Is AST nueroprotective?
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Neuroprotective Effects of AST: A Comprehensive Review
Introduction to AST Neuroprotection
Astaxanthin (AST) and Astragaloside IV (AST-IV) are compounds that have shown significant neuroprotective properties in various experimental models. This article synthesizes the findings from multiple studies to provide a clear understanding of the neuroprotective mechanisms and potential therapeutic applications of these compounds.
AST-IV and Neuroprotection in Ischemic Stroke
Mechanisms of Action
AST-IV, a principal component of Radix Astragali seu Hedysari, has demonstrated potential neuroprotective effects in experimental ischemic stroke models. The compound has been shown to improve neurological deficits, reduce infarct volume, and decrease blood-brain barrier permeability. The underlying mechanisms include antioxidative/nitration stress reactions, anti-inflammatory effects, and anti-apoptosis properties.
Experimental Evidence
In a systematic assessment of 13 studies involving 244 animals, AST-IV significantly ameliorated neurological function scores, reduced infarct volume, and decreased brain water content and Evans blue leakage compared to controls. These findings suggest that AST-IV could be a promising therapeutic agent for cerebral ischemia/reperfusion injury.
Astaxanthin (AST) and Neuroprotection in Various Neurological Disorders
Anti-Inflammatory and Antioxidative Properties
AST has gained interest as a multi-target pharmacological agent against neurological disorders such as Parkinson’s disease, Alzheimer’s disease, brain and spinal cord injuries, neuropathic pain, aging, depression, and autism. Its neuroprotective effects are primarily attributed to its anti-inflammatory, antioxidative, and anti-apoptotic properties.
Protection Against Excitotoxicity
AST has been shown to protect neurons from excitotoxic injuries by regulating ionotropic glutamate receptors, reducing reactive oxygen species (ROS) formation, and improving mitochondrial function. These actions help prevent neuronal death and maintain cellular homeostasis.
Cognitive Improvement in Alzheimer's Disease
In a study involving APP/PS1 transgenic mice, AST improved cognitive deficits by activating the mTOR pathway, which is essential for mitochondrial dynamics and synaptic plasticity. This activation led to increased expression of Aβ-degrading enzymes and synapse-associated proteins, suggesting that AST could be beneficial in treating cognitive impairments associated with Alzheimer's disease.
AST-004 and Traumatic Brain Injury (TBI)
Mechanisms of Action
AST-004, an adenosine A3 receptor (A3R) agonist, has shown neuroprotective efficacy in a mouse model of traumatic brain injury (TBI). The compound reduces secondary brain injury, cell death, and blood-brain barrier breakdown. It also decreases neuroinflammatory markers and enhances astrocyte energy production .
Experimental Evidence
In a controlled closed cortical injury model, AST-004 treatment significantly reduced impairment of long-term memory and spatial memory in male mice. The treatment also increased in vivo ATP production in astrocytes, supporting its proposed mechanism of action .
Conclusion
Both AST-IV and AST exhibit significant neuroprotective properties through various mechanisms, including antioxidative, anti-inflammatory, and anti-apoptotic effects. These compounds show promise in treating a range of neurological disorders, from ischemic stroke to neurodegenerative diseases and traumatic brain injuries. Further research and clinical trials are necessary to fully understand their therapeutic potential and optimize their use in clinical settings.
Sources and full results
Most relevant research papers on this topic
Astragaloside IV for Experimental Focal Cerebral Ischemia: Preclinical Evidence and Possible Mechanisms
The Neuroprotective Effects of Astaxanthin: Therapeutic Targets and Clinical Perspective
Neuroprotective Roles of the Adenosine A3 Receptor Agonist AST-004 in Mouse Model of Traumatic Brain Injury.
Neuroprotective Roles of the Adenosine A3 Receptor Agonist AST-004 in Mouse Model of Traumatic Brain Injury
Astaxanthin Protection against Neuronal Excitotoxicity via Glutamate Receptor Inhibition and Improvement of Mitochondrial Function
Astaxanthin alleviates brain aging in rats by attenuating oxidative stress and increasing BDNF levels.
Astragaloside IV inhibits experimental autoimmune encephalomyelitis by modulating the polarization of both microglia/macrophages and astrocytes.
Astaxanthin attenuates glutamate‐induced apoptosis via inhibition of calcium influx and endoplasmic reticulum stress
Astaxanthin Improved the Cognitive Deficits in APP/PS1 Transgenic Mice Via Selective Activation of mTOR
Antimicrobial susceptibility testing (AST) and associated clinical outcomes in individuals with cystic fibrosis: A systematic review.
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