Evidence map›Paper›PMID 32236586›Full record

ArticleInternational journal of molecular medicine2020

Ligustrazine ameliorates lipopolysaccharide‑induced neurocognitive impairment by activating autophagy via the PI3K/AKT/mTOR pathway.

Guangming Li, Sisi Liu, Huili Wang, Rui Pan, Haijie Tang, Xueqin Yan, Yanping Wang, Yongmei Fu, Fujun Jing, Jun Dong

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 25 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

10 authors at 2 institutions in 1 country.

Guangming LiDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Sisi LiuDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Huili WangDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Rui PanDepartment of Orthopedics, The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Haijie TangDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Xueqin YanDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Yanping WangDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Yongmei FuDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Fujun JingDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Jun DongDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Jinan University · CNFirst Affiliated Hospital of Jinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a lysosome‑mediated cell content‑dependent degradation pathway that leads to enhanced inflammation in an uncontrolled state. This study examined the role of autophagy in lipopolysaccharide (LPS)‑induced brain inflammation and the effects of the traditional Chinese medicine ligustrazine on LPS‑induced neurocognitive impairment in rats. Furthermore, the molecular mechanisms by which ligustrazine influences neurocognitive impairments were explored. The production of the inflammatory mediators interleukin (IL)‑1β and tumor necrosis factor (TNF)‑α was analyzed using ELISAs, and the expression levels of the autophagy marker microtubule‑associated protein light chain 3 (LC3) II/I were analyzed using western blotting. LPS exposure upregulated the expression of IL‑1β and TNF‑α and downregulated the expression of LC3 II/I. Ligustrazine activated autophagy by preventing the expression of phosphoinositide 3‑kinase (PI3K), phosphorylated protein kinase B (p‑AKT), and phosphorylated mammalian target of rapamycin (p‑mTOR). The present results suggest that ligustrazine improved LPS‑induced neurocognitive impairments by activating autophagy and ameliorated neuronal injury by regulating the PI3K/AKT/mTOR signaling pathway. These findings provide an important reference for the prevention and treatment of neuroinflammation.

Indexed as

AnimalsApoptosisAutophagyDown-RegulationFemaleInflammationInterleukin-1betaLipopolysaccharidesMaleNeurocognitive DisordersPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPyrazinesRatsRats, Sprague-DawleySignal TransductionInterleukin-1betaLipopolysaccharidesmTOR protein, ratPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPyrazinestetramethylpyrazineTOR Serine-Threonine Kinases

Identifiers

PMID32236586
PMCPMC7169653
OpenAlexW3012014897

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.