Evidence map›Paper›PMID 29273596›Full record

ArticleStroke2018

Dihydrolipoic Acid Inhibits Lysosomal Rupture and NLRP3 Through Lysosome-Associated Membrane Protein-1/Calcium/Calmodulin-Dependent Protein Kinase II/TAK1 Pathways After Subarachnoid Hemorrhage in Rat.

Keren Zhou, Budbazar Enkhjargal, Zhiyi Xie, Chengmei Sun, Lingyun Wu, Jay Malaguit, Sheng Chen, Jiping Tang, Jianmin Zhang, John H Zhang

Expression of concernOpen access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stroke, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 95 citations in OpenAlex.

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  14. Role of Estrogen-Related Receptor γ and PGC-1α/SIRT3 Pathway in Early Brain Injury After Subarachnoid Hemorrhage.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
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  20. A virulentVirulence · 2021
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Keren ZhouFrom the Department of Neurosurgery, Second Affiliated Hospital, School of Medicine (K.Z., S.C., J.Z.), Brain research institute (K.Z., S.C., J.Z.), and Collaborative Innovation Center for Brain Science (K.Z., S.C., J.Z.), Zhejiang University, Hangzhou, China; and Department of Physiology and Pharmacology, Loma Linda University, CA (K.Z., B.E., Z.X.,C.S., L.W., J.M., J.T., J.H.Z.).
Budbazar EnkhjargalFrom the Department of Neurosurgery, Second Affiliated Hospital, School of Medicine (K.Z., S.C., J.Z.), Brain research institute (K.Z., S.C., J.Z.), and Collaborative Innovation Center for Brain Science (K.Z., S.C., J.Z.), Zhejiang University, Hangzhou, China; and Department of Physiology and Pharmacology, Loma Linda University, CA (K.Z., B.E., Z.X.,C.S., L.W., J.M., J.T., J.H.Z.).
Zhiyi XieFrom the Department of Neurosurgery, Second Affiliated Hospital, School of Medicine (K.Z., S.C., J.Z.), Brain research institute (K.Z., S.C., J.Z.), and Collaborative Innovation Center for Brain Science (K.Z., S.C., J.Z.), Zhejiang University, Hangzhou, China; and Department of Physiology and Pharmacology, Loma Linda University, CA (K.Z., B.E., Z.X.,C.S., L.W., J.M., J.T., J.H.Z.).
Chengmei SunFrom the Department of Neurosurgery, Second Affiliated Hospital, School of Medicine (K.Z., S.C., J.Z.), Brain research institute (K.Z., S.C., J.Z.), and Collaborative Innovation Center for Brain Science (K.Z., S.C., J.Z.), Zhejiang University, Hangzhou, China; and Department of Physiology and Pharmacology, Loma Linda University, CA (K.Z., B.E., Z.X.,C.S., L.W., J.M., J.T., J.H.Z.).
Lingyun WuFrom the Department of Neurosurgery, Second Affiliated Hospital, School of Medicine (K.Z., S.C., J.Z.), Brain research institute (K.Z., S.C., J.Z.), and Collaborative Innovation Center for Brain Science (K.Z., S.C., J.Z.), Zhejiang University, Hangzhou, China; and Department of Physiology and Pharmacology, Loma Linda University, CA (K.Z., B.E., Z.X.,C.S., L.W., J.M., J.T., J.H.Z.).
Jay MalaguitFrom the Department of Neurosurgery, Second Affiliated Hospital, School of Medicine (K.Z., S.C., J.Z.), Brain research institute (K.Z., S.C., J.Z.), and Collaborative Innovation Center for Brain Science (K.Z., S.C., J.Z.), Zhejiang University, Hangzhou, China; and Department of Physiology and Pharmacology, Loma Linda University, CA (K.Z., B.E., Z.X.,C.S., L.W., J.M., J.T., J.H.Z.).
Sheng ChenFrom the Department of Neurosurgery, Second Affiliated Hospital, School of Medicine (K.Z., S.C., J.Z.), Brain research institute (K.Z., S.C., J.Z.), and Collaborative Innovation Center for Brain Science (K.Z., S.C., J.Z.), Zhejiang University, Hangzhou, China; and Department of Physiology and Pharmacology, Loma Linda University, CA (K.Z., B.E., Z.X.,C.S., L.W., J.M., J.T., J.H.Z.).
Jiping TangFrom the Department of Neurosurgery, Second Affiliated Hospital, School of Medicine (K.Z., S.C., J.Z.), Brain research institute (K.Z., S.C., J.Z.), and Collaborative Innovation Center for Brain Science (K.Z., S.C., J.Z.), Zhejiang University, Hangzhou, China; and Department of Physiology and Pharmacology, Loma Linda University, CA (K.Z., B.E., Z.X.,C.S., L.W., J.M., J.T., J.H.Z.).
Jianmin ZhangFrom the Department of Neurosurgery, Second Affiliated Hospital, School of Medicine (K.Z., S.C., J.Z.), Brain research institute (K.Z., S.C., J.Z.), and Collaborative Innovation Center for Brain Science (K.Z., S.C., J.Z.), Zhejiang University, Hangzhou, China; and Department of Physiology and Pharmacology, Loma Linda University, CA (K.Z., B.E., Z.X.,C.S., L.W., J.M., J.T., J.H.Z.). johnzhang3910@yahoo.com zjm135@zju.edu.cn.
John H ZhangFrom the Department of Neurosurgery, Second Affiliated Hospital, School of Medicine (K.Z., S.C., J.Z.), Brain research institute (K.Z., S.C., J.Z.), and Collaborative Innovation Center for Brain Science (K.Z., S.C., J.Z.), Zhejiang University, Hangzhou, China; and Department of Physiology and Pharmacology, Loma Linda University, CA (K.Z., B.E., Z.X.,C.S., L.W., J.M., J.T., J.H.Z.). johnzhang3910@yahoo.com zjm135@zju.edu.cn.
Loma Linda University · US

