Evidence map›Paper›PMID 28620824›Full record

ArticleNeurochemical research2017

L-3-n-Butylphthalide Activates Akt/mTOR Signaling, Inhibits Neuronal Apoptosis and Autophagy and Improves Cognitive Impairment in Mice with Repeated Cerebral Ischemia-Reperfusion Injury.

Jing Xu, Yaping Huai, Nan Meng, Yanhong Dong, Zhijuan Liu, Qianqian Qi, Ming Hu, Mingyue Fan, Wei Jin, Peiyuan Lv

Abstract read
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In one paragraph

Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
–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

33 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  3. Spatial metabolic analysis of the regulatory effects of DL-3-n-butylphthalide in a cerebral ischemia-reperfusion mouse model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
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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

10 authors.

Jing XuDepartment of Neurology, Hebei Medical University, Shijiazhuang, 050017, China.
Yaping HuaiDepartment of Rehabilitation Medicine, Hebei General Hospital, Shijiazhuang, 050051, China.
Nan MengDepartment of Neurology, Hebei General Hospital, Shijiazhuang, 050051, China.
Yanhong DongDepartment of Neurology, Hebei General Hospital, Shijiazhuang, 050051, China.
Zhijuan LiuDepartment of Neurology, Hebei Medical University, Shijiazhuang, 050017, China.
Qianqian QiDepartment of Neurology, Hebei Medical University, Shijiazhuang, 050017, China.
Ming HuDepartment of Neurology, Hebei General Hospital, Shijiazhuang, 050051, China.
Mingyue FanDepartment of Neurology, Hebei General Hospital, Shijiazhuang, 050051, China.
Wei JinDepartment of Neurology, Hebei General Hospital, Shijiazhuang, 050051, China.
Peiyuan LvDepartment of Neurology, Hebei Medical University, Shijiazhuang, 050017, China. peiyuanlu@163.com.

Funding

Hebei Province Major Medical Research Project of China zd2013005Hebei Province Natural Science Foundation of China H2013307046
6 · The paper itself

Abstract

L-3-n-Butylphthalide (L-NBP) exerts neuroprotective effects in animal models of cerebral ischemia, but its potential benefits in repeated cerebral ischemia-reperfusion (RCIR) injury remain unknown. We investigated the effect of L-NBP on cognitive impairment induced by RCIR in mice. Male C57Bl/6 mice received sham surgery or bilateral common carotid artery occlusion (3 times, 20 min each) and were orally administered preoperative L-NBP (30 mg/kg/day, 7 days), postoperative L-NBP (30 or 60 mg/kg/day, 28 days) or postoperative vehicle (28 days). Learning and memory were assessed by the Morris water maze task and step-down passive avoidance test. Nissl staining was used to identify pathologic changes in the hippocampal CA1 region. The expressions of proteins associated with signaling, apoptosis and autophagy were assessed by quantitative PCR and western blot. RCIR induced deficits in learning and memory that were alleviated by preoperative or postoperative L-NBP administration. Pathologic lesions in the hippocampal CA1 region induced by RCIR were less severe in mice treated with L-NBP. Preoperative or postoperative L-NBP administration in mice receiving RCIR promoted hippocampal expression of phospho-Akt and phospho-mTOR (suggesting activation of Akt/mTOR signaling), increased the Bcl-2/Bax ratio (indicating suppression of apoptosis) and reduced the LC3-II/LC3-I ratio (implying inhibition of autophagy). Preoperative or postoperative L-NBP administration also depressed hippocampal levels of beclin-1 mRNA (indicating suppression of autophagy). These findings suggest that the effect of L-NBP to alleviate learning and memory deficits in mice following RCIR may involve activation of Akt/mTOR signaling and regulation of the expressions of proteins related to apoptosis and autophagy.

Indexed as

AnimalsApoptosisAutophagyBenzofuransBrain IschemiaCognition DisordersCognitive DysfunctionDisease Models, AnimalMaleMemory DisordersMice, Inbred C57BLNeuroprotective AgentsProto-Oncogene Proteins c-aktReperfusionTOR Serine-Threonine Kinases3-n-butylphthalideBenzofuransmTOR protein, mouseNeuroprotective AgentsProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesApoptosisAutophagyL-3-n-ButylphthalideLearningMemoryRepeated cerebral ischemia–reperfusion

Identifiers

What OpenQuestion holds

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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.