Evidence map›Paper›PMID 33519423›Full record

ArticleFrontiers in aging neuroscience2020

Atorvastatin Attenuates Isoflurane-Induced Activation of ROS-p38MAPK/ATF2 Pathway, Neuronal Degeneration, and Cognitive Impairment of the Aged Mice.

Pengfei Liu, Quansheng Gao, Lei Guan, Weixuan Sheng, Yanting Hu, Teng Gao, Jingwen Jiang, Yongxing Xu, Hui Qiao, Xinying Xue and 2 more

Abstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

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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.

Pengfei LiuDepartment of Anesthesiology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Quansheng GaoDepartment of Operational Medicine, Tianjin Institute of Environmental and Operational Medicine, Tianjin, China.
Lei GuanDepartment of Anesthesiology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Weixuan ShengDepartment of Anesthesiology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Yanting HuDepartment of Anesthesiology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Teng GaoDepartment of Anesthesiology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Jingwen JiangDepartment of Anesthesiology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Yongxing XuDepartment of Nephrology, Chinese PLA Strategic Support Force Characteristic Medical Center, Beijing, China.
Hui QiaoDepartment of Anesthesiology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Xinying XueDepartment of Respiratory and Critical Care, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Sanhong LiuInstitute of Interdisciplinary Integrative Medicine Research, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Tianzuo LiDepartment of Anesthesiology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Isoflurane, a widely used volatile anesthetic, induces neuronal apoptosis and memory impairments in various animal models. However, the potential mechanisms and effective pharmacologic agents are still not fully understood. The p38MAPK/ATF-2 pathway has been proved to regulate neuronal cell survival and inflammation. Besides, atorvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, exerts neuroprotective effects. Thus, this study aimed to explore the influence of atorvastatin on isoflurane-induced neurodegeneration and underlying mechanisms. Aged C57BL/6 mice (20 months old) were exposed to isoflurane (1.5%) anesthesia for 6 h. Atorvastatin (5, 10, or 20 mg/kg body weight) was administered to the mice for 7 days. Atorvastatin attenuated the isoflurane-induced generation of ROS and apoptosis. Western blotting revealed a decrease in cleaved caspase-9 and caspase-3 expression in line with ROS levels. Furthermore, atorvastatin ameliorated the isoflurane-induced activation of p38MAPK/ATF-2 signaling. In a cellular study, we proved that isoflurane could induce oxidative stress and inflammation by activating the p38MAPK/ATF-2 pathway in BV-2 microglia cells. In addition, SB203580, a selected p38MAPK inhibitor, inhibited the isoflurane-induced inflammation, oxidative stress, and apoptosis. The results implied that p38MAPK/ATF-2 was a potential target for the treatment of postoperative cognitive dysfunction.

Indexed as

agingatorvastatinisofluranemitogen activated protein kinasesneuronal degenerationreactive oxygen species

Identifiers

PMID33519423
PMCPMC7840608

What Socratic holds

Textmetadata
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 Socratic graph.