Evidence map›Paper›PMID 30764838›Full record

ArticleLipids in health and disease2019

κ-Opioid receptor stimulation reduces palmitate-induced apoptosis via Akt/eNOS signaling pathway.

Yan Cui, Na Feng, Xiaoming Gu, Feng Fu, Jun Li, Haitao Guo, Yali Liu, Shumiao Zhang, Juan Li, Yuanbo Wang and 6 more

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 13 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

16 authors at 2 institutions in 1 country.

Yan CuiDepartment of Nursing, Medical College of Xi'an Peihua University, Xi'an, 710125, Shaanxi Province, China.
Na FengDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, Fourth Military Medical University, No. 169 West Changle Road, Xi'an, 710032, Shaanxi Province, China.
Xiaoming GuDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, Fourth Military Medical University, No. 169 West Changle Road, Xi'an, 710032, Shaanxi Province, China.
Feng FuDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, Fourth Military Medical University, No. 169 West Changle Road, Xi'an, 710032, Shaanxi Province, China.
Jun LiDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, Fourth Military Medical University, No. 169 West Changle Road, Xi'an, 710032, Shaanxi Province, China.
Haitao GuoDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, Fourth Military Medical University, No. 169 West Changle Road, Xi'an, 710032, Shaanxi Province, China.
Yali LiuDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, Fourth Military Medical University, No. 169 West Changle Road, Xi'an, 710032, Shaanxi Province, China.
Shumiao ZhangDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, Fourth Military Medical University, No. 169 West Changle Road, Xi'an, 710032, Shaanxi Province, China.
Juan LiDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, Fourth Military Medical University, No. 169 West Changle Road, Xi'an, 710032, Shaanxi Province, China.
Yuanbo WangDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, Fourth Military Medical University, No. 169 West Changle Road, Xi'an, 710032, Shaanxi Province, China.
Min JiaDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, Fourth Military Medical University, No. 169 West Changle Road, Xi'an, 710032, Shaanxi Province, China.
Lu YangDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, Fourth Military Medical University, No. 169 West Changle Road, Xi'an, 710032, Shaanxi Province, China.
Fuyang ZhangDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, Fourth Military Medical University, No. 169 West Changle Road, Xi'an, 710032, Shaanxi Province, China.
Yuemin WangDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, Fourth Military Medical University, No. 169 West Changle Road, Xi'an, 710032, Shaanxi Province, China.
Rong FanDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, Fourth Military Medical University, No. 169 West Changle Road, Xi'an, 710032, Shaanxi Province, China. heartj@fmmu.edu.cn.
Jianming PeiDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, Fourth Military Medical University, No. 169 West Changle Road, Xi'an, 710032, Shaanxi Province, China. jmpei8@fmmu.edu.cn.
Air Force Medical University · CNXi'an Peihua University · CN

Funding

a major project from Shaan Xi Province of China 2016KTCL03-11National Natural Science Foundation of China 81270402National Natural Science Foundation of China 81670354National Natural Science Foundation of China 81770243National Natural Science Foundation of China 81800226
6 · The paper itself

Abstract

backgroundThis study was designed to test the hypothesis that κ-opioid receptor (κ-OR) stimulation reduces palmitate-induced HUVECs apoptosis and to investigate its mechanisms.

methodsHUVECs were subjected to sodium palmitate, apoptosis and cell viability were determined, HUVECs were treated with specific inhibitors to PI3K, Akt, eNOS and siRNAs targeting κ-OR and Akt. Groups were divided as follows: the control group, the sodium palmitate group, the sodium palmitate+U50,488H (a selective κ-OR agonist) group and the sodium palmitate+U50,488H + nor-BNI (a selective κ-OR antagonist) group.

resultsTreatment with sodium palmitate significantly reduced cell viability and increased apoptosis rate which were significantly alleviated by pretreatment with U50,488H, the effect of U50,488H was abolished by nor-BNI. Phosphorylation of Akt and eNOS, as well as NO production were attenuated and accompanied by an increased expression of caspase 3 when HUVECs were subjected to sodium palmitate, and all these changes were restored by pretreatment with U50,488H, the effects of U50,488H were abolished by nor-BNI, and specific inhibitors to PI3K, Akt, eNOS, respectively. SiRNAs targeting κ-OR or Akt abolished the effects of U50,488H on phosphorylation of Akt and eNOS as well as the expressions of caspase 3, Bax and Bcl-2. SiRNAs targeting Akt elicited no effect on the expression of κ-OR.

conclusionThis study provides the evidence for the first time that κ-OR stimulation possesses anti-palmitate-induced apoptosis effect, which is mediated by PI3K/Akt/eNOS signaling pathway.

Indexed as

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-IsomerAnalgesics, OpioidApoptosisbcl-2-Associated X ProteinCaspase 3Cell SurvivalGene Expression RegulationHumansHuman Umbilical Vein Endothelial CellsNaltrexoneNarcotic AntagonistsNitric Oxide Synthase Type IIIPalmitic AcidPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphorylation3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-IsomerAnalgesics, OpioidBAX protein, humanbcl-2-Associated X ProteinBCL2 protein, humanCASP3 protein, humanCaspase 3NaltrexoneNarcotic AntagonistsNitric Oxide Synthase Type IIInorbinaltorphimineNOS3 protein, humanPalmitic AcidPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Receptors, Opioid, kappaRNA, Small InterferingAktApoptosiseNOSPalmitateκ-Opioid receptor

Identifiers

PMID30764838
PMCPMC6376663
OpenAlexW2925866256

What OpenQuestion holds

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LicenceCC BY
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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.