ArticleCurrent issues in molecular biology2024
The Autophagic and Apoptotic Death of Forebrain Neurons of Rats with Global Brain Ischemia Is Diminished by the Intranasal Administration of Insulin: Possible Mechanism of Its Action.
Article in Current issues in molecular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- High-dose intranasal insulin in an adaptive dose-escalation study in healthy human participants.Clinical and translational science · 2024Trial
- Intranasal Administration of Insulin and IGF-1 Protects Hippocampal CA1 Neurons Against Transient Global Forebrain Ischemia by Inhibiting Autophagy, Apoptosis and Neuroinflammation: A Comparative Study.International journal of molecular sciences · 2026Article
- Editorial for the Special Issue "Molecular Mechanisms and Treatment of Ischemia-Reperfusion Injury".Current issues in molecular biology · 2026Article
- Narrative review of rationale for IV deferoxamine plus intranasal insulin to ameliorate brain damage following resuscitation from cardiac arrest.Resuscitation plus · 2026Review
- Intranasal Formaldehyde Exposure Induces RAGE-Mediated Alteration of the ADAM10/BACE1 Expression Balance and Amyloid Deposition.Biomedicines · 2026Article
- The Regulatory Role of Non-Coding RNAs in Autophagy-Dependent Ischemia-Reperfusion Injury of the Brain.Current issues in molecular biology · 2025Review
- Physico-Chemical Characterization and Initial Evaluation of Carboxymethyl Chitosan-Hyaluronan Hydrocolloid Systems with Insulin Intended for Intranasal Administration.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Insulin is a promising neuroprotector. To better understand the mechanism of insulin action, it was important to show its ability to diminish autophagic neuronal death in animals with brain ischemic and reperfusion injury. In forebrain ischemia and reperfusion, the number of live neurons in the hippocampal CA1 region and frontal cortex of rats decreased to a large extent. Intracerebroventricular administration of the autophagy and apoptosis inhibitors to ischemic rats significantly increased the number of live neurons and showed that the main part of neurons died from autophagy and apoptosis. Intranasal administration of 0.5 IU of insulin per rat (before ischemia and daily during reperfusion) increased the number of live neurons in the hippocampal CA1 region and frontal brain cortex. In addition, insulin significantly diminished the level of autophagic marker LC3B-II in these forebrain regions, which markedly increased during ischemia and reperfusion. Our studies demonstrated for the first time the ability of insulin to decrease autophagic neuronal death, caused by brain ischemia and reperfusion. Insulin administered intranasally activated the Akt-kinase (activating the mTORC1 complex, which inhibits autophagy) and inhibited the AMP-activated protein kinase (which activates autophagy) in the hippocampus and frontal cortex of rats with brain ischemia and reperfusion.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.