Interleukin-1β, interleukin-1 receptor antagonist, interleukin-6, interleukin-10, and tumor necrosis factor-α levels in CSF and serum in relation to the clinical diversity of Parkinson’s disease

Karpenko, Marina N.; Василишина, А. А.; Громова, Е А; Muruzheva, Zamira M.; Bernadotte, Alexandra

doi:10.1016/j.cellimm.2018.02.011

Cited by 127 publications

(117 citation statements)

References 44 publications

Supporting

Mentioning

103

Contrasting

Unclassified

Order By: Relevance

“…Over-activation of microglia releases pro-inflammatory cytokines including IL-6, IL‐1β and TNF-α, which would lead to the damage of neurons and further active the inflammatory cascade [12]. It is reported that IL-6, IL‐1β and TNF-α are significantly elevated in patients with AD [13] and PD [14]. In addition, the activated microglial cells also produce harmful substances, such as iNOS, COX-2 and other free radicals, which may perturb neuronal death and induce the development of neurodegeneration [15].…”

Section: Discussionmentioning

confidence: 99%

Dihydromyricetin attenuates inflammation through TLR4/NF-kappaB pathway

Jing¹,

Li²

2019

Open Medicine

View full text Add to dashboard Cite

AbstractMicroglia plays a complex role in neuroinflammation, which has been implicated in neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. This study aims to explore the effect and mechanism of Dihydromyricetin (DHM) on lipopolysaccharide (LPS)-induced inflammation in microglial BV-2 cells. Cell viability was measured by 3-[4,5-dimethylthiazol-2-yl]2,5-diphenyltetrazolium bromide (MTT) assay. The pro-inflammatory mediators and cytokines including interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α); inducible nitric oxide synthase (iNOS); and cyclooxygenase 2 (COX-2) were measured by enzyme-linked immunosorbent assay (ELISA) and/or quantitative real-time PCR (qRT-PCR). The expression of p-p65, p-IκBα, toll-like receptor 4 (TLR4), and myeloid differentiation primary response 88 (MyD88) were analyzed by western blot. The present study showed that DHM treatment alleviated LPS-induced viability reduction, suppressed the mRNA levels of IL-6, IL‐1β and TNF-α, inhibited the mRNA and protein expression of iNOS and COX-2, and attenuated the activation of NF-кB and TLR4 signaling in a concentration-dependent manner. In conclusion, DHM exerts an anti-inflammatory effect on LPS-induced BV-2 microglial cells, possibly through TRL4/NF-κB signaling pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Dihydromyricetin attenuates inflammation through TLR4/NF-kappaB pathway

Jing¹,

Li²

2019

Open Medicine

View full text Add to dashboard Cite

show abstract

“…Pro‐inflammatory cytokines such as IL‐1, IL‐6, and TNF‐α secreted by activated microglial cells contribute the progress of PD (Alam et al, ). It has been shown that IL‐1β and IL‐6 in serum are significantly elevated in patients with PD (Karpenko, Vasilishina, Gromova, Muruzheva, & Bernadotte, ). Qin, Zhang, Cao, Loh, and Cheng () reported that higher peripheral concentrations of IL‐1β, IL‐2, IL‐6, and TNF‐α are observed in patients with PD, providing the clinical evidence that PD is accompanied by neuroinflammation.…”

Section: Discussionmentioning

confidence: 99%

Farrerol attenuates MPP⁺‐induced inflammatory response by TLR4 signaling in a microglia cell line

Cui

Guo

You³

et al. 2019

Phytotherapy Research

View full text Add to dashboard Cite

Farrerol was found to possess neuroprotective effect; however, the mechanism remains unknown. The aim of the present study was to explore the effect of farrerol on MPP + -induced inflammation in mouse microglial BV-2 cells and to elaborate the underlying mechanism. MTT assay was performed to measure the cell viability. The pro-inflammatory mediators and cytokines including interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α); inducible nitric oxide synthase; and cyclooxygenase 2 were measured. The expression of p-p65, p-IκBα, toll-like receptor 4 (TLR4), and myeloid differentiation primary response 88 were analyzed by western blot. We found that farrerol treatment improved cell viability in MPP + -induced BV-2 cells. MPP + -induced upregulation of IL-6, IL-1β, and TNF-α was inhibited by farrerol treatment. Farrerol treatment also attenuated MPP + -induced expression of inducible nitric oxide synthase and cyclooxygenase 2 as well as the activation of NF-κB in BV-2 cells. MPP + -induced TLR4 signaling was markedly diminished by farrerol treatment. Knockdown of TLR4 attenuated MPP + -induced inflammatory response in BV-2 cells. In conclusion, farrerol treatment attenuated MPP + -induced inflammatory response by inhibiting the TLR4 signaling pathway in BV-2 cells. The results indicated that farrerol could be used as a therapeutic agent for preventing or alleviating the neuroinflammation-related diseases, such as Parkinson's disease.

show abstract

“…Increased inflammatory responses have been described both in the brain and peripheral blood of PD patients (135). Depression correlated with a high serum level of IL-10 (136) and IL-6 (137). High levels of both sIL-2R and TNF-α in blood samples from PD patients were significantly associated with more severe depression and anxiety (119).…”

Section: Depressionmentioning

confidence: 98%

Biomarkers for Dementia, Fatigue, and Depression in Parkinson's Disease

2019

View full text Add to dashboard Cite

Parkinson's disease is a common multisystem neurodegenerative disorder characterized by typical motor and non-motor symptoms. There is an urgent need for biomarkers for assessment of disease severity, complications and prognosis. In addition, biomarkers reporting the underlying pathophysiology assist in understanding the disease and developing neuroprotective therapies. Ultimately, biomarkers could be used to develop a more efficient personalized approach for clinical trials and treatment strategies. With the goal to improve quality of life in Parkinson's disease it is essential to understand and objectively monitor non-motor symptoms. This narrative review provides an overview of recent developments of biomarkers (biofluid samples and imaging) for three common neuropsychological syndromes in Parkinson's disease: dementia, fatigue, and depression.

show abstract

Interleukin-1β, interleukin-1 receptor antagonist, interleukin-6, interleukin-10, and tumor necrosis factor-α levels in CSF and serum in relation to the clinical diversity of Parkinson’s disease

Cited by 127 publications

References 44 publications

Dihydromyricetin attenuates inflammation through TLR4/NF-kappaB pathway

Dihydromyricetin attenuates inflammation through TLR4/NF-kappaB pathway

Farrerol attenuates MPP⁺‐induced inflammatory response by TLR4 signaling in a microglia cell line

Biomarkers for Dementia, Fatigue, and Depression in Parkinson's Disease

Contact Info

Product

Resources

About

Interleukin-1β, interleukin-1 receptor antagonist, interleukin-6, interleukin-10, and tumor necrosis factor-α levels in CSF and serum in relation to the clinical diversity of Parkinson’s disease

Cited by 127 publications

References 44 publications

Dihydromyricetin attenuates inflammation through TLR4/NF-kappaB pathway

Dihydromyricetin attenuates inflammation through TLR4/NF-kappaB pathway

Farrerol attenuates MPP+‐induced inflammatory response by TLR4 signaling in a microglia cell line

Biomarkers for Dementia, Fatigue, and Depression in Parkinson's Disease

Contact Info

Product

Resources

About

Farrerol attenuates MPP⁺‐induced inflammatory response by TLR4 signaling in a microglia cell line