Resolvin D1 Prevents the Impairment in the Retention Memory and Hippocampal Damage in Rats Fed a Corn Oil-Based High Fat Diet by Upregulation of Nrf2 and Downregulation and Inactivation of p66Shc

Mostafa, Dalia G.; Satti, Huda H.

doi:10.1007/s11064-020-03022-1

Cited by 12 publications

(18 citation statements)

References 61 publications

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“…[24][25][26][27][28] RVD1 suppresses neural inflammation and apoptosis and improve recognition memory in several animal models with brain injury. [29][30][31] In the majority of these studies, the protective effect of RVD1 was attributed to the inhibition of inflammation and ROS production, at least, by preserving mitochondria haemostasis, inhibiting microglia and astrocytes activation, and regulating the activation of the the anti-inflmmatory and antioxidant transcription factors (i.e. nuclear factor κB [NF-κB] and the nuclear factor erythroid-2 related factor-2 [Nrf2]).…”

Section: Docosahexaenoic Acid [Dha] and Eicosapentaenoic Acids [Epa])mentioning

confidence: 99%

Resolvin D1 prevents cadmium chloride‐induced memory loss and hippocampal damage in rats by activation/upregulation of PTEN‐induced suppression of PI3K/Akt/mTOR signaling pathway

Shati

El‐kott

Alkhateeb

2021

Clin Exp Pharma Physio

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Intoxication with the heavy metal, cadmium (Cd), is associated with neurotoxicity in both humans and animals that is characterized by poor learning, low attention, neurodegeneration, neuropathy, memory loss, tau hyperphosphorylation and development of Parkinson's disease (PD) and Alzheimer's disease (AD). [1][2][3] Accordingly, Cd damages the cerebral cortices and the hippocampi of rodents by activating several mechanisms including the induction of oxidative stress, inflammation and apoptosis. 4,5 Yet, over-production of reactive oxygen species (ROS) and the associated alteration in multiple intracellular signaling pathways remains the most acceptable theory to explain the neurotoxic effect of Cd ions. 2,6,7 The phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) is the most common signaling pathway involved in neural proliferation, metabolism, neurotransmission, survival, and apoptosis. 8,9 Active PI3K phosphorylate and activate Akt which phoshorylates intacellular several targets including the glycogen synthase kinase-3-beta

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Section: Docosahexaenoic Acid [Dha] and Eicosapentaenoic Acids [Epa])mentioning

confidence: 99%

Resolvin D1 prevents cadmium chloride‐induced memory loss and hippocampal damage in rats by activation/upregulation of PTEN‐induced suppression of PI3K/Akt/mTOR signaling pathway

Shati

El‐kott

Alkhateeb

2021

Clin Exp Pharma Physio

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“…Similar to the protective effect of RVD1 reported here, aspirin-triggered resolvin D1 (AT-RVD1) prevented orthopedic surgery-induced cognitive decline. 39,98 Also, exogenous administration of RvD1 protected against traumatic brain injury (TBI)-induced cognitive impairment in mice by preserving the mitochondria of the astrocytes and reducing the generation of inflammatory cytokines and ROS. 98 RVD1 effectively prevented brain, lung, and hepatic injury in several animal models by suppressing the production of the inflammatory cytokines, reducing the generation of ROS, and upregulation of endogenous antioxidants mediated by inhibiting NF-κB and upregulation of Nrf-2.…”

Section: Discussionmentioning

confidence: 99%

“…[41][42][43][44][45][46][47] In a very recent elegant study, it has been demonstrated that chronic administration of RVD1 improved memory function and protected the hippocampal cells of high fat diet-induced oxidative stress, inflammation, and apoptosis by upregulation of Nrf-2 and suppression of P66 Sch . 39 In a single study, it has been shown that n-3 PUFAs can protect against cadmium chloride (CdCl 2 )-induced cortical injury and alleviate the reduction in antioxidant enzymes. 18 However, the authors showed that the co-treatment with n-3 PUFA has more beneficial effects than post-treatment.…”

Section: Introductionmentioning

confidence: 99%

Resolvin D1 protects against cadmium chloride-induced memory loss and hippocampal damage in rats: A comparison with docosahexaenoic acid

