Resveratrol limits diabetes-associated cognitive decline in rats by preventing oxidative stress and inflammation and modulating hippocampal structural synaptic plasticity
@article{Tian2016ResveratrolLD, title={Resveratrol limits diabetes-associated cognitive decline in rats by preventing oxidative stress and inflammation and modulating hippocampal structural synaptic plasticity}, author={Xia Tian and Yanlin Liu and Guang-Dong Ren and Ling Yin and Xi Liang and Tao Geng and Heqin Dang and Rufeng An}, journal={Brain Research}, year={2016}, volume={1650}, pages={1-9} }
59 Citations
Resveratrol prevents cognitive deficits by attenuating oxidative damage and inflammation in rat model of streptozotocin diabetes induced vascular dementia
- Biology, PsychologyPhysiology & Behavior
- 2019
SIRT1 Mediates H2S-Ameliorated Diabetes-Associated Cognitive Dysfunction in Rats: Possible Involvement of Inhibiting Hippocampal Endoplasmic Reticulum Stress and Synaptic Dysfunction.
- Biology, PsychologyNeurochemical research
- 2021
It is demonstrated that SIRT1 mediates the protection of H2S against cognitive dysfunction in STZ-diabetic rats partly via inhibiting hippocampal ER stress and synaptic dysfunction.
Berberine Ameliorates Diabetes-Associated Cognitive Decline through Modulation of Aberrant Inflammation Response and Insulin Signaling Pathway in DM Rats
- Biology, MedicineFront. Pharmacol.
- 2017
BBr inhibited the activation of inflammation pathway and insulin resistance in the mPFC of diabetic rats and improved the lesion of cognition in diabetic rats.
DL0410 Alleviates Memory Impairment in D-Galactose-Induced Aging Rats by Suppressing Neuroinflammation via the TLR4/MyD88/NF-κB Pathway
- Biology, ChemistryOxidative medicine and cellular longevity
- 2021
The results suggest that DL0410 exerts neuroprotective effects against hippocampus and cortex injury induced by D-galactose, and the possible mechanisms include antioxidative stress, antineuroinflammation, improving synaptic plasticity, and maintaining BBB integrity, which is mediated by the TLR4/MyD88/NF-κB signaling pathway inhibition.
Memory and Learning Improvement by Resveratrol and Probiotics via the Gut-Brain Axis and Antioxidant Activity in Diabetic Rats
- BiologyAvicenna Journal of Neuro Psycho Physiology
- 2021
Treatment with resveratrol and probiotics significantly normalized pyramidal cell densities in the hippocampus of diabetic rats, which reduced oxidative stress and activated the gut-brain axis in diabetic animals.
Resveratrol Improves Synaptic Plasticity in Hypoxic-Ischemic Brain Injury in Neonatal Mice via Alleviating SIRT1/NF-κB Signaling–Mediated Neuroinflammation
- BiologyJournal of molecular neuroscience : MN
- 2021
It is found that resveratrol improves HI-induced long-term cognitive and memory deficits and reduces hippocampal neuronal damage and increases dendritic spine density and the expression of synaptic proteins, and this effect may be exerted by regulating the neuroinflammatory response mediated by the SIRT1/NF-κB axis.
Review of the Effect of Natural Compounds and Extracts on Neurodegeneration in Animal Models of Diabetes Mellitus
- BiologyInternational journal of molecular sciences
- 2019
A wide range of natural extracts and compounds contribute to limit neurodegeneration and cognitive dysfunction under diabetic state, and could broaden therapeutic alternatives to reduce or slow down complications associated with diabetes at central level.
Neuroprotection elicited by resveratrol in a rat model of hypothyroidism: Possible involvement of cholinergic signaling and redox status
- Biology, MedicineMolecular and Cellular Endocrinology
- 2021
Effects of resveratrol on the levels of ATP, 5-HT and GAP-43 in the hippocampus of mice exposed to chronic unpredictable mild stress
- Biology, PsychologyNeuroscience Letters
- 2020
The Protective Effect of Astaxanthin on Cognitive Function via Inhibition of Oxidative Stress and Inflammation in the Brains of Chronic T2DM Rats
- BiologyFront. Pharmacol.
- 2018
Astaxanthin might inhibit oxidative stress and inflammatory responses by activating the Nrf2-ARE signaling pathway, which implies that AST ameliorated the impairment in the neurons of diabetic rats.
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