Evidence map›Paper›PMID 38745316›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

Polyphyllin I alleviates neuroinflammation after cerebral ischemia-reperfusion injury via facilitating autophagy-mediated M2 microglial polarization.

Chunyang Kang, Qiuling Sang, Dingxi Liu, Libo Wang, Jia Li, Xiaoyang Liu

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–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

20 citing papers in PubMed.

  1. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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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.

Chunyang Kang *Department of Neurology, China-Japan Union Hospital of Jilin University, No. 126 Xiantai Street, Changchun, 130000, China.
Qiuling Sang *Department of Neuroelectrophysiology, China-Japan Union Hospital of Jilin University, Changchun, 130000, China.
Dingxi LiuDepartment of Clinical Medicine, Zunyi Medical University, Zhuhai, 519041, China.
Libo WangDepartment of Neurology, China-Japan Union Hospital of Jilin University, No. 126 Xiantai Street, Changchun, 130000, China.
Jia LiDepartment of Neurology, China-Japan Union Hospital of Jilin University, No. 126 Xiantai Street, Changchun, 130000, China. lijia33233@jlu.edu.cn.
Xiaoyang LiuDepartment of Neurology, China-Japan Union Hospital of Jilin University, No. 126 Xiantai Street, Changchun, 130000, China. liuxy48@jlu.edu.cn.ORCID 0009-0005-6184-4869

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglial activation and polarization play a central role in poststroke inflammation and neuronal damage. Modulating microglial polarization from pro-inflammatory to anti-inflammatory phenotype is a promising therapeutic strategy for the treatment of cerebral ischemia. Polyphyllin I (PPI), a steroidal saponin, shows multiple bioactivities in various diseases, but the potential function of PPI in cerebral ischemia is not elucidated yet. In our study, the influence of PPI on cerebral ischemia-reperfusion injury was evaluated. Mouse middle cerebral artery occlusion (MCAO) model and oxygen-glucose deprivation and reoxygenation (OGD/R) model were constructed to mimic cerebral ischemia-reperfusion injury in vivo and in vitro. TTC staining, TUNEL staining, RT-qPCR, ELISA, flow cytometry, western blot, immunofluorescence, hanging wire test, rotarod test and foot-fault test, open-field test and Morris water maze test were performed in our study. We found that PPI alleviated cerebral ischemia-reperfusion injury and neuroinflammation, and improved functional recovery of mice after MCAO. PPI modulated microglial polarization towards anti-inflammatory M2 phenotype in MCAO mice in vivo and post OGD/R in vitro. Besides, PPI promoted autophagy via suppressing Akt/mTOR signaling in microglia, while inhibition of autophagy abrogated the effect of PPI on M2 microglial polarization after OGD/R. Furthermore, PPI facilitated autophagy-mediated ROS clearance to inhibit NLRP3 inflammasome activation in microglia, and NLRP3 inflammasome reactivation by nigericin abolished the effect of PPI on M2 microglia polarization. In conclusion, PPI alleviated post-stroke neuroinflammation and tissue damage via increasing autophagy-mediated M2 microglial polarization. Our data suggested that PPI had potential for ischemic stroke treatment.

Indexed as

AutophagyDisease Models, AnimalMicrogliaNeuroinflammatory DiseasesReperfusion InjuryAnimalsBrain IschemiaCell PolarityDiosgeninInfarction, Middle Cerebral ArteryMaleMiceMice, Inbred C57BLSignal TransductionTOR Serine-Threonine KinasesDiosgeninTOR Serine-Threonine KinasesAutophagyCerebral ischemiaMicroglial polarizationNLRP3 inflammasomePolyphyllin I (PPI)

Identifiers

PMID38745316
PMCPMC11094947

What OpenQuestion holds

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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.