Evidence map›Paper›PMID 29098460›Full record

ArticleLasers in medical science2018

Low-level laser therapy prevents endothelial cells from TNF-α/cycloheximide-induced apoptosis.

Yu-Hsiu Chu, Shu-Ya Chen, Yueh-Ling Hsieh, Yi-Hsien Teng, Yu-Jung Cheng

Abstract read
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Article in Lasers in medical science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

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

  1. Pooled it
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  14. Luteolin-Induced Activation of Mitochondrial BKAntioxidants (Basel, Switzerland) · 2022
    Article
  15. Laser acupuncture for claudication symptoms in peripheral artery disease - Does it work? A randomized trial.Hong Kong physiotherapy journal : official publication of the Hong Kong Physiotherapy Association Limited = Wu li chih liao · 2022
    Article
  16. Article
  17. Article
  18. Article
  19. Cellular Signalling and Photobiomodulation in Chronic Wound Repair.International journal of molecular sciences · 2021
    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

5 authors.

Yu-Hsiu ChuDepartment of Physical Therapy and Graduate Institute of Rehabilitation Science, China Medical University, Taichung, Taiwan.
Shu-Ya ChenDepartment of Physical Therapy and Graduate Institute of Rehabilitation Science, China Medical University, Taichung, Taiwan.
Yueh-Ling HsiehDepartment of Physical Therapy and Graduate Institute of Rehabilitation Science, China Medical University, Taichung, Taiwan.
Yi-Hsien TengDepartment of Physical Therapy and Graduate Institute of Rehabilitation Science, China Medical University, Taichung, Taiwan.
Yu-Jung ChengDepartment of Physical Therapy and Graduate Institute of Rehabilitation Science, China Medical University, Taichung, Taiwan. chengyu@mail.cmu.edu.tw.

Funding

Ministry of Science and Technology, Taiwan MOST 105-2314-B-039-009
6 · The paper itself

Abstract

Low-level laser therapy (LLLT), widely used in physiotherapy, has been known to enhance wound healing and stimulate cell proliferation, including fibroblast and endothelial cells. Applying LLLT can increase cell proliferation in many kinds of cells including fibroblasts and endothelial cells. However, the protective mechanisms of LLLT on endothelial apoptosis remain unclear. We hypothesized LLLT can protect endothelial cells from inflammation-induced apoptosis. Human endothelial cell line, EA.hy926 cells, and TNF-α/cycloheximide (TNF/CHX) were used to explore the protective effects of LLLT (660 nm) on inflammation-induced endothelial apoptosis. Cell viability, apoptosis, caspase-3/7/8/9 activity, MAPKs signaling, NF-κB activity, and inducible/endothelial nitric oxide synthase (iNOS/eNOS) expression were measured. Our results showed that LLLT increased EA.hy926 cell proliferation, attenuated the TNF/CHX-induced apoptosis, and reduced the TNF/CHX-mediated caspase-3/7/8/9 activation. In addition, LLLT increased ERK MAPK phosphorylation and suppressed the TNF/CHX-increased p38 MAPK, JNK, IKK phosphorylation, NF-κB translocation, and iNOS expression. The caspases-3 cleavage and cell death were not increased in cells treating with ERK inhibitor U0126, which implicated that ERK is not to be responsible for the protective effects of LLLT. After treating with p38 mitogen-activated protein kinase (MAPK) activator, the protection of LLLT in cell apoptosis was no longer existed, showing that LLLT protected the endothelial cells by suppressing p38 MAPK signaling. Our results provide a new insight into the possible molecular mechanisms in which LLLT protects against inflammatory-induced endothelial dysfunction.

Indexed as

Low-Level Light TherapyApoptosisCaspase 3Cell LineCell ProliferationCell SurvivalCycloheximideEndothelial CellsEnzyme ActivationExtracellular Signal-Regulated MAP KinasesHumansMAP Kinase Signaling SystemNF-kappa BNitric Oxide Synthase Type IIp38 Mitogen-Activated Protein KinasesPhosphorylationCaspase 3CycloheximideExtracellular Signal-Regulated MAP KinasesNF-kappa BNitric Oxide Synthase Type IIp38 Mitogen-Activated Protein KinasesTumor Necrosis Factor-alphaApoptosisCaspasesInflammationLLLTMAPKTNF-α

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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.