ArticleMetabolic brain disease2021
Amelioration of oxidative stress and neuroinflammation in lipopolysaccharide-induced memory impairment using Rosmarinic acid in mice.
Article in Metabolic brain disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 56 citations in OpenAlex.
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- Neuroprotective Effects of Carnosine Against Corticosterone-Induced Depression and Memory Impairment.Food science & nutrition · 2026Article
- Chronic uropathogenic Escherichia coli infections in adolescence: in vitro analysis of clinical isolates, multidrug resistance, and in vivo hippocampal cognitive impacts.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Rosemary (Iranian journal of basic medical sciences · 2026Review
- Investigation of neuroprotective and antiapoptotic effects of rosmarinic acid in anIranian journal of basic medical sciences · 2026Article
- Potent Ameliorative Effects of Rosmarinic Acid on Tramadol-Induced Neurotoxicity in the Brain and Hippocampus; by Suppressing Oxidative stress, Apoptosis, ER stress, and Regulating Cognitive Functions.Molecular neurobiology · 2025Article
- [Ameliorative effects and mechanisms of an integrated endoplasmic reticulum stress inhibitor on lipopolysaccharide-induced cognitive impairment in mice].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Article
- Subchronic Toxicity and Effect of the Methanolic Extract ofPlants (Basel, Switzerland) · 2025Article
- Gallic acid enhances memory, learning and reduces neuroinflammation in a rat model of scopolamine-induced cholinergic dysfunction.Inflammopharmacology · 2025Article
- Barbigerone against Lipopolysaccharide-Induced Memory Deficit in Rats via Alteration of Inflammatory and Oxidative Stress Pathway:CNS & neurological disorders drug targets · 2025Article
- Ambroxol confers neuroprotection against scopolamine-induced Alzheimer's-like pathology by modulating oxidative stress, neuroinflammation, and cognitive deficits via Nrf-2/JNK/GSK-3β signaling pathways.Frontiers in aging neuroscience · 2025Article
- Rosmarinic acid ameliorated oxidative stress, neuronal injuries, and mitochondrial dysfunctions mediated by polyglutamine and ɑ-synuclein in Caenorhabditis elegans models.Molecular neurobiology · 2024Article
- Carotenoid Supplementation for Alleviating the Symptoms of Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Novel Insights into Changes in Gene Expression within the Hypothalamus in Two Asthma Mouse Models: A Transcriptomic Lung-Brain Axis Study.International journal of molecular sciences · 2024Article
- Kojic acid reverses LPS-induced neuroinflammation and cognitive impairment by regulating the TLR4/NF-κB signaling pathway.Frontiers in pharmacology · 2024Article
- Knockdown and inhibition of hippocampal GPR17 attenuates lipopolysaccharide-induced cognitive impairment in mice.Journal of neuroinflammation · 2023Article
- Minocycline Protects Against Lipopolysaccharide-Induced Cognitive Impairment and Oxidative Stress: Possible Role of the CREB-BDNF Signaling Pathway.Neurochemical research · 2023Article
- Yomogin, Isolated fromAntioxidants (Basel, Switzerland) · 2022Article
- Phytochemistry, Pharmacology and Molecular Mechanisms of Herbal Bioactive Compounds for Sickness Behaviour.Metabolites · 2022Review
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Oxidative stress plays a pivotal part in the manifestation of neuroinflammation, which further leads to neurodegenerative diseases like Alzheimer's disease (AD). Systemic administration of lipopolysaccharide (LPS) induces neuroinflammation resulting in memory impairment (MI) and cognitive decline. In this study, we evaluated whether prophylactic administration of Rosmarinic acid (RA), a naturally occurring compound, exerts a neuroprotective effect in LPS-induced MI and cognitive decline. Herein, Swiss albino mice were pre-treated with RA (0.5 mg/kg and 1 mg/kg i.p.) for 28 days and were intermittently exposed to LPS (0.25 mg/kg i.p.) for 7 days. LPS caused poor memory retention and increased cognitive decline in Morris water maze (MWM) and Y maze paradigms respectively. Additionally, LPS increased oxidative stress which was denoted by a decrease in superoxide dismutase (SOD) activity, decrease in reduced glutathione (GSH) levels, and increased lipid peroxidation in the brain. Imbalance in the cholinergic system was analyzed by measuring the acetylcholinesterase (AChE) activity. Pre-treatment with RA improved memory and behavioral disturbances by alleviating oxidative stress and AChE activity. LPS augmented levels of tumor necrosis factor (TNF-α), interleukin (IL)-6, caspase-3, and c-Jun. Pre-treatment with RA revitalized the elevated levels of proinflammatory cytokines and apoptotic proteins. In conclusion, this study showcases the amelioration of MI by RA in LPS-challenged memory and cognitive decline, which could be credited to its anti-oxidant effect, inhibitory effect on both proinflammatory cytokines and apoptotic regulators, and reduction in AChE activity.
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