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The protective effects of propofol against CoCl2-induced HT22 cell hypoxia injury via PP2A/CAMKIIα/nNOS pathway

Overview of attention for article published in BMC Anesthesiology, February 2017
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Title
The protective effects of propofol against CoCl2-induced HT22 cell hypoxia injury via PP2A/CAMKIIα/nNOS pathway
Published in
BMC Anesthesiology, February 2017
DOI 10.1186/s12871-017-0327-1
Pubmed ID
Authors

Yan Lu, Wei Chen, Chen Lin, Jiaqiang Wang, Minmin Zhu, Jiawei Chen, Changhong Miao

Abstract

Perioperative cerebral ischemia/hypoxia could induce hippocampal injury and has been reported to induce cognitive impairment. In this study, we used cobalt chloride (CoCl2) to build a hypoxia model in mouse hippocampal cell lines. Propofol, a widely used intravenous anesthetic agent, has been demonstrated to have neuroprotective effect. Here, we explored whether and how propofol attenuated CoCl2-induced mouse hippocampal HT22 cell injury. Mouse hippocampal HT22 cells were pretreated with propofol, and then stimulated with CoCl2. Cell viability was measured by cell counting kit 8 (CCK8). The effect of propofol on CoCl2-modulated expressions of B-cell lymphoma 2 (Bcl-2), BAX, cleaved caspase 3, phosphatase A2 (PP2A), and the phosphorylation of Ca(2+)/Calmodulin (CaM)-dependent protein kinase II (pCAMKIIα), neuron nitric oxide synthase at Ser(1412) (pnNOS-Ser(1412)), neuron nitric oxide synthase at Ser(847) (pnNOS-Ser(847)) were detected by Western blot analysis. Compared with control, CoCl2 treatment could significantly decrease cell viability, which could be reversed by propofol. Further, we found CoCl2 treatment could up-regulate the expression of PP2A, BAX, cleaved caspase three and cause the phosphorylation of nNOS-Ser(1412), but it down-regulated the expression of Bcl-2 and the phosphorylation of CAMKIIα and nNOS-Ser(847). More importantly, these CoCl2-mediated effects were attentuated by propofol. In addition, we demonstrated that propofol could exert similar effect to that of the PP2A inhibitor (okadaic acid). Further, the PP2A activator (FTY720) and the CAMKIIα inhibitor (KN93) could reverse the neuroprotective effect of propofol. Our data indicated that propofol could attenuate CoCl2-induced HT22 cells hypoxia injury via PP2A/CAMKIIα/nNOS pathway.

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

Mendeley readers

The data shown below were compiled from readership statistics for 19 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 19 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 4 21%
Student > Ph. D. Student 3 16%
Student > Bachelor 2 11%
Professor 2 11%
Student > Postgraduate 2 11%
Other 4 21%
Unknown 2 11%
Readers by discipline Count As %
Medicine and Dentistry 4 21%
Agricultural and Biological Sciences 3 16%
Biochemistry, Genetics and Molecular Biology 2 11%
Pharmacology, Toxicology and Pharmaceutical Science 2 11%
Neuroscience 2 11%
Other 2 11%
Unknown 4 21%
Attention Score in Context

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 22 September 2017.
All research outputs
#17,880,829
of 22,957,478 outputs
Outputs from BMC Anesthesiology
#850
of 1,504 outputs
Outputs of similar age
#223,970
of 310,855 outputs
Outputs of similar age from BMC Anesthesiology
#21
of 46 outputs
Altmetric has tracked 22,957,478 research outputs across all sources so far. This one is in the 19th percentile – i.e., 19% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,504 research outputs from this source. They receive a mean Attention Score of 3.1. This one is in the 33rd percentile – i.e., 33% 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 310,855 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 23rd percentile – i.e., 23% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 46 others from the same source and published within six weeks on either side of this one. This one is in the 45th percentile – i.e., 45% of its contemporaries scored the same or lower than it.