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Dexmedetomidine attenuates lung apoptosis induced by renal ischemia–reperfusion injury through α2AR/PI3K/Akt pathway

Overview of attention for article published in Journal of Translational Medicine, March 2018
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Title
Dexmedetomidine attenuates lung apoptosis induced by renal ischemia–reperfusion injury through α2AR/PI3K/Akt pathway
Published in
Journal of Translational Medicine, March 2018
DOI 10.1186/s12967-018-1455-1
Pubmed ID
Authors

Juanjuan Li, Qian Chen, Xinhai He, Azeem Alam, Jiaolin Ning, Bin Yi, Kaizhi Lu, Jianteng Gu

Abstract

Acute lung injury caused by renal ischemia-reperfusion is one of the leading causes of acute kidney injury-related death. Dexmedetomidine, an α2-adrenergic agonist sedative, has been found to have protective effects against acute kidney injury and remote lung injury. We sought to determine whether dexmedetomidine can exert its anti-apoptotic effects in acute lung injury after acute kidney injury, in addition to its common anti-inflammatory effects, and to determine the underlying mechanisms. In vivo, acute kidney injury was induced by 60 min of kidney ischemia (bilateral occlusion of renal pedicles) followed by 24 h of reperfusion. Mice received dexmedetomidine (25 µg/kg, i.p.) in the absence or presence of α2-adrenergic antagonist atipamezole (250 µg/kg, i.p.) before IR. Histological assessment of the lung was conducted by HE staining and arterial blood gases were measured. Lung apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay. The expression of caspase 3 and p-Akt in lung tissue was detected by western blot. In vitro, C57BL/6J mice pulmonary microvascular endothelial cells were treated with serum from mice obtained following sham or IR. Dexmedetomidine was given before serum stimulation in cells, alone or with atipamezole or LY294002. Cell viability was assessed by CCK 8 assay. Cell apoptosis was examined by Hoechst staining and Annexin V-FITC/PI staining flow cytometry analysis. Mitochondrial membrane potential was measured by flow cytometry. The expression of p-Akt, caspase 3, Bcl-2 and Bax was measured by western blot. In vivo, dexmedetomidine remarkably mitigated pathohistological changes and apoptosis and significantly increased p-Akt expression in the lung. In addition, dexmedetomidine also slightly improved oxygenation in mice after IR, which can be abolished by atipamezole. In vitro, dexmedetomidine significantly inhibited IR serum-induced loss of viability and apoptosis in PMVECs. Dexmedetomidine increased p-Akt in a time- and dose-dependent manner, and down-regulated the expression of caspase 3 and Bax and up-regulated the Bcl-2 expression in PMVECs. The changes of MMP were also improved by dexmedetomidine. Whilst these effects were abolished by Atipamezole or LY294002. Our results demonstrated that dexmedetomidine attenuates lung apoptosis induced by IR, at least in part, via α2AR/PI3K/Akt pathway.

Twitter Demographics

The data shown below were collected from the profiles of 2 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 16 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 16 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 3 19%
Student > Bachelor 2 13%
Lecturer > Senior Lecturer 1 6%
Student > Doctoral Student 1 6%
Other 1 6%
Other 3 19%
Unknown 5 31%
Readers by discipline Count As %
Pharmacology, Toxicology and Pharmaceutical Science 3 19%
Biochemistry, Genetics and Molecular Biology 3 19%
Medicine and Dentistry 3 19%
Agricultural and Biological Sciences 1 6%
Nursing and Health Professions 1 6%
Other 0 0%
Unknown 5 31%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 30 March 2018.
All research outputs
#12,214,415
of 16,024,783 outputs
Outputs from Journal of Translational Medicine
#2,285
of 3,027 outputs
Outputs of similar age
#195,967
of 282,105 outputs
Outputs of similar age from Journal of Translational Medicine
#1
of 2 outputs
Altmetric has tracked 16,024,783 research outputs across all sources so far. This one is in the 20th percentile – i.e., 20% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,027 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.2. This one is in the 20th percentile – i.e., 20% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 282,105 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 24th percentile – i.e., 24% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 2 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them