Tannic Acid Ameliorates STZ-Induced Alzheimer’s Disease-Like Impairment of Memory, Neuroinflammation, Neuronal Death and Modulates Akt Expression

Gerzson, Mariana Freire Barbieri; Bona, Natália Pontes; Soares, Mayara Sandrielly Pereira; Teixeira, Fernanda Cardoso; Rahmeier, Francine Luciano; Carvalho, Fabiano B.; Fernandes, Marilda da Cruz; Onzi, Giovana R.; Lenz, Guido; Gonçales, Relber Aguiar; Spanevello, Rosélia Maria; Stefanello, Francieli Moro

doi:10.1007/s12640-020-00167-3

Cited by 33 publications

(13 citation statements)

References 56 publications

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“…30 Tannic acid is known to activate nuclear factor erythroid 2-related factor 2 (Nrf2) transcription factor; in response to oxidative stress Nrf2 is activated and translocated to the nucleus where it binds to the Antioxidant Response Elements (AREs) to up-regulate the expression of enzymes that are responsible for GSH homeostasis including heme oxygenase 1 and NAD(P)H: quinone oxidoreductase 1. 31 Furthermore, TA prevents PTZ-induced production of pro-inflammatory cytokines such as IL-6 and TNF-α 29 ; this anti-inflammatory effect of TA may result from its ability to suppress ROS-induced NF-κB pathway activation. 16 This anti-neuroinflammatory effect of TA, in association with antioxidant properties, is suggested to be responsible, at least in part, for the prevention of neurotoxic agents-induced cell death and memory deficits.…”

Section: Discussionmentioning

confidence: 99%

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RETRACTED: Neuroprotective effects of tannic acid against kainic acid-induced seizures in mice

et al. 2022

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Background Epileptic seizures are associated with the release of potentially neurotoxic amount of glutamate, which results in the over-production of free radicals and inflammatory factors, and induction of neuronal cell death. Current study evaluated the effect of tannic acid (TA) on Kainic acid (KA)-induced seizures in mice. Methods Mice were divided into the six groups. Group I was administrated with normal saline (NS; 1 mL/kg, intraperitoneally (i.p.)), Group II was injected with KA (15 mg/kg, i.p.), Groups III was treated with diazepam (DZ; 20 mg/kg, i.p.) and KA (15 mg/kg, i.p.), Groups IV-VI were treated with TA (25, 50 and 100 mg/kg, i.p.) and KA (15 mg/kg, i.p.). Animals received all treatments 30 min before injection of KA. After the injection of KA, mice were observed for seizure (latency, activity and duration) and mortality for 2 h. In the brain tissue, oxidative stress, apoptosis, and inflammatory markers were evaluated in addition to the determination of histological alterations in the CA1 molecular layer of hippocampus. Results Treatment with TA significantly increased seizure latency and decreased seizure duration and activity, but could not significantly decrease mice mortality. This effect was associated with the reduction of oxidative stress, inflammation, and apoptosis. Furthermore, treatment with TA significantly improved KA-induced pyramidal cell loss and change in the arrangement of CA1 molecular layer. Conclusions Tannic acid may be useful in the control of epileptic seizures through regulating oxidative stress, inflammation and apoptosis.

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Section: Discussionmentioning

confidence: 99%

“…16 This anti-neuroinflammatory effect of TA, in association with antioxidant properties, is suggested to be responsible, at least in part, for the prevention of neurotoxic agents-induced cell death and memory deficits. 29…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Neuroprotective effects of tannic acid against kainic acid-induced seizures in mice

et al. 2022

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“…The detected histological lesions in the hippocampus prove the role of AD in changing memory and spatial learning potentials [ 78 ]. Nissl stain of the cerebral cortex showed marked reduction in the number of surviving neurons in the STZ administrated group, this neuronal degeneration resulted in synaptic dysfunction of the brain regions responsible for cognitive functions, with further memory disorders [ 79 ]. Previous studies have confirmed the relation of neuronal degeneration with memory impairment [ 80 , 81 ].…”

