Emerging immune and cell death mechanisms in stroke: Saponins as therapeutic candidates

García-Pupo, Laura; San, Emily Van; Hernández, René Delgado; Berghe, Tom Vanden; Berghe, Wim Vanden

doi:10.1016/j.bbih.2020.100152

Cited by 5 publications

(2 citation statements)

References 123 publications

(162 reference statements)

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“…Ischemic stroke results in neural death through complex pathophysiological pathways, including excitotoxicity [70], oxidative stress [71][72][73][74], blood-brain barrier disruption [75], and inflammation [76]. Based on the proposed role for NAAG in preventing excitotoxicity, a neuroprotective effect in stroke seems intuitive.…”

Section: Naag In Strokementioning

confidence: 99%

N-Acetyl-Aspartyl-Glutamate in Brain Health and Disease

Morland

Nordengen

2022

IJMS

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N-acetyl-aspartyl-glutamate (NAAG) is the most abundant dipeptide in the brain, where it acts as a neuromodulator of glutamatergic synapses by activating presynaptic metabotropic glutamate receptor 3 (mGluR3). Recent data suggest that NAAG is selectively localized to postsynaptic dendrites in glutamatergic synapses and that it works as a retrograde neurotransmitter. NAAG is released in response to glutamate and provides the postsynaptic neuron with a feedback mechanisms to inhibit excessive glutamate signaling. A key regulator of synaptically available NAAG is rapid degradation by the extracellular enzyme glutamate carboxypeptidase II (GCPII). Increasing endogenous NAAG—for instance by inhibiting GCPII—is a promising treatment option for many brain disorders where glutamatergic excitotoxicity plays a role. The main effect of NAAG occurs through increased mGluR3 activation and thereby reduced glutamate release. In the present review, we summarize the transmitter role of NAAG and discuss the involvement of NAAG in normal brain physiology. We further present the suggested roles of NAAG in various neurological and psychiatric diseases and discuss the therapeutic potential of strategies aiming to enhance NAAG levels.

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Section: Naag In Strokementioning

confidence: 99%

N-Acetyl-Aspartyl-Glutamate in Brain Health and Disease

Morland

Nordengen

2022

IJMS

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“…Saponins are known as surface-active compounds that are widely distributed in the plant kingdom ( 171 ). They comprise a non-polar aglycone or non-saccharide moiety, coupled with polar mono or oligosaccharides.…”

Section: Cardioprotective Phytochemicals Attenuating Myocardial I/r I...mentioning

confidence: 99%

Promising Therapeutic Candidate for Myocardial Ischemia/Reperfusion Injury: What Are the Possible Mechanisms and Roles of Phytochemicals?

Chen

Cheng

et al. 2022

Front. Cardiovasc. Med.

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Percutaneous coronary intervention (PCI) is one of the most effective reperfusion strategies for acute myocardial infarction (AMI) despite myocardial ischemia/reperfusion (I/R) injury, causing one of the causes of most cardiomyocyte injuries and deaths. The pathological processes of myocardial I/R injury include apoptosis, autophagy, and irreversible cell death caused by calcium overload, oxidative stress, and inflammation. Eventually, myocardial I/R injury causes a spike of further cardiomyocyte injury that contributes to final infarct size (IS) and bound with hospitalization of heart failure as well as all-cause mortality within the following 12 months. Therefore, the addition of adjuvant intervention to improve myocardial salvage and cardiac function calls for further investigation. Phytochemicals are non-nutritive bioactive secondary compounds abundantly found in Chinese herbal medicine. Great effort has been put into phytochemicals because they are often in line with the expectations to improve myocardial I/R injury without compromising the clinical efficacy or to even produce synergy. We summarized the previous efforts, briefly outlined the mechanism of myocardial I/R injury, and focused on exploring the cardioprotective effects and potential mechanisms of all phytochemical types that have been investigated under myocardial I/R injury. Phytochemicals deserve to be utilized as promising therapeutic candidates for further development and research on combating myocardial I/R injury. Nevertheless, more studies are needed to provide a better understanding of the mechanism of myocardial I/R injury treatment using phytochemicals and possible side effects associated with this approach.

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