Evidence map›Paper›PMID 32905277›Full record

ArticleToxicology research2020

Lidocaine promotes autophagy of SH-SY5Y cells through inhibiting PI3K/AKT/mTOR pathway by upregulating miR-145.

Zhong Wang, Qin Liu, Jun Lu, Jian Cao, Xiao-Yan Wang, Yong Chen

Open access · bronzeAbstract read
In one paragraph

Article in Toxicology research, 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
2.8field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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  6. Review
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  9. Sufentanil promotes autophagy and improves ischemiaZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
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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

6 authors at 1 institution in 1 country.

Zhong WangDepartment of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province P. R. China.
Qin LiuDepartment of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province P. R. China.
Jun LuDepartment of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province P. R. China.
Jian CaoDepartment of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province P. R. China.
Xiao-Yan WangDepartment of Medical Administration , The Second Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province P. R. China.
Yong ChenDepartment of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province P. R. China.ORCID 0000-0001-7115-7951
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lidocaine is one of the most common local anesthetics (LA) used in clinical practice and it is neurotoxic. Recent studies suggested that LA, including lidocaine, could exert protective effect over neurotoxicity by promoting autophagy. However, the underlying mechanism was not sufficiently elucidated. This study aimed to explore the mechanism behind. Human neuroblastoma cell line SH-SY5Y was used throughout the whole study. The effect of lidocaine on viability, toxicity of SH-SY5Y cells were analyzed by MTT and lactate dehydrogenase (LDH) assays, respectively. The relative expression of miR-145 was assessed by quantitative reverse transcription-polymerase chain reaction. The impact which lidocaine brought on PI3K/AKT/mTOR pathway and autophagy-related proteins were examined by the western blot assay. LC3B was assessed by immunofluorescence staining. The interaction between miR-145 and AKT3 was conducted by the dual-luciferase reporting assay. Lidocaine inhibited viability of SH-SY5Y cells in a time and dose dependent manner and enhanced the release of LDH in SH-SY5Y cells. Furthermore, the expression of miR-145 and autophagy were enhanced by lidocaine. Transfection with miR-145 inhibitor inhibited the release of LDH and autophagy. miR-145 targeted AKT3 to inhibit PI3K/AKT/mTOR pathway. Finally, lidocaine inactivated PI3K/AKT/mTOR pathways via upregulation of miR-145, and it subsequently promoted autophagy of SH-SY5Y cells. However, silence of miR-145 could reverse the promotion of the autophagy of SH-SY5Y cells. Our results showed that lidocaine promoted autophagy of nerve cells via regulating miR-145 expression and further inactivation of PI3K/AKT/mTOR signaling pathway.

Indexed as

autophagylidocainemiR-145neurotoxicity

Identifiers

PMID32905277
PMCPMC7467247
OpenAlexW3042714785

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.