The effect of propofol postconditioning on the expression of K+-Cl--co-transporter 2 in GABAergic inhibitory interneurons of acute ischemia/reperfusion injury rats

Wang, Hongbai; Liu, Shuying; Wang, Haiyun; Wang, Guolin; Ai, Zhu

doi:10.1016/j.brainres.2014.11.036

Cited by 15 publications

(12 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…After ischemia or excitotoxicity, GluR2 expression is decreased in survival neurons [20]. NR1 represents a basic functional unit of NMDA receptor, while NR2 is of great importance for regulatory function of NMDA receptor, which is correlated with neuronal excitotoxicity, neuronal injury after brain ischemia-reperfusion [21].…”

Section: Discussionmentioning

confidence: 99%

The effect of dexmedetomidine on GluR2 and NR2B expression of cortical neurons after cerebral ischemia-reperfusion in rats

Li¹,

Liu²

2018

biomedicalresearch

View full text Add to dashboard Cite

Objective: Neurotransmitter plays a crucial role in ischemia cerebrovascular disease. Study has shown that Dexmedetomidine (Dex) contributes to neuroprotective functions. We thus observed the regulatory effect of Dex on the expressions of Glutamate Receptor-2 (GluR2) and N-Methyl-D-Aspartic Acid (NMDA) receptor 2B (NR2B) in cerebral cortical neurons with an ischemia-reperfusion rat model. Patients and methods: Healthy male SD rats were randomly divided into sham, model and Dex treatment groups (N=20 each). Whole-brain ischemia-reperfusion model was generated by the clipping of bilateral common carotid artery with hypotension. Dex (9 μg/kg) was infused immediately after reperfusion, while the other two groups received equal volume of saline. Morris water maze was employed to detect learning and memory function of rats. Brain tissues were extracted at 6, 24 and 72 h after reperfusion. Immunohistochemistry (IHC) was used to detect GluR2 and NR2B receptor levels, the mRNA levels of which were determined by real-time PCR. Results: The longer escape latency and fewer number of crossing platform in water maze were shown in Model rats group. Cortical GluR2 expression was down-regulated while NR2B level was increased. Dex treatment inhibited escape latency and increased crossing times, along with the rise of cortical GluR2 expression and reduction of NR2B expression (p<0.05) in a time-dependent manner (p<0.05). Conclusion: Dex could alleviate ischemia-reperfusion injury of rat brain via down-regulating GluR2 while increasing NR2B expression.

show abstract

Section: Discussionmentioning

confidence: 99%

The effect of dexmedetomidine on GluR2 and NR2B expression of cortical neurons after cerebral ischemia-reperfusion in rats

Li¹,

Liu²

2018

biomedicalresearch

View full text Add to dashboard Cite

show abstract

“…Extensive recent laboratory investigations (in particular, in-vitro and in-vivo rodent models) has, however, revealed different potential molecular pathways by which propofol may offer protection against hypoxic damage. Results of these studies suggest that the mechanisms of postconditioning effect of propofol administered after cerebral ischemia/reperfusion injury was the result of increased neuronal tolerance to hypoxia or improved recovery [19][20][21], attenuated inflammatory reactions [22,23], or reduced endoplasmic reticulum stress-induced apoptosis [24]. Administration of a combination of propofol and dexmedetomidine seems to have a stronger neuroprotective effect in rats [25].…”

Section: Propofolmentioning

confidence: 99%

Update on anesthetic neuroprotection

Zwerus

Absalom

2015

Current Opinion in Anaesthesiology

View full text Add to dashboard Cite

The evidence of benefit of current strategies remains sparse. Given the complex pathophysiology of cerebral ischemia and hypoxia, a multimodal approach to neuroprotective strategies seems sensible. The many variables and confounds associated with the clinical setting of patients, their comorbidities and concurrent medications, pose challenges to translate from experimental studies to clinical practice.

show abstract

“…Ischemic postconditioning can also inhibit some types of NMDA receptors, such as kainate receptors, in order to reduce glutamine toxicity and promote the recovery of cognitive function [21]. Cerebral ischemic postconditioning also influences KCC2 pathways and regulates the expression of gamma-aminobutyric acid receptors, resulting in improvements in cognitive dysfunction following stroke [59]. …”

Section: Neuroprotective Effects Of Ischemic Postconditioningmentioning

confidence: 99%

Overview of Experimental and Clinical Findings regarding the Neuroprotective Effects of Cerebral Ischemic Postconditioning

Feng

Deng

et al. 2017

BioMed Research International

View full text Add to dashboard Cite

Research on attenuating the structural and functional deficits observed following ischemia-reperfusion has become increasingly focused on the therapeutic potential of ischemic postconditioning. In recent years, various methods and animal models of ischemic postconditioning have been utilized. The results of these numerous studies have indicated that the mechanisms underlying the neuroprotective effects of ischemic postconditioning may involve reductions in the generation of free radicals and inhibition of calcium overload, as well as the release of endogenous active substances, alterations in membrane channel function, and activation of protein kinases. Here we review the novel discovery, mechanism, key factors, and clinical application of ischemic postconditioning and discuss its implications for future research and problem of clinical practice.

show abstract

The effect of propofol postconditioning on the expression of K+-Cl--co-transporter 2 in GABAergic inhibitory interneurons of acute ischemia/reperfusion injury rats

Cited by 15 publications

References 52 publications

The effect of dexmedetomidine on GluR2 and NR2B expression of cortical neurons after cerebral ischemia-reperfusion in rats

The effect of dexmedetomidine on GluR2 and NR2B expression of cortical neurons after cerebral ischemia-reperfusion in rats

Update on anesthetic neuroprotection

Overview of Experimental and Clinical Findings regarding the Neuroprotective Effects of Cerebral Ischemic Postconditioning

Contact Info

Product

Resources

About