Shati

El‐kott

2021

Hum Exp Toxicol

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Background Intoxication with cadmium (Cd) ions leads to hippocampal damage and cognitive impairment. However, omega-3 polyunsaturated fatty acids (n-3 PUFAs) exert neuroprotective effects in different animal models of neurodegeneration. Purpose This study compared the neuroprotective effect of the n-3 PUFA, docosahexaenoic acid (DHA), and its downstream metabolite, resolvin D1 (RVD1), on hippocampal damage and memory deficits in cadmium chloride (CdCl2)-treated rats. Research design Control or CdCl2 (0.5 mg/kg)-treated rats were subdivided into three groups ( n = 18/each) and treated for 6 weeks as follows: (1) fed control diet, (2) fed DHA-rich diets (0.7 g/100 g), or (3) treated with RVD1 (0.2 μg/kg, i.p). Results Treatment with a DHA-rich diet or RVD1 significantly increased the levels of docosahexaenoic acid and RVD1, respectively, in the hippocampal of CdCl2-treated rats without affecting the reduction in the expression of the 15-lipooxygenase-1 (ALOX15). These effects were associated with improvements in rats’ memory function and hippocampal structure, as well as a redction in the hippocampal levels of reactive oxygen species (ROS), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), nuclear localization of the nuclear factor-kappa beta p65 (NF-κB p65), and expression of cleaved caspase-3. Concomitantly, hippocampi of both groups of rats showed significantly higher levels of Bcl-2, superoxide dismutase (SOD), and glutathione (GSH), as well as enhanced nuclear levels of the nuclear factor erythroid 2–related factor 2 (Nrf-2). The effects of RVD1 on all these markers in the CdCl2-induced rats were more profound than those of DHA. Also, the increase in the nuclear protein levels of Nrf-2 and the decrease in the levels of Bax and nuclear protein levels of NF-κB p65 were only seen in the hippocampal of CdCl2 + RVD1-treated rats. Conclusion RVD1 is more powerful than DHA in preventing CdCl2-induced memory loss and hippocampal damage in rats.

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“…Various studies have reported that HFD triggers oxidative stress in the brain and hippocampus [17,28]. It has been shown that increased MDA levels and decreased GSH levels in the hippocampus [29], and brain [30] in rats receiving HFD. Similar to the aforementioned studies in this study HFD administration caused an increase in the MDA level and decrease in the GSH level.…”

Section: Discussionmentioning

confidence: 99%

Myrtus communis extract ameliorates high-fat diet induced brain damage and cognitive function

Özbeyli¹,

YARIMBAŞ²,

Ertaş³

et al. 2020

JRP

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Obesity causes cognitive weakening and increases the risk of neurodegenerative diseases. Myrtus communis extract (MC) has anti-inflammatory and antioxidant properties. In this study, it is aimed to investigate the effects of Myrtus communis on oxidative brain damage caused by a high-fat diet (HFD), using behavioral and biochemical parameters. Twenty-four Wistar albino rats (200-250 g) were divided into three groups. The control group (C) received a standard diet, while HFD groups were received HFD for 16 weeks. MC (100 mg/kg, oral) was given to the HFD + MC group for the last 4 weeks. At the end of the study, the novel object recognition test (NORT) was performed and the hippocampus and blood samples were collected. Acetylcholinesterase (AChE) and Na + /K +-ATPase activities, malondialdehyde (MDA), 8-hydroxy-2'-deoxyguanosine (8-OHdG) and reduced glutathione (GSH) levels were measured in the hippocampal samples and cholesterol levels were analyzed in sera. Findings have shown that NORT performance of the HFD group was reduced, while administration of MC prevents this reduction and in parallel, increased AChE and decreased Na⁺ /K⁺-ATPase activities were ameliorated by administration of MC. Increased MDA and 8-OHdG levels observed in the HFD group, were decreased in the MC treated HFD group. Our results point out that MC has ameliorative effects on hippocampal oxidative stress and cognitive impairment in high fat nutritioninduced obesity.

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Resolvin D1 Prevents the Impairment in the Retention Memory and Hippocampal Damage in Rats Fed a Corn Oil-Based High Fat Diet by Upregulation of Nrf2 and Downregulation and Inactivation of p66Shc

Cited by 12 publications

References 61 publications

Resolvin D1 prevents cadmium chloride‐induced memory loss and hippocampal damage in rats by activation/upregulation of PTEN‐induced suppression of PI3K/Akt/mTOR signaling pathway

Resolvin D1 prevents cadmium chloride‐induced memory loss and hippocampal damage in rats by activation/upregulation of PTEN‐induced suppression of PI3K/Akt/mTOR signaling pathway

Resolvin D1 protects against cadmium chloride-induced memory loss and hippocampal damage in rats: A comparison with docosahexaenoic acid

Myrtus communis extract ameliorates high-fat diet induced brain damage and cognitive function

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