| Title |
Dexmedetomidine attenuates the propofol-induced long-term neurotoxicity in the developing brain of rats by enhancing the PI3K/Akt signaling pathway
|
|---|---|
| Published in |
Neuropsychiatric Disease and Treatment, August 2018
|
| DOI | 10.2147/ndt.s169099 |
| Pubmed ID | |
| Authors |
Yong Xiao, Lifang Zhou, Youbing Tu, Yuantao Li, Yubing Liang, Xu Zhang, Jing Lv, Yu Zhong, Yubo Xie |
| Abstract |
Propofol induces short- and long-term neurotoxicity. Our previous study showed that dexmedetomidine (Dex) can attenuate the propofol-induced acute neurotoxicity in rodents by enhancing the PI3K/Akt signaling. However, whether treatment of young rats with Dex could protect them from long-term neurotoxicity induced by propofol is unclear. Seven-day-old male Sprague Dawley rats were randomized and injected intraperitoneally with saline (100 μL, NS), propofol (100 mg/kg), Dex (75 μg/kg), propofol (100 mg/kg) plus Dex (25, 50 or 75 μg/kg), 10% dimethyl sulfoxide (DMSO, 100 μL) or TDZD-8 (a GSK3β inhibitor, 1 mg/kg), or intracerebroventricularly with DMSO (5 μL) or LY294002 (a PI3K inhibitor, 25 μg/5 μL DMSO). Other rats in the experimental group were injected with the same doses of propofol, Dex and LY294002 or TDZD-8. All the rats were monitored until they were 9 weeks old. Their spatial learning and memory were tested by Morris water maze. The neuronal apoptosis, expression of PSD95, expression and phosphorylation of Akt and GSK3β and synaptic ultrastructures were determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, immunohistochemistry, Western blot and transmission electron microscopy assays, respectively. Compared with the NS control group, young rats injected with intralipid, Dex, TDZD-8, LY294002 or DMSO alone did not show any significant change as they aged. Propofol significantly increased the escape latency time, hippocampal neuroapoptosis and synaptic ultrastructural changes but decreased the relative levels of PSD95 expression, and Akt and GSK3β phosphorylation in the developing hippocampus of the rats. The neuronal toxic effects of propofol were significantly mitigated by the pretreatment with a higher dose of Dex. The neuroprotective effect of Dex was enhanced by the treatment with TDZD-8, but was completely abrogated by the treatment with LY294002. Our results indicated that the pretreatment of young rats with Dex attenuated the propofol-induced long-term neurotoxicity in their developing hippocampus by enhancing the PI3K/Akt signaling. |
Mendeley readers
The data shown below were compiled from readership statistics for 14 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 14 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Ph. D. Student | 4 | 29% |
| Student > Bachelor | 1 | 7% |
| Professor | 1 | 7% |
| Student > Master | 1 | 7% |
| Researcher | 1 | 7% |
| Other | 1 | 7% |
| Unknown | 5 | 36% |
| Readers by discipline | Count | As % |
|---|---|---|
| Medicine and Dentistry | 3 | 21% |
| Biochemistry, Genetics and Molecular Biology | 2 | 14% |
| Pharmacology, Toxicology and Pharmaceutical Science | 2 | 14% |
| Neuroscience | 2 | 14% |
| Agricultural and Biological Sciences | 1 | 7% |
| Other | 0 | 0% |
| Unknown | 4 | 29% |
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 August 2018.
All research outputs
#22,767,715
of 25,385,509 outputs
Outputs from Neuropsychiatric Disease and Treatment
#2,583
of 3,131 outputs
Outputs of similar age
#299,007
of 341,886 outputs
Outputs of similar age from Neuropsychiatric Disease and Treatment
#48
of 79 outputs
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