Effect of Glycyrrhizic Acid on Scopolamine-Induced Cognitive Impairment in Mice

Ban, Ju Yeon; Park, Hyun Kyung; Kim, Su Kang

doi:10.5213/inj.2040154.077

Cited by 28 publications

(11 citation statements)

References 33 publications

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“…As per animal ethics committee recommendations, all of the research animals were handled with care and empathy. The doses of scopolamine and friedelin were selected and optimized from the literature review [ 22 ]. Friedelin isolated from different plants had already been reported to have significant in vivo activities in animal models of hepatotoxicity [ 15 ], gastro-protective activities [ 12 ], and anti-inflammatory and antipyretic activities [ 23 ].…”

Section: Methodsmentioning

confidence: 99%

Friedelin Attenuates Neuronal Dysfunction and Memory Impairment by Inhibition of the Activated JNK/NF-κB Signalling Pathway in Scopolamine-Induced Mice Model of Neurodegeneration

et al. 2022

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Oxidative stress (OS) and c-Jun N-terminal kinase (JNK) are both key indicators implicated in neuro-inflammatory signalling pathways and their respective neurodegenerative diseases. Drugs targeting these factors can be considered as suitable candidates for treatment of neuronal dysfunction and memory impairment. The present study encompasses beneficial effects of a naturally occurring triterpenoid, friedelin, against scopolamine-induced oxidative stress and neurodegenerative pathologies in mice models. The treated animals were subjected to behavioural tests i.e., Y-maze and Morris water maze (MWM) for memory dysfunction. The underlying mechanism was determined via western blotting, antioxidant enzymes and lipid profile analyses. Molecular docking studies were carried out to predict the binding modes of friedelin in the binding pocket of p-JNK protein. The results reveal that scopolamine caused oxidative stress by (1) inhibiting catalase (CAT), peroxidase enzyme (POD), superoxide dismutase (SOD), and reduced glutathione enzyme (GSH); (2) the up-regulation of thiobarbituric acid reactive substances (TBARS) in mice brain; and (3) affecting the neuronal synapse (both pre- and post-synapse) followed by associated memory dysfunction. In contrast, friedelin administration not only abolished scopolamine-induced oxidative stress, glial cell activation, and neuro-inflammation but also inhibited p-JNK and NF-κB and their downstream signaling molecules. Moreover, friedelin administration improved neuronal synapse and reversed scopolamine-induced memory impairment accompanied by the inhibition of β-secretase enzyme (BACE-1) to halt amyloidogenic pathways of amyloid-β production. In summary, all of the results show that friedelin is a potent naturally isolated neuro-therapeutic agent to reverse scopolamine-induced neuropathology, which is characteristic of Alzheimer’s disease.

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Section: Methodsmentioning

confidence: 99%

Friedelin Attenuates Neuronal Dysfunction and Memory Impairment by Inhibition of the Activated JNK/NF-κB Signalling Pathway in Scopolamine-Induced Mice Model of Neurodegeneration

et al. 2022

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“…Glycyrrhizic acid (GA), as a major component of Glycyrrhiza glabra roots, belongs to flavonoids, which exhibits antioxidant, anti-inflammatory, and antiexcitotoxic properties [108]. GA substantially increases the expression rate and 14 Oxidative Medicine and Cellular Longevity mass of mitochondrial genes subsequent to aluminum toxicity [109].…”

Section: Amla C2c12 Myotubesmentioning

confidence: 99%

Targeting Mitochondrial Biogenesis with Polyphenol Compounds

Chodari

Aytemir

Vahedi

et al. 2021

Oxidative Medicine and Cellular Longevity

118

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Appropriate mitochondrial physiology is an essential for health and survival. Cells have developed unique mechanisms to adapt to stress circumstances and changes in metabolic demands, by meditating mitochondrial function and number. In this context, sufficient mitochondrial biogenesis is necessary for efficient cell function and haemostasis, which is dependent on the regulation of ATP generation and maintenance of mitochondrial DNA (mtDNA). These procedures play a primary role in the processes of inflammation, aging, cancer, metabolic diseases, and neurodegeneration. Polyphenols have been considered as the main components of plants, fruits, and natural extracts with proven therapeutic effects during the time. These components regulate the intracellular pathways of mitochondrial biogenesis. Therefore, the current review is aimed at representing an updated review which determines the effects of different natural polyphenol compounds from various plant kingdoms on modulating signaling pathways of mitochondrial biogenesis that could be a promising alternative for the treatment of several disorders.

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“…DG can reduce TNF-α, NF-κB, IL-1, IL-6, and IL-17. [9][10][11] In addition, it increases the expression and activity of superoxide dismutase and catalase, 12 and decreases the production of nitric oxide synthase 13 and reactive oxygen species. 14 Previous studies have found these factors play important roles in the pathogenesis of rosacea.…”

Section: Discussionmentioning

confidence: 99%