Evidence map›Paper›PMID 39698073›Full record

ArticleHeliyon2024

Tibetan golden acupuncture inhibits JNK/caspase-3 signaling pathway to alleviate neuronal apoptosis in cerebral ischemia-reperfusion injury.

Yaru Liu, Yixilamu, Guilin Jin, Mingke Feng, Chunhua, Dawa

Abstract read
In one paragraph

Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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.

Yaru LiuSchool of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, Beijing, China.
YixilamuUniversity of Tibetan Medicine, Lhasa, China.
Guilin JinUniversity of Tibetan Medicine, Lhasa, China.
Mingke FengUniversity of Tibetan Medicine, Lhasa, China.
ChunhuaUniversity of Tibetan Medicine, Lhasa, China.
DawaUniversity of Tibetan Medicine, Lhasa, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Apoptosis induced by cerebral ischemia-reperfusion is one of the key pathological processes of nerve injury. Tibetan golden acupuncture (GA) is a common treatment for ischemic brain injury in Tibetan. The aim of this study was to explore whether GA prevents cerebral ischemia-reperfusion-induced apoptosis in mice by blocking the JNK/caspase-3 pathway. Methods: In experiment I, 36 mice were randomly divided into a Sham group, CI/RI group, CI/RI + GA group. Morris water maze tests, TdT-mediated dUTP-biotin nick end labeling (TUNEL) staining and flow cytometry (FCM) were used to evaluate the effect of the GA intervention on CI/RI. In experiment II, 30 mice were randomly divided into a Sham group, CI/RI group, CI/RI + GA group, CI/RI + SP group and CI/RI + SP + EA group. Western blotting was used to detect protein expression of key factors in the JNK signaling pathway in the hippocampus. Results: After 7 and 14 interventions, behavioral evaluations in CI/RI + GA group was significantly different from those in CI/RI groups (p < 0.01), pathological injury and apoptosis were significantly reduced (p < 0.01). Compared with CI/RI group, the expression of P-JNK/JNK, Cleaved caspase-3/caspase-3, Bax, and Bad proteins in CI/RI + GA group, CI/RI + SP and CI/RI + SP + GA groups were significantly decreased (p < 0.01). The expression of B-cell lymphoma 2 (Bcl-2) was significantly increased (p < 0.01, p < 0.05). Conclusions: GA can restore neurological dysfunction and inhibit hippocampal neuronal apoptosis in CI/RI mice, at least partially through inhibition of the JNK/Caspase-3 signaling pathway and regulation of apoptosis signals.

Indexed as

ApoptosisCerebral ischemia/reperfusion injuryHippocampusJNK/Caspase-3 signaling pathwayNeurological deficitTibetan golden acupuncture

Identifiers

PMID39698073
PMCPMC11652837

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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.