Impact of levetiracetam on cognitive impairment, neuroinflammation, oxidative stress, and neuronal apoptosis caused by lipopolysaccharides in rats

Mani, Vasudevan; Almutairi, Salem Rashed

doi:10.1016/j.jsps.2023.101728

Cited by 6 publications

(2 citation statements)

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“…), APZ1 + LPS (aripiprazole 1 mg/kg+ LPS), and APZ2 + LPS (aripiprazole 2 mg/kg+ LPS). The choice of APZ doses at 1 and 2 mg/kg [14,15] and the schedule for inducing LPS-related neurotoxicity were determined based on insights from early publications [24]. To evaluate cognitive performance, all animals were allowed to participate in the NOR test on days 29 and 30.…”

Section: Experimental Designmentioning

confidence: 99%

“…The exploration time was determined as "the period during which an animal directs its nose toward an object located within a distance of 2 cm or less". To assess the rat's ability to discriminate between FOs and NOs, the discrimination index (DI% = (ENO − EFO/ ENO + EFO) × 100; ENO-Exploration time of an NO; EFO-Exploration time of an FO) was computed [24,25].…”

Section: Novel Object Recognition (Nor)mentioning

confidence: 99%

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Aripiprazole Attenuates Cognitive Impairments Induced by Lipopolysaccharide in Rats through the Regulation of Neuronal Inflammation, Oxidative Stress, and Apoptosis

Mani,

Alshammeri

2023

Medicina

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Background and Objectives: Aripiprazole (APZ), an atypical antipsychotic, is mainly prescribed for conditions such as schizophrenia and bipolar disorder, while ongoing research indicates promising neuroprotective qualities. APZ’s mechanism of action, involving the regulation of neurotransmitter levels, appears to contribute to its potential to shield neural tissues from specific forms of harm and degeneration. Materials and Methods: To investigate its neuroprotective mechanisms, groups of rats were orally administered APZ at 1 or 2 mg/kg once daily for a 30-day period. In addition, neuronal toxicity was induced through intraperitoneal injection of four doses of lipopolysaccharide (LPS) at a concentration of 1 mg/kg. To evaluate cognitive function, particularly, short-term recognition memory, the procedure implemented the novel object recognition (NOR) task. Subsequently, brain tissues were gathered to examine markers linked with neuroinflammation, oxidative stress, and apoptosis. Results: The administration of LPS led to a decline in memory performance during the NOR tasks. Simultaneously, this LPS treatment raised inflammatory markers like cyclooxygenase (COX)-2, tumor necrosis factor (TNF)-α, and nuclear factor kappa B (NF-κB), increased oxidative markers such as malondialdehyde (MDA), and triggered apoptosis markers like Caspase-3 and Bcl2 associated X protein (Bax) within the brain. Furthermore, it decreased levels of antioxidants like reduced glutathione (GSH) and catalase, as well as the anti-apoptotic marker B-cell lymphoma (Bcl)-2 in brain tissue. The use of APZ resulted in enhanced recognition memory performance, as indicated by improved exploration and discrimination abilities of the objects in the NOR task. Moreover, APZ lowered the markers associated with neuronal vulnerability, such as COX-2, NF-κB, MDA, Caspase-3, and Bax. Additionally, it increased the levels of protective markers, including GSH, catalase, and Bcl-2 in LPS-challenged brains. Conclusions: In summary, the findings suggest that APZ exhibits protective properties against neuronal inflammation, oxidative stress, and apoptosis markers in the context of inflammatory-related neurodegeneration. Additional in-depth investigations are needed to further explore potential applications.

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Section: Experimental Designmentioning

confidence: 99%

Section: Novel Object Recognition (Nor)mentioning

confidence: 99%