Amelioration of oxidative stress and neuroinflammation in lipopolysaccharide-induced memory impairment using Rosmarinic
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ORIGINAL ARTICLE
Amelioration of oxidative stress and neuroinflammation in lipopolysaccharide-induced memory impairment using Rosmarinic acid in mice Chetan Thingore 1 & Viplav Kshirsagar 1 & Archana Juvekar 1 Received: 5 June 2020 / Accepted: 11 October 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
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 LPSchallenged 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. Keywords Rosmarinic acid . Alzheimer’s disease . Neuroinflammation . Memory impairment
Abbreviations AChE Acetylcholinesterase AcSCh Acetyl thio-choline iodide AD Alzheimer’s disease ANOVA Analysis of variance DTNB 5, 5’- dithiobis (2- nitrobenzoic acid) IL Interleukin IAEC Institutional Animal Ethics Committee JNK c-Jun N-terminal kinase (JNK) LPO Lipid peroxidation LPS Lipopolysaccharide
* Archana Juvekar [email protected] 1
Department of Pharmaceutical Sciences and Technology, Institute of Chemical Technology, Nathalal Parekh Marg, Matunga, Mumbai, Maharashtra, India
MI MWM NFTs NSAIDs Nrf2 NIBS PBS ROS GSH RVS RA SOD SAB TBA TBARS TCA TNF WHO
Memory impairment Morris water maze test Neurofibrillary tangles Non-steroidal anti-inflammatory drugs Nuclear factor erythroid 2-related factor 2 National Institute of Biosciences Phosphate buffer saline Reactive oxygen species Reduced glutathione Rivastigmine Rosmarinic acid Superoxide dismutase Spontaneous alteration behaviours Thiobarbituric acid Thiobarbituric ac
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