Saffron (Crocus Sativus L.), Combined with Endurance Exercise, Synergistically Enhances BDNF, Serotonin, and NT-3 in Wistar Rats

Akbari‐Fakhrabadi, Maryam; Najafi, Mohammad; Mortazavian, Soudabehsadat; Memari, Amir Hossein; Shidfar, Farzad; Shahbazi, Ali; Heshmati, Javad

doi:10.52547/rbmb.9.4.426

Cited by 16 publications

(10 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Data from animal studies indicate that exercise significantly increases the synthesis and metabolism of central 5-HT ( Dey et al, 1992 ), and is required for the exercise-induced neurogenic response, especially adult hippocampal neurogenesis ( Klempin et al, 2013 , 2018 ). Furthermore, saffron combined with endurance exercise increased levels of hippocampal 5-HIAA, and this change was associated with improved short-term memory ( Akbari-Fakhrabadi et al, 2021 ). Regulation of central 5-HT synthesis and metabolism by exercise may represent a therapeutic opportunity in depression and age-related cognitive decline.…”

Section: Serotonergic Systemmentioning

confidence: 99%

Understanding How Physical Exercise Improves Alzheimer’s Disease: Cholinergic and Monoaminergic Systems

Zong

Zhang

et al. 2022

Front. Aging Neurosci.

View full text Add to dashboard Cite

Alzheimer’s disease (AD) is an age-related neurodegenerative disorder, characterized by the accumulation of proteinaceous aggregates and neurofibrillary lesions composed of β-amyloid (Aβ) peptide and hyperphosphorylated microtubule-associated protein tau, respectively. It has long been known that dysregulation of cholinergic and monoaminergic (i.e., dopaminergic, serotoninergic, and noradrenergic) systems is involved in the pathogenesis of AD. Abnormalities in neuronal activity, neurotransmitter signaling input, and receptor function exaggerate Aβ deposition and tau hyperphosphorylation. Maintenance of normal neurotransmission is essential to halt AD progression. Most neurotransmitters and neurotransmitter-related drugs modulate the pathology of AD and improve cognitive function through G protein-coupled receptors (GPCRs). Exercise therapies provide an important alternative or adjunctive intervention for AD. Cumulative evidence indicates that exercise can prevent multiple pathological features found in AD and improve cognitive function through delaying the degeneration of cholinergic and monoaminergic neurons; increasing levels of acetylcholine, norepinephrine, serotonin, and dopamine; and modulating the activity of certain neurotransmitter-related GPCRs. Emerging insights into the mechanistic links among exercise, the neurotransmitter system, and AD highlight the potential of this intervention as a therapeutic approach for AD.

show abstract

Section: Serotonergic Systemmentioning

confidence: 99%

Understanding How Physical Exercise Improves Alzheimer’s Disease: Cholinergic and Monoaminergic Systems

Zong

Zhang

et al. 2022

Front. Aging Neurosci.

View full text Add to dashboard Cite

show abstract

“…Moreover, they indicated that aerobic exercise and administration of the Crocus sativus L. reduced muscle damage in rats (Akbari‐Fakhrabadi et al, 2019). Moreover, evidence has shown that exercise and bioactive compounds could affect the serotonin and brain‐derived neurotrophic factor (BDNF) in the hippocampus of rats (Akbari‐Fakhrabadi et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

The effect of resistance and endurance training with ursolic acid on atrophy‐related biomarkers in muscle tissue of diabetic male rats induced by streptozotocin and ahigh‐fatdiet

