Evidence map›Paper›PMID 26901291›Full record

ArticlePloS one2016

Jujuboside B Reduces Vascular Tension by Increasing Ca2+ Influx and Activating Endothelial Nitric Oxide Synthase.

Yixiu Zhao, Xin Zhang, Jiannan Li, Yu Bian, Miaomiao Sheng, Bin Liu, Zidong Fu, Yan Zhang, Baofeng Yang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.3field-weighted citation impact, top 7% 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

13 citing papers in PubMed, 30 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

9 authors at 1 institution in 1 country.

Yixiu ZhaoDepartment of Pharmacology, Harbin Medical University, Harbin, Heilongjiang, PR China.
Xin ZhangDepartment of Pharmacology, Harbin Medical University, Harbin, Heilongjiang, PR China.
Jiannan LiDepartment of Pharmacology, Harbin Medical University, Harbin, Heilongjiang, PR China.
Yu BianDepartment of Pharmacology, Harbin Medical University, Harbin, Heilongjiang, PR China.
Miaomiao ShengDepartment of Pharmacology, Harbin Medical University, Harbin, Heilongjiang, PR China.
Bin LiuDepartment of Pharmacology, Harbin Medical University, Harbin, Heilongjiang, PR China.
Zidong FuDepartment of Pharmacology, Harbin Medical University, Harbin, Heilongjiang, PR China.
Yan ZhangDepartment of Pharmacology, Harbin Medical University, Harbin, Heilongjiang, PR China.
Baofeng YangDepartment of Pharmacology, Harbin Medical University, Harbin, Heilongjiang, PR China.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Jujuboside B has been reported to have protective effect on many cardiovascular diseases. However, the effects of Jujuboside B on vascular tension and endothelial function are unknown. The present study investigated the effects of Jujuboside B on reducing vascular tension, protecting endothelial function and the potential mechanisms. The tension of isolated rat thoracic aorta ring was measured by Wire myograph system. The concentration of nitric oxide (NO) and the activity of endothelial nitric oxide synthase (eNOS) in human aortic endothelial cells (HAECs) were determined by Griess reagent method and enzyme-linked immune sorbent assay. The protein levels of eNOS and p-eNOS at Serine-1177 were determined by western blot analysis. Intracellular Ca2+ concentration in HAECs was measured by laser confocal imaging microscopy. Results showed that Jujuboside B reduced the tension of rat thoracic aorta rings with intact endothelium in a dose-dependent manner. L-NAME, KN93, EGTA, SKF96365, iberiotoxin and glibenclamide significantly attenuated Jujuboside B-induced vasodilation in endothelium-intact tissues. In contrast, indometacin and 4-DAMP had no such effects. Jujuboside B also promoted NO generation and increased eNOS activity, which were attenuated by L-NAME, EGTA and SKF96365. Moreover, Jujuboside B increased intracellular Ca2+ concentration dose-dependently, which was inhibited by EGTA and SKF96365. Besides, Jujuboside B induced a rapid Ca2+ influx instantaneously after depleting intracellular Ca2+ store, which was significantly inhibited by SKF96365. In conclusion, this study preliminarily confirmed that Jujuboside B reduced vascular tension endothelium-dependently. The underlying mechanisms involved that Jujuboside B increased extracellular Ca2+ influx through endothelial transient receptor potential cation (TRPC) channels, phosphorylated eNOS and promoted NO generation in vascular endothelial cells. In addition, Jujuboside B-induced vasodilation involved endothelium-dependent hyperpolarizaiton through endothelial potassium channels. Jujuboside B is a natural compound with new pharmacological effects on improving endothelial dysfunction and treating vascular diseases.

Indexed as

AnimalsAorta, ThoracicCalcium SignalingDose-Response Relationship, DrugEndothelium, VascularEnzyme ActivationEnzyme InhibitorsHumansMaleNitric OxideNitric Oxide Synthase Type IIIRatsRats, Sprague-DawleySaponinsVasodilationEnzyme Inhibitorsjujuboside BNitric OxideNitric Oxide Synthase Type IIINos3 protein, ratSaponins

Identifiers

PMID26901291
PMCPMC4762982
OpenAlexW2283066865

What OpenQuestion holds

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LicenceCC BY
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.