Evidence map›Paper›PMID 30666561›Full record

ArticleMolecular neurobiology2019

Steroid-Enriched Fraction of Achyranthes bidentata Protects Amyloid β Peptide 1-40-Induced Cognitive Dysfunction and Neuroinflammation in Rats.

Li-Wei Lin, Fan-Hsuan Tsai, Wan-Cheng Lan, Yih-Dih Cheng, Sheng-Chi Lee, Chi-Rei Wu

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Metformin mitigates amyloid βMetabolic brain disease · 2023
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Nobiletin prevents amyloid βMetabolic brain disease · 2022
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
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

6 authors at 3 institutions in 1 country.

Li-Wei LinSchool of Chinese Medicines for Post-Baccalaureate, I-Shou University, Kaohsiung, 82445, Taiwan.
Fan-Hsuan TsaiSchool of Chinese Medicines for Post-Baccalaureate, I-Shou University, Kaohsiung, 82445, Taiwan.
Wan-Cheng LanDepartment of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung, 40402, Taiwan.
Yih-Dih ChengDepartment of Pharmacy, China Medical University Hospital, Taichung, 40402, Taiwan.
Sheng-Chi LeePintung Branch, Kaohsiung Veterans General Hospital, Pitung, 91245, Taiwan. osclee.tw@msa.hinet.net.
Chi-Rei WuDepartment of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung, 40402, Taiwan. crw@mail.cmu.edu.tw.ORCID http://orcid.org/0000-0002-7036-5035
China Medical University · TWI-Shou University · TWKaohsiung Veterans General Hospital · TW

Funding

Ministry of Science and Technology NSC 100-2320-B-214-001
6 · The paper itself

Abstract

The roots of Achyranthes bidentata Blume (AB) is commonly used in the treatment of osteoporosis and dementia in traditional Chinese medicine. Pharmacological reports evidenced that AB possessed anti-osteoarthritis effects. However, there is little literature about the anti-dementia activities of AB. The present study was designed to prepare steroid-enriched fraction of AB (ABS) and investigate whether ABS can protect from cognitive dysfunction and neuroinflammation against Aβ 1-40-induced Alzheimer's disease (AD) model in rats. ABS only contained 135.11 ± 4.28 mg of ecdysterone per gram. ABS (50 mg/kg) reversed the dysfunction of exploratory activity and memory function on plus-maze and Morris water maze caused by Aβ 1-40 in rats. ABS (50 mg/kg) also decreased amyloid deposition, neurofibrillary tangle, neural damage, activated astrocyte, and microglial caused by Aβ 1-40. Furthermore, ABS reversed the phenomenon of neural oxidative damage and neuroinflammation, including the higher levels of MDA and cytokines, and the lower activities of antioxidant enzymes and GSH levels caused by Aβ 1-40 in rat cortex and hippocampus. Finally, ABS restored the activation of ERK pathway and decreased NF-κB phosphorylation and translocation altered by Aβ 1-40. ABS alone (50 mg/kg) promoted cognitive function, activated brain antioxidant defense system, and decreased brain TNF-α levels in sham group. Therefore, ABS has the cognition-promoting and antidementia potential. Steroids especial ecdysterone are major active components of AB. The action mechanism is due to decreasing oxidative stress and neuroinflammation through modulating ERK pathway, NF-κB phosphorylation, and translocation in Aβ 1-40-induced AD rat model.

Indexed as

AcetylcholinesteraseAchyranthesAmyloid beta-PeptidesAnimalsAntioxidantsAstrocytesBehavior, AnimalBrainCognitive DysfunctionCytokinesEcdysteroneGlutathioneHippocampusInflammationMaleMalondialdehydeAcetylcholinesteraseAmyloid beta-Peptidesamyloid beta-protein (1-40)AntioxidantsCytokinesEcdysteroneGlutathioneMalondialdehydeNeuroprotective AgentsNF-kappa BOleanolic AcidPeptide FragmentsSteroidsTriterpenesUrsolic AcidAchyranthes bidentataAβ 1–40EcdysteroneERK/NF-κB pathwayHippocampusNeuroinflammationOxidative stress

Identifiers

PMID30666561
OpenAlexW2917128008

What OpenQuestion holds

Textmetadata
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.