A Comparison of Resveratrol and Vitamin C Therapy on Expression of BDNF in Stressed Rat Brain Homogenate

Ashwin, R.

doi:10.9790/3013-0310022-27

Cited by 6 publications

(4 citation statements)

References 34 publications

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“…The (LPS + Esc) group showed a significant decrease in BDNF compared to the control, this decrease was normalized in the presence of vitamins C and D. Although Little is known about the influence of SSRIs or vitamins C and D on BDNF expression, one study showed that the chronic administration of fluoxetine upregulated cortical BDNF in mice (Mendez-David et al 2015 ), on the other hand, our finding is consistent with existing literature vitamin C was shown to upregulate BDNF in chronic stress models, although in that study the upregulation did still lower than the control, however, the mechanism needs further elucidation (Rai 2013 ), some studies pointed out towards involvement of cognitive restoring function, morphological brain changes of vitamin C beside the antioxidant theory (El-Sokkary and Awadalla 2011 ; Tagliari et al 2011 ).…”

Section: Discussionsupporting

confidence: 89%

Unraveling the potential of vitamins C and D as adjuvants in depression treatment with escitalopram in an LPS animal model

Gammoh,

Akasheh,

Qnais

et al. 2024

Inflammopharmacol

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Depression is linked with oxidative stress and inflammation, where key players include nitric oxide (NO), nuclear factor erythroid 2-related factor 2 (Nrf2), Brain-Derived Neurotrophic Factor (BDNF), and Heme Oxidase-1 (HO-1). Augmenting the efficacy of antidepressants represents a compelling avenue of exploration. We explored the potential of vitamins C and D as adjuncts to escitalopram (Esc) in a lipopolysaccharide (LPS)-induced depression model focusing on the aforementioned biomarkers. Male Swiss albino mice were stratified into distinct groups: control, LPS, LPS + Esc, LPS + Esc + Vit C, LPS + Esc + Vit D, and LPS + Esc + Vit C + Vit D. After a 7-day treatment period, a single LPS dose (2 mg/kg), was administered, followed by comprehensive assessments of behavior and biochemical parameters. Notably, a statistically significant (p < 0.05) alleviation of depressive symptoms was discerned in the Esc + Vit C + Vit D group versus the LPS group, albeit with concomitant pronounced sedation evident in all LPS-treated groups (p < 0.05). Within the cortex, LPS reduced (p < 0.05) the expression levels of NOx, Nrf2, BDNF, and HO-1, with only HO-1 being reinstated to baseline in the LPS + Esc + Vit D and the LPS + Esc + Vit C + Vit D groups. Conversely, the hippocampal NOx, Nrf2, and HO-1 levels remained unaltered following LPS administration. Notably, the combination of Esc, Vit C, and Vit D effectively restored hippocampal BDNF levels, which had been diminished by Esc alone. In conclusion, vitamins C and D enhance the therapeutic effects of escitalopram through a mechanism independent of Nrf2. These findings underscore the imperative need for in-depth investigations.

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Section: Discussionsupporting

confidence: 89%

Unraveling the potential of vitamins C and D as adjuvants in depression treatment with escitalopram in an LPS animal model

Gammoh,

Akasheh,

Qnais

et al. 2024

Inflammopharmacol

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“…The nerve growth factor (NGF), neurotrophin 3 (NT-3), neurotrophin 4/5 (NT-4/5), and the brain-derived neurotrophic factor (BDNF) are the proteins, which specifically help the survival of neurons in AD patients (Hock et al 2000 ). BDNF is one of the significant neurotrophins, which protect the neurons by promoting their survival against the various neuronal insults in different brain regions, including the hippocampus (Rai et al 2013 ). The primary source for the BDNF is the neuron.…”

