Abstract
Risperidone (RIS), an atypical antipsychotic has been found to show anti-inflammatory effect against lipopolysaccharide (LPS)-induced inflammation. In vitro study has revealed that RIS inhibits the LPS-induced reactive oxygen species (ROS) formation. We investigated the antioxidant effects of RIS on LPS-induced oxidative stress markers in Swiss albino mice. Ten weeks old male Swiss albino mice (30 ± 2 g) were pretreated with either distilled water (control) or RIS (3 mg/kg) for 7 days. On day 8, animals were challenged with a single dose of LPS (0.8 mg/kg) while control animals received distilled water only. The animals were sacrificed after 24 h of LPS administration and tissue samples were collected. RIS administration significantly (p < 0.05) reduced the LPS-induced elevated levels of lipid peroxidation product malondialdehyde (MDA), advanced protein oxidation products, and nitric oxide (NO) in the cortex. Catalase (CAT) and superoxide dismutase (SOD) levels were also diminished while the level of glutathione (GSH) was enhanced. Hippocampus data showed that RIS significantly (p < 0.05) reduced the LPS-induced increased levels of MDA and NO, and SOD activity. Our results suggest that LPS-induced neuronal oxidative damage can be alleviated by the pretreatment with RIS and the effect is shown presumably by scavenging of the ROS by risperidone as an antioxidant.
Highlights
IntroductionEndothelial cells, astrocytes, and microglial cells are the vital elements that conserve the features of blood–brain barrier (BBB)
The brain is a specialized restricted region separated by blood–brain barrier (BBB)
We report that the administration of RIS in LPS-induced stress model might be promising in improving the deficits due to oxidative stress
Summary
Endothelial cells, astrocytes, and microglial cells are the vital elements that conserve the features of BBB. Astrocytes and microglial cells provide a distinct immune mechanism to the brain. Under inflammatory state, BBB becomes leaky and allows the access of undesirable components, such as immune cells, inflammatory molecules, and albumin to the brain. Microglia becomes activated resulting in the release of cytotoxic mediators; such as NO, TNF-α, IL-1β, and ROS. Overproduction of these mediators has been found to be toxic to the neurons which leads to neuronal death (Cui et al, 2012)
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