in ghrelin levels may be associated with decreased energy intake due to gastrointestinal dysfunction, increased energy expenditure caused by motor manifestations of the disease, or increased glucose metabolism with the use of drugs and changes in the eating behavior of patients.  

scholarly journals Protective Effects of an Ancient Chinese Kidney-Tonifying Formula against H2O2-Induced Oxidative Damage to MES23.5 Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-9
Author(s):  
Yihui Xu ◽  
Wei Lin ◽  
Shuifen Ye ◽  
Huajin Wang ◽  
Tingting Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Oxidative Damage ◽  
Cell Damage ◽  
Critical Role ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protective Effects ◽  
Transmission Electron ◽  
Potential Strategy

Oxidative damage plays a critical role in the etiology of neurodegenerative disorders including Parkinson’s disease (PD). In our study, an ancient Chinese kidney-tonifying formula, which consists ofCistanche,Epimedii,andPolygonatum cirrhifolium, was investigated to protect MES23.5 dopaminergic neurons against hydrogen peroxide- (H2O2-) induced oxidative damage. The damage effects of H2O2on MES23.5 cells and the protective effects of KTF against oxidative stress were evaluated using MTT assay, transmission electron microscopy (TEM), immunocytochemistry (ICC), enzyme-linked immunosorbent assay (ELISA), and immunoblotting. The results showed that cell viability was dramatically decreased after a 12 h exposure to 150 μM H2O2. TEM observation found that the H2O2-treated MES23.5 cells presented cellular organelle damage. However, when cells were incubated with KTF (3.125, 6.25, and 12.5 μg/ml) for 24 h after H2O2exposure, a significant protective effect against H2O2-induced damage was observed in MES23.5 cells. Using ICC, we found that KTF inhibited the reduction of the tyrosine hydroxylase (TH) induced by H2O2, upregulated the mRNA and protein expression of HO-1, CAT, and GPx-1, and downregulated the expression of caspase 3. These results indicated that KTF may provide neuron protection against H2O2-induced cell damage through ameliorating oxidative stress, and our findings provide a new potential strategy for the prevention and treatment of Parkinson’s disease.

scholarly journals Therapeutic effect of TO901317 on 6-OHDA-induced Parkinson rats in vitro and in vivo

2020 ◽  
Author(s):  
Miaomiao Li ◽  
Junqing Yang ◽  
Oumei Cheng ◽  
Zhe Peng ◽  
Yin Luo ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Stem Cells ◽  
Parkinson's Disease ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Dopamine Neurons ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Fibroblast Growth ◽  
Fibroblast Growth Factor 8

Abstract Background: Stem cells from different sources could differentiate into dopamine-producing cells and ameliorate behavioral deficits in Parkinsonian models. Especially, human bone marrow mesenchymal stem cells (hBMSCs) have many advantages without ethical dispute. Liver X receptor s (LXRs) are involved in the maintenance of the normal function of the central nervous system myelin. We have reported the induction of cocktail-induced da phenotypes from adult rat BMSCs by using sonic hedgehog (SHH), fibroblast growth factor 8 (FGF8), basic fibroblast growth factor (bFGF) and TO901317 (agonist of LXRs) with 87.42% of efficiency in 6 days of period of induction. But the previous work did not verify whether the induced cells had the corresponding neural function. Methods: In this study, we demonstrated that TO901317 could promote the differentiation of hBMSCs into dopaminergic neurons. Neuronal markers (Tuj1, Neun and Nestin), dopamine neuron markers (tyrosine hydroxylase, TH), LXRa and LXRb were detected by immunofluorescence. RT-qPCR was used to measure the mRNA expressions of adenosine triphosphate-binding cassette transporter A1 (ABCA1). Western Blotting detected the changes of LXRa, LXRb and TH expression. Results: TO901317 significantly enhanced the differentiation from hBMSCs to DA neurons. Only the LXR+GF group released dopamine by the result of enzyme linked immunosorbent assay (ELISA). Compared with the control group and GF group, the optimal time for differentiation of hBMSCs treated by 0.5mM TO901317 combined with GF was six days. And the maximum induction efficiency was 91.67%. After transplanting induced-cells into Parkinson's disease rats, the symptoms of Parkinson's rats decreased, and the number of dopamine neurons increased in the substantia nigra and striatum. Conclusions: TO901317 promoted differentiation of hBMSCs into dopamine neurons may be related to activation of LXR-ABCA1 signaling pathway. These data suggest that TO901317 may serve as a potential therapeutic methods for Parkinson's disease.

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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