Evidence map›Paper›PMID 26550302›Full record

ArticleInternational journal of clinical and experimental medicine2015

Allopregnanolone attenuates Aβ25-35-induced neurotoxicity in PC12 cells by reducing oxidative stress.

Xiaowei Qian, Hong Cao, Qian Ma, Qinsai Wang, Wei He, Peishun Qin, Bin Ji, Kaiming Yuan, Fanghua Yang, Xuhua Liu and 2 more

Abstract read
In one paragraph

Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 22 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

12 authors at 1 institution in 1 country.

Xiaowei QianDepartment of Anesthesiology, Critical Care and Pain Medicine, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
Hong CaoDepartment of Anesthesiology, Critical Care and Pain Medicine, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
Qian MaDepartment of Anesthesiology, Critical Care and Pain Medicine, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
Qinsai WangDepartment of Anesthesiology, Critical Care and Pain Medicine, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
Wei HeDepartment of Anesthesiology, Critical Care and Pain Medicine, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
Peishun QinDepartment of Anesthesiology, Critical Care and Pain Medicine, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
Bin JiDepartment of Anesthesiology, Critical Care and Pain Medicine, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
Kaiming YuanDepartment of Anesthesiology, Critical Care and Pain Medicine, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
Fanghua YangDepartment of Anesthesiology, Critical Care and Pain Medicine, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
Xuhua LiuDepartment of Anesthesiology, Critical Care and Pain Medicine, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
Qingquan LianDepartment of Anesthesiology, Critical Care and Pain Medicine, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
Jun LiDepartment of Anesthesiology, Critical Care and Pain Medicine, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Massive accumulation of amyloid beta (Aβ) has been implicated as a pivotal event in the pathogenesis of Alzheimer's disease. The underlying mechanisms of Aβ-induced neurotoxicity include generation of reactive oxidative species (ROS), inflammation, and neurons loss. Allopregnano-lone (APα), a neurosteroid derive from neuroactive progesterone, has been demonstrated to have neuroprotective properties in vivo and vitro. In the present study, the effects of APα on oxidative damage in Aβ25-35-treated pheochromocytoma (PC12) cells were investigated. Pretreatment of APα significantly attenuated Aβ25-35-induced neuronal death. APα decreased the intracellular ROS generation and reduced lipid peroxidation induced by Aβ25-35. In addition, APα treatment enhanced antioxidant enzyme superoxide dismutase (SOD) activity. This study demonstrates that APα exerts a protective effect against Aβ25-35-induced neurotoxicity in PC12 cells. The protective role of APα likely results from inhibition of oxidative stress.

Indexed as

Allopregnanoloneamyloid betaPC12 cellsreactive oxidative species

Identifiers

PMID26550302
PMCPMC4612987
OpenAlexW2173908654

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.