Section: Resultsmentioning

confidence: 99%

Novel Luteolin-Loaded Chitosan Decorated Nanoparticles for Brain-Targeting Delivery in a Sporadic Alzheimer’s Disease Mouse Model: Focus on Antioxidant, Anti-Inflammatory, and Amyloidogenic Pathways

et al. 2022

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Preparation and evaluation of a non-invasive intranasal luteolin delivery for the management of cognitive dysfunction in Alzheimer’s disease (AD) using novel chitosan decorated nanoparticles. Development of luteolin-loaded chitosomes was followed by full in vitro characterization. In vivo efficacy was evaluated using a sporadic Alzheimer’s disease (SAD) animal model via intracerebroventricular injection of 3 mg/kg streptozotocin (ICV-STZ). Treatment groups of luteolin suspension and chitosomes (50 mg/kg) were then intranasally administered after 5 h of ICV-STZ followed by everyday administration for 21 consecutive days. Behavioral, histological, immunohistochemical, and biochemical studies were conducted. Chitosomes yielded promising quality attributes in terms of particle size (PS) (412.8 ± 3.28 nm), polydispersity index (PDI) (0.378 ± 0.07), Zeta potential (ZP) (37.4 ± 2.13 mv), and percentage entrapment efficiency (EE%) (86.6 ± 2.05%). Behavioral findings showed obvious improvement in the acquisition of short-term and long-term spatial memory. Furthermore, histological evaluation revealed an increased neuronal survival rate with a reduction in the number of amyloid plaques. Biochemical results showed improved antioxidant effects and reduced pro-inflammatory mediators’ levels. In addition, a suppression by half was observed in the levels of both Aβ aggregation and hyperphosphorylated-tau protein in comparison to the model control group which in turn confirmed the capability of luteolin-loaded chitosomes (LUT-CHS) in attenuating the pathological changes of AD. The prepared nanoparticles are considered a promising safe, effective, and non-invasive nanodelivery system that improves cognitive function in SAD albino mice as opposed to luteolin suspension.

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“…Furthermore, it has been reported that tannic acid, a hydrolysable glycosidic polyphenol polymer of gallic acid, has neuroprotective, anti-inflammatory, and pro-cognitive properties. It indeed prevented streptozotocin (STZ)-induced memory impairment, and restored the increased level of the pro-inflammatory cytokines IL-6 and TNF-α as well as the decreased level of Akt and pAkt [54]. Gallic acid also showed neuroprotective effects in a rat model of traumatic brain injury (TBI) ameliorating memory and long-term potentiation (LTP) impairment through the decrease in brain lipid peroxidation (MDA) and pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) in the brain.…”

Section: Gallic Acidmentioning

confidence: 90%

Phenolic Acids and Prevention of Cognitive Decline: Polyphenols with a Neuroprotective Role in Cognitive Disorders and Alzheimer’s Disease

et al. 2022

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Cognitive impairment, also known as cognitive decline, can occur gradually or suddenly and can be temporary or more permanent. It represents an increasingly important public health problem and can depend on normal aging or be linked to different neurodegenerative disorders, including Alzheimer’s disease (AD). It is now well-established that lifestyle factors including dietary patterns play an important role in healthy aging as well as in the prevention of cognitive decline in later life. Among the natural compounds, dietary polyphenols including phenolic acids have been recently the focus of major attention, with their supplementation being associated with better cognitive status and prevention of cognitive decline. Despite their therapeutic potential, human studies investigating the relation between phenolic acids intake and cognitive outcomes are rather scarce. In this review, we provide preclinical evidence that different dietary polyphenols such as rosmarinic acid, ellagic acid, and cinnamic aldehyde can exert neuroprotective and pro-cognitive activities through different molecular mechanisms including the modulation of pro-oxidant and antioxidant machinery as well as inflammatory status. Future and more numerous in vivo studies are needed to strengthen the promising results obtained at the preclinical level. Despite the excellent pharmacokinetic properties of phenolic acids, which are able to be accumulated in the brain at pharmacologically relevant levels, future studies should also identify which among the different metabolites produced as a consequence of phenolic acids’ consumption may be responsible for the potential neuroprotective effects of this subgroup of polyphenols.

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Tannic Acid Ameliorates STZ-Induced Alzheimer’s Disease-Like Impairment of Memory, Neuroinflammation, Neuronal Death and Modulates Akt Expression

Cited by 33 publications

References 56 publications

RETRACTED: Neuroprotective effects of tannic acid against kainic acid-induced seizures in mice

RETRACTED: Neuroprotective effects of tannic acid against kainic acid-induced seizures in mice

Novel Luteolin-Loaded Chitosan Decorated Nanoparticles for Brain-Targeting Delivery in a Sporadic Alzheimer’s Disease Mouse Model: Focus on Antioxidant, Anti-Inflammatory, and Amyloidogenic Pathways

Phenolic Acids and Prevention of Cognitive Decline: Polyphenols with a Neuroprotective Role in Cognitive Disorders and Alzheimer’s Disease

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