Funding

Vascular Biology Core FacilityP01NS082184 · NINDS · LOMA LINDA UNIVERSITY · PI PEARCE, WILLIAM J. · 2014 to 2018
$6.1M
Neurovascular Protection for Early Brain Injury after SAHR01NS081740 · NINDS · LOMA LINDA UNIVERSITY · PI ZHANG, JOHN H · 2013 to 2017
$1.6M
NINDS NIH HHS P01 NS082184NINDS NIH HHS R01 NS081740
6 · The paper itself

Abstract

background and purposeThe NLRP3 (nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3) inflammasome is a crucial component of the inflammatory response in early brain injury after subarachnoid hemorrhage (SAH). In this study, we investigated a role of dihydrolipoic acid (DHLA) in lysosomal rupture, NLRP3 activation, and determined the underlying pathway.

methodsSAH was induced by endovascular perforation in male Sprague-Dawley rats. DHLA was administered intraperitoneally 1 hour after SAH. Small interfering RNA for lysosome-associated membrane protein-1 and CaMKIIα (calcium/calmodulin-dependent protein kinase II α) was administered through intracerebroventricular 48 hours before SAH induction. SAH grade evaluation, short- and long-term neurological function testing, Western blot, and immunofluorescence staining experiments were performed.

resultsDHLA treatment increased the expression of lysosome-associated membrane protein-1 and decreased phosphorylated CaMKIIα and NLRP3 inflammasome, thereby alleviating neurological deficits after SAH. Lysosome-associated membrane protein-1 small interfering RNA abolished the neuroprotective effects of DHLA and increased the level of phosphorylated CaMKIIα, p-TAK1 (phosphorylated transforming growth factor-β-activated kinase), p-JNK (phosphorylated c-Jun-N-terminal kinase), and NLRP3 inflammasome. CaMKIIα small interfering RNA downregulated the expression of p-TAK1, p-JNK, and NLRP3 and improved the neurobehavior after SAH.

conclusionsDHLA treatment improved neurofunction and alleviated inflammation through the lysosome-associated membrane protein-1/CaMKII/TAK1 pathway in early brain injury after SAH. DHLA may provide a promising treatment to alleviate early brain injury after SAH.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Lysosomal-Associated Membrane Protein 1Lysosomal Membrane ProteinsLysosomesMaleMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMAP Kinase Signaling SystemNLR Family, Pyrin Domain-Containing 3 ProteinRatsRats, Sprague-DawleySubarachnoid HemorrhageThioctic AcidCalcium-Calmodulin-Dependent Protein Kinase Type 2Camk2a protein, ratdihydrolipoic acidLamp1 protein, ratLysosomal-Associated Membrane Protein 1Lysosomal Membrane ProteinsMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratThioctic Acidcalcium-calmodulin-dependent protein kinase type 2dihydrolipoic acidinflammasomeslysosomal-associated membrane protein 1subarachnoid hemorrhage

Identifiers

PMID29273596
PMCPMC5744882
OpenAlexW2780417897

What OpenQuestion holds

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Read underepoch 390

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.