Evidence map›Paper›PMID 35965824›Full record

ArticleAnnals of translational medicine2022

The neuroprotective effect of YaoYi-moxibustion on ischemic stroke by attenuating NK-κB expression in rats.

Zheyi Zhou, Linglu Dun, Hong Xu, Peishan Yu, Cuilan Chen, Tao Si, Hongwei An, Junlei Lu, Bingxin Wei, Dongli Guo and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 43% 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

2 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.

  1. Pooled it
  2. Review
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

13 authors at 1 institution in 1 country.

Zheyi Zhou *Department of Neurology Laboratory, Liuzhou Traditional Chinese Medical Hospital Affiliated to Guangxi University of Chinese Medicine, Liuzhou, China.
Linglu Dun *Department of Neurology Laboratory, Liuzhou Traditional Chinese Medical Hospital Affiliated to Guangxi University of Chinese Medicine, Liuzhou, China.
Hong XuDepartment of Neurology Laboratory, Liuzhou Traditional Chinese Medical Hospital Affiliated to Guangxi University of Chinese Medicine, Liuzhou, China.
Peishan YuDepartment of Neurology Laboratory, Liuzhou Traditional Chinese Medical Hospital Affiliated to Guangxi University of Chinese Medicine, Liuzhou, China.
Cuilan ChenDepartment of Neurology Laboratory, Liuzhou Traditional Chinese Medical Hospital Affiliated to Guangxi University of Chinese Medicine, Liuzhou, China.
Tao SiDepartment of Neurology Laboratory, Liuzhou Traditional Chinese Medical Hospital Affiliated to Guangxi University of Chinese Medicine, Liuzhou, China.
Hongwei AnDepartment of Neurology Laboratory, Liuzhou Traditional Chinese Medical Hospital Affiliated to Guangxi University of Chinese Medicine, Liuzhou, China.
Junlei LuDepartment of Neurology Laboratory, Liuzhou Traditional Chinese Medical Hospital Affiliated to Guangxi University of Chinese Medicine, Liuzhou, China.
Bingxin WeiDepartment of Neurology Laboratory, Liuzhou Traditional Chinese Medical Hospital Affiliated to Guangxi University of Chinese Medicine, Liuzhou, China.
Dongli GuoDepartment of Neurology Laboratory, Liuzhou Traditional Chinese Medical Hospital Affiliated to Guangxi University of Chinese Medicine, Liuzhou, China.
Qian YangDepartment of Neurology Laboratory, Liuzhou Traditional Chinese Medical Hospital Affiliated to Guangxi University of Chinese Medicine, Liuzhou, China.
Na ZhengDepartment of Neurology Laboratory, Liuzhou Traditional Chinese Medical Hospital Affiliated to Guangxi University of Chinese Medicine, Liuzhou, China.
Ping YiDepartment of Neurology Laboratory, Liuzhou Traditional Chinese Medical Hospital Affiliated to Guangxi University of Chinese Medicine, Liuzhou, China.
Guangxi University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Traditional Chinese medicine (TCM) has become a crucial direction for ischemic stroke treatment. This study sought to explore the underlying roles of YaoYi-moxibustion (YY-moxi) in ischemic stroke. Methods: A total of 75 Sprague-Dawley rats were randomly divided into the following 5 groups: (I) the sham-operated group; (II) the middle cerebral artery occlusion model (MCAO) group; (III) the YY-moxi group; (IV) the antioxidant (N-acetylcysteine, NAC) group; and (V) the NAC + YY-moxi group. After the model had been established, the NAC group received intracerebroventricular injections of NAC, the YY-moxi group received YY-moxi, and the NAC + YY-moxi group received a combination of these 2 interventions. The neurological deficit score was confirmed, and the cerebral infarction was examined by triphenyl tetrazolium chloride (TTC) staining. In the ischemia site of stroke, terminal deoxynucleotidyl transferase-mediated Dutp nick end labeling staining was applied to examine the apoptotic cells. Additionally, the apoptosis-associated genes and protein expressions in the ischemic brains were investigated by the reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR), immunohistochemistry, and western blot analysis. Results: YY-moxi alone and YY-moxi combined with NAC significantly reduced the neurological scores and cerebral infarction area of the MCAO rats. Additionally, YY-moxi alone and the combined application of YY-moxi and NAC improved the pathological status of ischemic brain tissues. Further, we found that YY-moxi alone and YY-moxi in combination with NAC could enhanced the antioxidation ability and reduced the inflammatory response of the MCAO model rats. We also proved that YY-moxi alone and YY-moxi combined with NAC significantly suppressed apoptosis-related proteins in the MCAO model rats. Conclusions: These findings indicate that YY-moxi exerts a protective effect on cerebral ischemic injury by reducing apoptosis. The study suggests that the mechanism may be related to its downregulating the expression of nuclear factor kappa B (NK-κB).

Indexed as

apoptosis pathwaycerebral ischemic injurymoxa-moxibustionnuclear factor kappa B (NK-κB)YaoYi-moxibustion (YY-moxi)

Identifiers

PMID35965824
PMCPMC9372685
OpenAlexW4286948794

What Socratic 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 Socratic graph.