Evidence map›Paper›PMID 35428182›Full record

ArticleBMC anesthesiology2022

Ropivacaine inhibits wound healing by suppressing the proliferation and migration of keratinocytes via the PI3K/AKT/mTOR Pathway.

Xiaoyang Wu, Quanyu Sun, Simeng He, Ya Wu, Shihan Du, Lirong Gong, Jianbo Yu, Haifeng Guo

Open access · goldAbstract read
In one paragraph

Article in BMC anesthesiology, 2022. 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
1.5field-weighted citation impact, top 17% 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, 13 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Ropivacaine as a novel AKT1 specific inhibitor regulates the stemness of breast cancer.Journal of experimental & clinical cancer research : CR · 2024
    Article
  8. Targeting Signalling Pathways in Chronic Wound Healing.International journal of molecular sciences · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Article
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

8 authors at 4 institutions in 1 country.

Xiaoyang Wu *School of Medicine, Nankai University, Tianjin, China.
Quanyu Sun *the First Clinical Medical College, Mudanjiang Medical University, Mudanjiang, , Heilongjiang, China.
Simeng He *School of Medicine, Nankai University, Tianjin, China.
Ya WuDepartment of Anesthesiology and Critical Care Medicine, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, China.
Shihan DuDepartment of Anesthesiology and Critical Care Medicine, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, China.
Lirong GongDepartment of Anesthesiology and Critical Care Medicine, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, China.
Jianbo YuSchool of Medicine, Nankai University, Tianjin, China. 30717008@nankai.edu.cn.
Haifeng GuoDepartment of General Surgery, Hongqi Hospital Affiliated to Mudanjiang Medical University, Mudanjiang, Heilongjiang, China. 13555006398@163.com.
Tianjin Nankai Hospital · CNMudanjiang Medical University · CNNankai University · CNTianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAfter surgery, millions of people suffer from delayed healing or wound dehiscence with subsequent severe complications, even death. Previous studies have reported that ropivacaine exhibits anti-proliferative and anti-migratory activities on numerous cells. Whether ropivacaine is able to influence the proliferation and migration of keratinocytes is still unclear. This study aimed to investigate the effect of ropivacaine on keratinocytes and its underlying molecular mechanism.

methodsAdult male Sprague-Dawley rats were allocated to establish wound healing models with or without 0.75% ropivacaine treatment and assessed the epidermal thickness by HE staining. HaCaT cells were cultured to evaluate the effect of ropivacaine on wound healing. The cell proliferation, apoptosis status and migration were detected in vitro. Moreover, western blotting was used to examine expression to with PI3K/AKT/mTOR signaling pathways for molecular studies and the changes in inflammatory factors (IL-6, IL-10, TNF-α) were detected by ELISA.

resultsIn the present study, we found that ropivacaine delayed wound closure in vivo. In vitro experiments, it was demonstrated that ropivacaine significantly inhibited the proliferation and migration of HaCaT cells via the suppression of PI3K/AKT/mTOR signaling pathway. Activation of PI3K/AKT/mTOR signaling pathway reversed the effects of ropivacaine on the proliferation and migration of HaCaT cells. Furthermore, ropivacaine contributed to the release of pro-inflammatory cytokines (IL-6 and TNF-α) and inhibited the secretion of anti-inflammatory cytokines of keratinocytes (IL-10).

conclusionsOur research demonstrated that ropivacaine treatment showed a more decreased wound closure rate. Mechanistically, we found that ropivacaine suppressed the proliferation and migration of keratinocytes and altered the expression of cytokines by inhibiting PI3K/AKT/mTOR pathway.

Indexed as

Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAnimalsCell ProliferationCytokinesHumansInterleukin-10Interleukin-6KeratinocytesMaleRatsRats, Sprague-DawleyRopivacaineTOR Serine-Threonine KinasesTumor Necrosis Factor-alphaWound HealingCytokinesInterleukin-10Interleukin-6MTOR protein, humanmTOR protein, ratPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRopivacaineTOR Serine-Threonine KinasesTumor Necrosis Factor-alphaAKTmTOR PathwayPI3KRopivacaineWound healing

Identifiers

PMID35428182
PMCPMC9011930
OpenAlexW4226198880

What OpenQuestion holds

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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 OpenQuestion graph.