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Tenuigenin protects dopaminergic neurons from inflammation via suppressing NLRP3 inflammasome activation in microglia

Overview of attention for article published in Journal of Neuroinflammation, December 2017
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Title
Tenuigenin protects dopaminergic neurons from inflammation via suppressing NLRP3 inflammasome activation in microglia
Published in
Journal of Neuroinflammation, December 2017
DOI 10.1186/s12974-017-1036-x
Pubmed ID
Authors

Zheng Fan, Zhigang Liang, Hui Yang, Yuting Pan, Yan Zheng, Xiaomin Wang

Abstract

Emerging evidence indicates that nod-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome-induced inflammation plays a crucial role in the pathogenesis of Parkinson's disease (PD). Thus, inhibition of NLRP3 inflammasome activation may offer a therapeutic benefit in the treatment of PD. Tenuigenin, a major active component of Polygala tenuifolia, has been shown to have potential anti-inflammatory activity, but the underlying mechanisms remain obscure. In the present study, the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model of PD was established to explore the effect of tenuigenin on dopaminergic neurons in substantia nigra. We next activated NLRP3 inflammasome in both BV2 microglia cells and adult mice to investigate the mechanisms for the neuroprotective effect of tenuigenin. We demonstrated that treatment with tenuigenin increased striatal dopaminergic levels and improved motor impairment induced by MPTP. Also, tenuigenin significantly ameliorated the degeneration of dopaminergic neurons and inhibited NLRP3 inflammasome activation in substantia nigra of MPTP mouse model. We further found that tenuigenin reduced intracellular reactive oxygen species (ROS) production and suppressed NLRP3 inflammasome activation, subsequent caspase-1 cleavage, and interleukin-1β secretion in BV2 microglia cells. These data indicate that tenuigenin inhibits the activation of NLRP3 inflammasome via downregulating ROS. Correspondingly, in vivo data showed that tenuigenin attenuates microglia activation induced by lipopolysaccharide (LPS) in substantia nigra via suppressing NLRP3 inflammasome. Our findings reveal that tenuigenin protects dopaminergic neurons from inflammation partly through inhibition of NLRP3 inflammasome activation in microglia, and suggest the promising clinical use of tenuigenin for PD therapy.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 74 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 74 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 9 12%
Student > Master 9 12%
Student > Ph. D. Student 7 9%
Student > Bachelor 6 8%
Student > Postgraduate 3 4%
Other 11 15%
Unknown 29 39%
Readers by discipline Count As %
Neuroscience 12 16%
Pharmacology, Toxicology and Pharmaceutical Science 5 7%
Biochemistry, Genetics and Molecular Biology 5 7%
Medicine and Dentistry 4 5%
Agricultural and Biological Sciences 3 4%
Other 10 14%
Unknown 35 47%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 22 December 2017.
All research outputs
#18,579,736
of 23,012,811 outputs
Outputs from Journal of Neuroinflammation
#2,084
of 2,654 outputs
Outputs of similar age
#328,880
of 440,645 outputs
Outputs of similar age from Journal of Neuroinflammation
#44
of 65 outputs
Altmetric has tracked 23,012,811 research outputs across all sources so far. This one is in the 11th percentile – i.e., 11% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,654 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.6. This one is in the 12th percentile – i.e., 12% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 440,645 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 14th percentile – i.e., 14% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 65 others from the same source and published within six weeks on either side of this one. This one is in the 18th percentile – i.e., 18% of its contemporaries scored the same or lower than it.