Evidence map›Paper›PMID 33805302›Full record

ArticleAntioxidants (Basel, Switzerland)2021

Icaritin Provides Neuroprotection in Parkinson's Disease by Attenuating Neuroinflammation, Oxidative Stress, and Energy Deficiency.

Hao Wu, Xi Liu, Ze-Yu Gao, Ming Lin, Xin Zhao, Yi Sun, Xiao-Ping Pu

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.2field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 49 citations in OpenAlex.

  1. Frontiers in medicine · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Hao WuNational Key Research Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China.
Xi LiuNational Key Research Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China.
Ze-Yu GaoNational Key Research Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China.
Ming LinNational Key Research Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China.
Xin ZhaoNational Key Research Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China.
Yi SunNational Key Research Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China.ORCID 0000-0001-7043-5251
Xiao-Ping PuNational Key Research Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China.ORCID 0000-0002-7932-5603
Peking University · CN

Funding

Science and Technology Major Projects: Significant New-Drugs Creation 2018ZX09711001-009-006
6 · The paper itself

Abstract

Neuroinflammation, oxidative stress, and mitochondrial dysfunction are all important pathogenic mechanisms underlying motor dysfunction and dopaminergic neuronal damage observed in patients with Parkinson's disease (PD). However, despite extensive efforts, targeting inflammation and oxidative stress using various approaches has not led to meaningful clinical outcomes, and mitochondrial enhancers have also failed to convincingly achieve disease-modifying effects. We tested our hypothesis that treatment approaches in PD should simultaneously reduce neuroinflammation, oxidative stress, and improve alterations in neuronal energy metabolism using the flavonoid icaritin in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. Using matrix-assisted laser desorption/ionization-mass spectrometry imaging (MALDI-MSI), coupled with biochemical analyses and behavioral tests, we demonstrate that icaritin improves PD by attenuating the the NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome activity and stabilizing mitochondrial function, based on our extensive analyses showing the inhibition of NLRP3 inflammasome, reduction of NLRP3-mediated IL-1β secretion, and improvements in the levels of antioxidant molecules. Our data also indicated that icaritin stabilized the levels of proteins related to mitochondrial function, such as voltage-dependent anion channel (VDAC) and ATP synthase subunit beta (ATP5B), as well as those of molecules related to energy metabolism, such as ATP and ADP, ultimately improving mitochondrial dysfunction. By employing molecular docking, we also discovered that icaritin can interact with NLRP3, VDAC, ATP5B, and several blood-brain barrier (BBB)-related proteins. These data provide insights into the promising therapeutic potential of icaritin in PD.

Indexed as

1-methyl-4-phenyl-1,2,3,6-tetrahydropyridineicaritininflammationmitochondrial disfunctionoxidative stressParkinson’s disease

Identifiers

PMID33805302
PMCPMC8066334
OpenAlexW3146492162

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.