Section: Introductionmentioning

confidence: 99%

Hippocampus and its involvement in Alzheimer’s disease: a review

et al. 2022

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Hippocampus is the significant component of the limbic lobe, which is further subdivided into the dentate gyrus and parts of Cornu Ammonis. It is the crucial region for learning and memory; its sub-regions aid in the generation of episodic memory. However, the hippocampus is one of the brain areas affected by Alzheimer’s (AD). In the early stages of AD, the hippocampus shows rapid loss of its tissue, which is associated with the functional disconnection with other parts of the brain. In the progression of AD, atrophy of medial temporal and hippocampal regions are the structural markers in magnetic resonance imaging (MRI). Lack of sirtuin (SIRT) expression in the hippocampal neurons will impair cognitive function, including recent memory and spatial learning. Proliferation, differentiation, and migrations are the steps involved in adult neurogenesis. The microglia in the hippocampal region are more immunologically active than the other regions of the brain. Intrinsic factors like hormones, glia, and vascular nourishment are instrumental in the neural stem cell (NSC) functions by maintaining the brain’s microenvironment. Along with the intrinsic factors, many extrinsic factors like dietary intake and physical activity may also influence the NSCs. Hence, pro-neurogenic lifestyle could delay neurodegeneration.

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“…Accordingly, in the BCCAO/R model, RVT pre-treatment restores the tissue concentration of docosahexaenoic acid (DHA), a structural component of neural cell membranes, and increases expression of synapse-associated proteins [4]. In this context, it is not surprising that RVT has also been shown to modulate the expression of brain-derived neurotrophic factor (BDNF) [35,36,37,38], a member of the neurotrophin family that signals through the tyrosine kinase receptor B (trkB). The BDNF-trkB system plays an instructive role for synaptic plasticity [39], involving activation of cytoskeleton dynamics in dendritic spines.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol Regulates BDNF, trkB, PSA-NCAM, and Arc Expression in the Rat Cerebral Cortex after Bilateral Common Carotid Artery Occlusion and Reperfusion

et al. 2019

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The polyphenol resveratrol (RVT) may drive protective mechanisms of cerebral homeostasis during the hypoperfusion/reperfusion triggered by the transient bilateral common carotid artery occlusion followed by reperfusion (BCCAO/R). This immunochemical study investigates if a single dose of RVT modulates the plasticity-related markers brain-derived neurotrophic factor (BDNF), the tyrosine kinase trkB receptor, Polysialylated-Neural Cell Adhesion Molecule (PSA-NCAM), and Activity-regulated cytoskeleton-associated (Arc) protein in the brain cortex after BCCAO/R. Frontal and temporal-occipital cortical regions were examined in male Wistar rats randomly subdivided in two groups, sham-operated and submitted to BCCAO/R. Six hours prior to surgery, half the rats were gavage fed a dose of RVT (180 mg·kg−1 in 300 µL of sunflower oil as the vehicle), while the second half was given the vehicle alone. In the frontal cortex of BCCAO/R vehicle-treated rats, BDNF and PSA-NCAM decreased, while trkB increased. RVT pre-treatment elicited an increment of all examined markers in both sham- and BCCAO/R rats. No variations occurred in the temporal-occipital cortex. The results highlight a role for RVT in modulating neuronal plasticity through the BDNF-trkB system and upregulation of PSA-NCAM and Arc, which may provide both trophic and structural local support in the dynamic changes occurring during the BCCAO/R, and further suggest that dietary supplements such as RVT are effective in preserving the tissue potential to engage plasticity-related events and control the functional response to the hypoperfusion/reperfusion challenge.

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A Comparison of Resveratrol and Vitamin C Therapy on Expression of BDNF in Stressed Rat Brain Homogenate

Cited by 6 publications

References 34 publications

Unraveling the potential of vitamins C and D as adjuvants in depression treatment with escitalopram in an LPS animal model

Unraveling the potential of vitamins C and D as adjuvants in depression treatment with escitalopram in an LPS animal model

Hippocampus and its involvement in Alzheimer’s disease: a review

Resveratrol Regulates BDNF, trkB, PSA-NCAM, and Arc Expression in the Rat Cerebral Cortex after Bilateral Common Carotid Artery Occlusion and Reperfusion

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