Evidence map›Paper›PMID 34080089›Full record

ArticleInflammation2021

Baicalin Inhibits NLRP3 Inflammasome Activity Via the AMPK Signaling Pathway to Alleviate Cerebral Ischemia-Reperfusion Injury.

Wen-Xia Zheng, Wen-Qi He, Qian-Rui Zhang, Jin-Xin Jia, Sheng Zhao, Fang-Jian Wu, Xiao-Lu Cao

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2021. 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
2.5field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Wen-Xia ZhengDepartment of Pharmacy, General Hospital of the Yangtze River Shipping, Wuhan, 430010, Hubei Province, China.
Wen-Qi HeDepartment of Pharmacy, College of Medical, Wuhan University of Science and Technology, Hubei Province Key Laboratory of Occupational Hazard Identification and Control, Wuhan, 430065, Hubei Province, China.
Qian-Rui ZhangDepartment of Pharmacy, General Hospital of the Yangtze River Shipping, Wuhan, 430010, Hubei Province, China.
Jin-Xin JiaDepartment of Pharmacy, College of Medical, Wuhan University of Science and Technology, Hubei Province Key Laboratory of Occupational Hazard Identification and Control, Wuhan, 430065, Hubei Province, China.
Sheng ZhaoDepartment of Pharmacy, General Hospital of the Yangtze River Shipping, Wuhan, 430010, Hubei Province, China.
Fang-Jian WuDepartment of Pharmacy, General Hospital of the Yangtze River Shipping, Wuhan, 430010, Hubei Province, China. wu_fangjian@163.com.
Xiao-Lu CaoDepartment of Pharmacy, College of Medical, Wuhan University of Science and Technology, Hubei Province Key Laboratory of Occupational Hazard Identification and Control, Wuhan, 430065, Hubei Province, China. caoxiaolu1126@163.com.ORCID http://orcid.org/0000-0002-7909-0306
Yangtze River Pharmaceutical Group (China) · CNWuhan University of Science and Technology · CN

Funding

National Natural Science Foundation of China 81801307Wuhan Municipal Health Commission 2018 Medical Scientific Research Project WX18C28
6 · The paper itself

Abstract

Baicalin has been reported to have ameliorative effects on nerve-induced hypoxic ischemia injury; however, its role in the NLRP3 inflammasome-dependent inflammatory response during cerebral ischemia-reperfusion remains unclear. To investigate the molecular mechanisms involved in baicalin alleviating cerebral ischemia-reperfusion injury, we investigated the AMPK signaling pathway which regulates NLRP3 inflammasome activity. SD rats were treated with baicalin at doses of 100 mg/kg and 200 mg/kg, respectively, after middle cerebral artery occlusion at 2 h and reperfusion for 24 h (MCAO/R). MCAO/R treatment significantly increased cerebral infarct volume, changed the ultrastructure of nerve cells, and activated the NLRP3 inflammasome, manifesting as significantly increased expression of NLRP3, ASC, cleaved caspase-1, IL-1β, and IL-18. Our results demonstrated that baicalin treatment effectively reversed these phenomena in a dose-dependent manner. Additionally, inhibition of NLRP3 expression was found to promote the neuroprotective effects of baicalin on cortical neurons. Furthermore, baicalin remarkably increased the expression of p-AMPK following oxygen glucose deprivation/reperfusion (OGD/R). The expression of the NLRP3 inflammasome was also increased when the AMPK pathway was blocked by compound C. Taken together, our findings reveal that baicalin reduces the activity of the NLRP3 inflammasome and consequently inhibits cerebral ischemia-reperfusion injury through activation of the AMPK signaling pathway.

Indexed as

AMP-Activated Protein Kinase KinasesAnimalsAnti-Inflammatory Agents, Non-SteroidalBrain IschemiaCells, CulturedFlavonoidsNeuronsNLR Family, Pyrin Domain-Containing 3 ProteinPyroptosisRatsRats, Sprague-DawleyReperfusion InjurySignal TransductionAMP-Activated Protein Kinase KinasesAnti-Inflammatory Agents, Non-SteroidalbaicalinFlavonoidsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratAMPK signaling pathwaybaicalincerebral ischemia-reperfusionNLRP3 inflammasome

Identifiers

PMID34080089
OpenAlexW3164223060

What OpenQuestion holds

Textmetadata
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.