Evidence map›Paper›PMID 35103832›Full record

ArticlePsychopharmacology2022

Baicalin attenuates amyloid β oligomers induced memory deficits and mitochondria fragmentation through regulation of PDE-PKA-Drp1 signalling.

Hai-Yang Yu, Ye Zhu, Xin-Li Zhang, Lei Wang, Yan-Meng Zhou, Fang-Fang Zhang, Han-Ting Zhang, Xiao-Min Zhao

Abstract read
PubMed Publisher
In one paragraph

Article in Psychopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Hai-Yang YuSchool of Pharmaceutical Sciences, Shandong First Medical University & Shandong Academy of Medical Sciences, Tai'an, 210046, People's Republic of China. yuhaiyang_15@163.com.
Ye ZhuSchool of Radiology, Shandong First Medical University & Shandong Academy of Medical Sciences, Tai'an, 210046, People's Republic of China.
Xin-Li ZhangSchool of Pharmaceutical Sciences, Shandong First Medical University & Shandong Academy of Medical Sciences, Tai'an, 210046, People's Republic of China.
Lei WangSchool of Pharmaceutical Sciences, Shandong First Medical University & Shandong Academy of Medical Sciences, Tai'an, 210046, People's Republic of China.
Yan-Meng ZhouSchool of Pharmaceutical Sciences, Shandong First Medical University & Shandong Academy of Medical Sciences, Tai'an, 210046, People's Republic of China.
Fang-Fang ZhangSchool of Pharmaceutical Sciences, Shandong First Medical University & Shandong Academy of Medical Sciences, Tai'an, 210046, People's Republic of China.
Han-Ting ZhangSchool of Pharmacy, Qingdao University, Qingdao, 266073, People's Republic of China.
Xiao-Min ZhaoSchool of Chemistry and Pharmaceutical Engineering, Shandong First Medical University & Shandong Academy of Medical Sciences, Tai'an, 210046, People's Republic of China.
Shandong First Medical University · CNQingdao University · CN

Funding

Natural Science Foundation of Shandong Province ZR2020MH127Shandong Administration of traditional Chinese Medicine 2019-0354Shandong Administration of traditional Chinese Medicine 2019-0356
6 · The paper itself

Abstract

rationaleMitochondrial fragmentation contributes to the initiation of Alzheimer's disease (AD) pathology. Baicalin plays a significant role in rescuing mitochondrial dysfunction. However, the effect of baicalin treatment on the modulation of mitochondrial fragmentation has not yet been assessed.

objectivesThe present study was designed to evaluate the effect of baicalin on memory and understand its mechanism of action.

resultsBaicalin treatment significantly reversed the altered learning and memory behaviours in AD mouse model. We found that baicalin treatment significantly improved the levels of microtubule association protein-2 and enhanced the expression of synaptophysin and postsynaptic density protein 95 (PSD95). Moreover, treatment with baicalin reversed amyloid-β oligomer (AβO)-induced abnormalities in the succinate dehydrogenase complex iron sulphur subunit B (SDHB) and cytochrome c oxidase components I (COXI) and mitochondrial fragmentation in the hippocampus. Further, we found that baicalin decreased the PDE4 levels and upregulated the levels of phosphorylated Ser157 site of vasodilator-stimulated phosphoprotein (pVASP

conclusionThe effect of baicalin on memory improvement may be due to improved synaptic plasticity, mitochondrial fragmentation, and rescue of dysfunction via the inhibition of PDE4, which leads to activation of pDrp1

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsFlavonoidsMemory DisordersMiceMitochondriaNeuronsAmyloid beta-PeptidesbaicalinFlavonoidsAlzheimer’s diseaseBaicalinMitochondria fragmentationPDEPKA-pDrp1S637

Identifiers

PMID35103832
OpenAlexW4210538436

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.