Evidence map›Paper›PMID 37256377›Full record

ArticlePsychopharmacology2023

Neuroprotection of isookanin against MPTP-induced cell death of SH-SY5Y cells via BCL2/BAX and PI3K/AKT pathways.

Rong Zhang, Lili Teng, Yi Zhong, Pei Ma, Lijia Xu, Peigen Xiao

Abstract read
PubMed Publisher
In one paragraph

Article in Psychopharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
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 1 institution in 1 country.

Rong ZhangInstitute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences & Peking Union Medical College, No. 151 Malianwa North Road, Haidian District, 100193, Beijing, China.
Lili TengInstitute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences & Peking Union Medical College, No. 151 Malianwa North Road, Haidian District, 100193, Beijing, China.
Yi ZhongInstitute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences & Peking Union Medical College, No. 151 Malianwa North Road, Haidian District, 100193, Beijing, China.
Pei MaInstitute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences & Peking Union Medical College, No. 151 Malianwa North Road, Haidian District, 100193, Beijing, China. pma@implad.ac.cn.
Lijia XuInstitute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences & Peking Union Medical College, No. 151 Malianwa North Road, Haidian District, 100193, Beijing, China. ljxu@implad.ac.cn.
Peigen XiaoInstitute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences & Peking Union Medical College, No. 151 Malianwa North Road, Haidian District, 100193, Beijing, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

CAMS Innovation Fund for Medical Sciences CIFMS 2022-I2M-2-002Hainan Academician Innovation Platform Scientific Research Project. YSPTZX202117the National Natural Science Foundation of China Grant 82174046
6 · The paper itself

Abstract

background and purposeIsookanin, an important antioxidant component in Coreopsis tinctoria Nutt., has shown remarkable hypolipidemic, hypoglycemic, and hypotensive effects. However, the neuroprotective effect of isookanin has not been reported yet. Here, the neuroprotective effects and relevant molecular mechanisms of isookanin are explored for the first time.

methodsThe SH-SY5Y cells were exposed to neurotoxic H

resultsAmong the three in vitro models, isookanin showed the best neuroprotection against MPTP-induced damage. Isookanin attenuated the levels of LDH, intracellular ROS, and mitochondrial membrane potential. Isookanin upregulated phosphorylation of AKT and PI3K, and increased BCL2/BAX ratio. Isookanin possessed a powerful affinity toward AKT. Besides, the protective effects of isookanin disappeared when cells were co-treated with an AKT inhibitor (AZD5363).

conclusionIsookanin regulated BCL2/BAX and PI3K/AKT pathways to reduce mitochondrial damage and cellular apoptosis. Isookanin may be a new protector for neurodegenerative diseases.

Indexed as

Neuroprotective AgentsApoptosisbcl-2-Associated X ProteinCell Line, TumorCell SurvivalChalconesHumansHydrogen PeroxideMolecular Docking SimulationNeuroprotectionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Reactive Oxygen Speciesbcl-2-Associated X ProteinBCL2 protein, humanChalconesHydrogen PeroxideisookaninNeuroprotective AgentsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesIsookaninMitochondrial damageNeurodegenerative diseaseNeuroprotection

Identifiers

PMID37256377
OpenAlexW4378781442

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.