ArticleMetabolic brain disease2023
Inhibition of hyperpolarization-activated cyclic nucleotide-gated cation channel attenuates cerebral ischemia reperfusion-induced impairment of learning and memory by regulating apoptotic pathway.
Article in Metabolic brain disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Clonidine protects rat hippocampal and cortical neurons from oxygen-glucose deprivation and reoxygenation-induced injury through HCN Channels.Scientific reports · 2026Article
- Inhibition of HCN Channels Enhances Oxidative Stress and Autophagy of NRK-52E Cells Under NHInternational journal of molecular sciences · 2025Article
- ZD7288 ameliorates long-term cerebral ischemia reperfusion-induced deterioration of spatial memory by regulating the expressions of NMDA receptor subunits in rats.Scientific reports · 2025Article
- Downregulation of the HCN1 Channel Alleviates Anxiety- and Depression-Like Behaviors in Mice With Cerebral Ischemia-Reperfusion Injury by Suppressing the NLRP3 Inflammasome.Journal of the American Heart Association · 2025Article
- Topological functional network analysis of cortical blood flow in hyperacute ischemic rats.Brain structure & function · 2024Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Stroke is the second leading cause of death globally. Cognitive dysfunction is a common complication of stroke, which seriously affects the patient's quality of life. Previous studies have shown that the expression of hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channel is closely related to ischemia-reperfusion (IR) injury and subsequent cognitive impairment. We also found that ZD7288, a specific inhibitor of the HCN channel, attenuated IR injury during short-term reperfusion. Since apoptosis can induce cell necrosis and aggravate cognitive impairment after IR, the purpose of this study is to define whether ZD7288 could improve cognitive impairment after prolonged cerebral reperfusion in rats by regulating apoptotic pathways. Our data indicated that ZD7288 can ameliorate spatial cognitive behavior and synaptic plasticity, protect the morphology of hippocampal neurons, and alleviate hippocampal apoptotic cells in IR rats. This effect may be related to down-regulating the expressions of pro-apoptotic proteins such as AIF, p53, Bax, and Caspase-3, and increasing the ratio of Bcl-2/Bax. Taken together, it suggested that inhibition of the HCN channel improves cognitive impairment after IR correlated with its regulation of apoptotic pathways.
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