Evidence map›Paper›PMID 33989759›Full record

ArticleFree radical biology & medicine2021

Kisspeptin-54 attenuates oxidative stress and neuronal apoptosis in early brain injury after subarachnoid hemorrhage in rats via GPR54/ARRB2/AKT/GSK3β signaling pathway.

Yi Huang, Yong Guo, Lei Huang, Yuanjian Fang, Dujuan Li, Rui Liu, Qin Lu, Reng Ren, Lihui Tang, Lifei Lian and 4 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-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

25 citing papers in PubMed, 35 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 2 countries.

Yi HuangDepartment of Neurosurgery, Ningbo Hospital, Zhejiang University School of Medicine, Ningbo, Zhejiang, 315010, China; Department of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, 92350, USA; Department of Neurosurgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310009, China.
Yong GuoDepartment of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, 92350, USA; Cerebrovascular Center, Henan Provincial People's Hospital, Zhengzhou University, Zhengzhou, Henan, 450003, China.
Lei HuangDepartment of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, 92350, USA; Department of Neurosurgery, Loma Linda University, Loma Linda, CA, 92350, USA.
Yuanjian FangDepartment of Neurosurgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310009, China.
Dujuan LiDepartment of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, 92350, USA.
Rui LiuDepartment of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, 92350, USA.
Qin LuDepartment of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, 92350, USA.
Reng RenDepartment of Neurosurgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310009, China.
Lihui TangDepartment of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, 92350, USA.
Lifei LianDepartment of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, 92350, USA.
Yongmei HuDepartment of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, 92350, USA.
Jiping TangDepartment of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, 92350, USA.
Gao ChenDepartment of Neurosurgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310009, China. Electronic address: d-chengao@zju.edu.cn.
John H ZhangDepartment of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, 92350, USA; Department of Neurosurgery, Loma Linda University, Loma Linda, CA, 92350, USA; Department of Anesthesiology, Loma Linda University, Loma Linda, CA, 92350, USA. Electronic address: johnzhang3910@yahoo.com.
Loma Linda University · USSecond Affiliated Hospital of Zhejiang University · CNNingbo University · CN

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

Oxidative stress-induced neuron apoptosis plays a crucial role in the early brain injury (EBI) after subarachnoid hemorrhage (SAH). Kisspeptin has been reported as antioxidant to reduce oxidative stress-induced neuronal cell death through G protein-coupled receptor 54 (GPR54). The goal of this study was to determine the neuroprotection of the Kisspeptin/GRP54 signaling pathway against EBI after SAH. Two hundred and ninety-two Sprague Dawley male rats were used and SAH was induced by the endovascular perforation. Exogenous Kisspeptin 54 (KP54) was delivered intranasally. Small interfering ribonucleic acid (siRNA) for endogenous KISS1, a selective GPR54 antagonist kisspeptin 234, or β-arrestin 2 siRNA for ARRB2 (a functional adaptor of GPR54) were administered intracerebroventricularly. Post-SAH evaluations included neurobehavioral tests, SAH grade, Western blot, immunofluorescence, Fluoro-Jade C, TUNEL, and Nissl staining. The results showed that endogenous KISS1 knockdown aggravated but exogenous KP54 (1.0 nmol/kg) treatment attenuated neurological deficits, brain oxidative stress, and neuronal apoptosis at 24 h after SAH. The benefits of KP54 persisted to 28 days after SAH, which significantly improved cognitive function in SAH rats. The GPR54 blockade or the ARRB2 knockout offset the neuroprotective effects of KP54 in SAH rats. In conclusion, our results suggested that administration of KP54 attenuated oxidative stress, neuronal apoptosis and neurobehavioral impairments through GPR54/ARRB2/AKT/GSK3β signaling pathway after SAH in rat. Thus, KP54 may provide an effective treatment strategy for SAH patients.

Indexed as

Brain InjuriesNeuroprotective AgentsSubarachnoid HemorrhageAnimalsApoptosisbeta-Arrestin 2Glycogen Synthase Kinase 3 betaHumansKisspeptinsMaleNeuronsOxidative StressProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyReceptors, Kisspeptin-1ARRB2 protein, humanbeta-Arrestin 2Glycogen Synthase Kinase 3 betaKISS1 protein, humanKisspeptinsNeuroprotective AgentsProto-Oncogene Proteins c-aktReceptors, Kisspeptin-1GPR 54Kisspeptin 54Neuronal apoptosisOxidative stressRatSubarachnoid hemorrhage

Identifiers

PMID33989759
PMCPMC8388553
OpenAlexW3160445151

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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.