Zolfaghari

Faramarzi

Hedayati

et al. 2022

Journal of Food Biochemistry

View full text Add to dashboard Cite

In this study, the effect of resistance and endurance training with/without ursolic acid supplementation was evaluated to identify atrophy‐related biomarkers in elderly rats induced by diabetes and a high‐fat diet (HFD) based on in silico analysis algorithms and pharmaceutical methods. The visualizer software found differential gene expression levels in skeletal muscle atrophy via computed hub gene network parameters. Also, the impact of ursolic acid, as a potent inducer of the Trp53 protein in ameliorating decreased muscle mass, was analyzed in diabetic rats. Fifty‐six‐old male Wistar rats were randomly assigned into seven groups, including healthy control (Control), diabetic control (DM), Ursolic acid supplementation (UA), resistance training (RT), endurance training (ET), resistance training+ Ursolic acid supplementation (RT + U), and endurance training in combination with Ursolic acid supplementation (ET + U). Exercise intervention included 8 weeks of resistance or endurance training programs. Biomedical informatic outputs determined the P53 signaling pathway as a remarkable causative factor in the pathomechanism of atrophy. In addition, the results demonstrated that exercise and supplementation of UA impeded the interactions among p53/ATF4/p21. Moreover, ET and ursolic acid had a synergetic effect on the signaling pathway of p53/ATF4/p21 and probably could inhibit the aging process and modulate the p53/ATF4/p21 molecular pathway. The interaction between UA and endurance exercise significantly modified the activity of the p53/ATF4/p21 signaling pathway. Based on in silico studies, the p53/ATF4/p21 pathway plays an essential role in aging, and the inhibition of this pathway would be beneficial in decelerating the aging process. Practical applications Ursolic acid (UA) is a natural pentacyclic triterpenoid carboxylic acid found in apples (a major compound of apple wax) and other fruits; it is known to improve skeletal muscle function and reduce the muscular atrophy pathways. We indicated that p53/ATF4/p21 signaling is an essential factor in aging, and the suppression of this pathway could be beneficial in the deceleration of the aging process. Therefore, this work would shed light on understanding the effect of exercise and nutrition interventions on preventing atrophy markers of skeletal muscle in diabetic rats. Further studies are needed to seek the precise mechanism of the synergism between UA and exercise in ameliorating atrophy markers.

show abstract

“…BDNF mRNA is increased in neurons and in newborn neurons of the injured area after TBI in telencephalon of adult zebrafish, and this increase is maintained up to 15 dpi [ 39 ]. Studies imply that saffron anti-depressant and cognitive effects could be mediated via neurotrophin upregulations such as BDNF, neurotrophin-3 (NT-3) and the neurotrophin-inducible neuropeptide VGF [ 67 , 68 ]. The anxiolytic effect of saffron in the novel tank test when comparing treated TBI to untreated TBI seems exacerbated when comparing treated TBI to control.…”

Section: Discussionmentioning

confidence: 99%

Saffron Extract Attenuates Anxiogenic Effect and Improves Cognitive Behavior in an Adult Zebrafish Model of Traumatic Brain Injury

Chaoul

Awad

Harb

et al. 2022

IJMS

View full text Add to dashboard Cite

Traumatic brain injury (TBI) has the highest mortality rates worldwide, yet effective treatment remains unavailable. TBI causes inflammatory responses, endoplasmic reticulum stress, disruption of the blood–brain barrier and neurodegeneration that lead to loss of cognition, memory and motor skills. Saffron (Crocus sativus L.) is known for its anti-inflammatory and neuroprotective effects, which makes it a potential candidate for TBI treatment. Zebrafish (Danio rerio) shares a high degree of genetic homology and cell signaling pathways with mammals. Its active neuro-regenerative function makes it an excellent model organism for TBI therapeutic drug identification. The objective of this study was to assess the effect of saffron administration to a TBI zebrafish model by investigating behavioral outcomes such as anxiety, fear and memory skills using a series of behavioral tests. Saffron exhibited anxiolytic effect on anxiety-like behaviors, and showed prevention of fear inhibition observed after TBI. It improved learning and enhanced memory performance. These results suggest that saffron could be a novel therapeutic enhancer for neural repair and regeneration of networks post-TBI.

show abstract

Saffron (Crocus Sativus L.), Combined with Endurance Exercise, Synergistically Enhances BDNF, Serotonin, and NT-3 in Wistar Rats

Cited by 16 publications

References 31 publications

Understanding How Physical Exercise Improves Alzheimer’s Disease: Cholinergic and Monoaminergic Systems

Understanding How Physical Exercise Improves Alzheimer’s Disease: Cholinergic and Monoaminergic Systems

The effect of resistance and endurance training with ursolic acid on atrophy‐related biomarkers in muscle tissue of diabetic male rats induced by streptozotocin and ahigh‐fatdiet

Saffron Extract Attenuates Anxiogenic Effect and Improves Cognitive Behavior in an Adult Zebrafish Model of Traumatic Brain Injury

Contact Info

Product

Resources

About