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      Histopathological and Biochemical Assessment of Neuroprotective Effects of Sodium Valproate and Lutein on the Pilocarpine Albino Rat Model of Epilepsy

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      1 , , 2
      Behavioural Neurology
      Hindawi

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          Abstract

          Epilepsy is one of the most frequent neurological disorders characterized by an enduring predisposition to generate epileptic seizures. Oxidative stress is believed to directly participate in the pathways of neurodegenerations leading to epilepsy. Approximately, one-third of the epileptic patients who suffer from seizures do not receive effective medical treatment. Sodium valproate (SVP) is a commonly used antiepileptic drug (AED); however, it has toxic effects. Lutein (L), a carotenoid, has potent antioxidant and anti-inflammatory properties. The aim of this study was to determine the neuroprotective effect of sodium valproate (SVP) and lutein (L) in a rat model of pilocarpine- (PLC-) induced epilepsy. To achieve this aim, fifty rats were randomly divided into five groups. Group I: control, group II: received PLC (400 mg/kg intraperitoneally), group III: received PLC + SVP (500 mg/kg orally), group IV: received PLC + SVP + L (100 mg/kg orally), and group V: received (PLC + L). Racine Scale (RC) and latency period to onset seizure were calculated. After eight weeks, the hippocampus rotarod performance and histological investigations were performed. Oxidative stress was investigated in hippocampal homogenates. Results revealed that SVP and L, given alone or in combination, reduced the RC significantly, a significant delay in latency to PLC-kindling onset, and improved rotarod performance of rats compared with the PLC group. Moreover, L was associated with a reduction of oxidative stress in hippocampal homogenate, a significant decrease in serum tumor necrosis factor-alpha (TNF- α) level, and inhibition of cerebral injury and displayed antiepileptic properties in the PLC-induced epileptic rat model. Data obtained from the current research elucidated the prominent neuroprotective, antioxidant, and anti-inflammatory activities of lutein in this model. In conclusion, lutein cotreatment with AEDs is likely to be a promising strategy to improve treatment efficacy in patients suffering from epilepsy.

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          Astaxanthin: Sources, Extraction, Stability, Biological Activities and Its Commercial Applications—A Review

          There is currently much interest in biological active compounds derived from natural resources, especially compounds that can efficiently act on molecular targets, which are involved in various diseases. Astaxanthin (3,3′-dihydroxy-β, β′-carotene-4,4′-dione) is a xanthophyll carotenoid, contained in Haematococcus pluvialis, Chlorella zofingiensis, Chlorococcum, and Phaffia rhodozyma. It accumulates up to 3.8% on the dry weight basis in H. pluvialis. Our recent published data on astaxanthin extraction, analysis, stability studies, and its biological activities results were added to this review paper. Based on our results and current literature, astaxanthin showed potential biological activity in in vitro and in vivo models. These studies emphasize the influence of astaxanthin and its beneficial effects on the metabolism in animals and humans. Bioavailability of astaxanthin in animals was enhanced after feeding Haematococcus biomass as a source of astaxanthin. Astaxanthin, used as a nutritional supplement, antioxidant and anticancer agent, prevents diabetes, cardiovascular diseases, and neurodegenerative disorders, and also stimulates immunization. Astaxanthin products are used for commercial applications in the dosage forms as tablets, capsules, syrups, oils, soft gels, creams, biomass and granulated powders. Astaxanthin patent applications are available in food, feed and nutraceutical applications. The current review provides up-to-date information on astaxanthin sources, extraction, analysis, stability, biological activities, health benefits and special attention paid to its commercial applications.
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            The Interleukin-10 Family of Cytokines and Their Role in the CNS

            Resident cells of the central nervous system (CNS) play an important role in detecting insults and initiating protective or sometimes detrimental host immunity. At peripheral sites, immune responses follow a biphasic course with the rapid, but transient, production of inflammatory mediators giving way to the delayed release of factors that promote resolution and repair. Within the CNS, it is well known that glial cells contribute to the onset and progression of neuroinflammation, but it is only now becoming apparent that microglia and astrocytes also play an important role in producing and responding to immunosuppressive factors that serve to limit the detrimental effects of such responses. Interleukin-10 (IL-10) is generally considered to be the quintessential immunosuppressive cytokine, and its ability to resolve inflammation and promote wound repair at peripheral sites is well documented. In the present review article, we discuss the evidence for the production of IL-10 by glia, and describe the ability of CNS cells, including microglia and astrocytes, to respond to this suppressive factor. Furthermore, we review the literature for the expression of other members of the IL-10 cytokine family, IL-19, IL-20, IL-22 and IL-24, within the brain, and discuss the evidence of a role for these poorly understood cytokines in the regulation of infectious and sterile neuroinflammation. In concert, the available data indicate that glia can produce IL-10 and the related cytokines IL-19 and IL-24 in a delayed manner, and these cytokines can limit glial inflammatory responses and/or provide protection against CNS insult. However, the roles of other IL-10 family members within the CNS remain unclear, with IL-20 appearing to act as a pro-inflammatory factor, while IL-22 may play a protective role in some instances and a detrimental role in others, perhaps reflecting the pleiotropic nature of this cytokine family. What is clear is that our current understanding of the role of IL-10 and related cytokines within the CNS is limited at best, and further research is required to define the actions of this understudied family in inflammatory brain disorders.
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              On the Neuroprotective Role of Astaxanthin: New Perspectives?

              Astaxanthin is a carotenoid with powerful antioxidant and anti-inflammatory activity produced by several freshwater and marine microorganisms, including bacteria, yeast, fungi, and microalgae. Due to its deep red-orange color it confers a reddish hue to the flesh of salmon, shrimps, lobsters, and crayfish that feed on astaxanthin-producing organisms, which helps protect their immune system and increase their fertility. From the nutritional point of view, astaxanthin is considered one of the strongest antioxidants in nature, due to its high scavenging potential of free radicals in the human body. Recently, astaxanthin is also receiving attention for its effect on the prevention or co-treatment of neurological pathologies, including Alzheimer and Parkinson diseases. In this review, we focus on the neuroprotective properties of astaxanthin and explore the underlying mechanisms to counteract neurological diseases, mainly based on its capability to cross the blood-brain barrier and its oxidative, anti-inflammatory, and anti-apoptotic properties.
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                Author and article information

                Contributors
                Journal
                Behav Neurol
                Behav Neurol
                bn
                Behavioural Neurology
                Hindawi
                0953-4180
                1875-8584
                2021
                3 June 2021
                : 2021
                : 5549638
                Affiliations
                1Medical Laboratory Technology Department, Faculty of Applied Medical Sciences, King Abdul Aziz University, Saudi Arabia
                2Department of Anatomy, Faculty of Medicine, Najran University, Najran, Saudi Arabia
                Author notes

                Academic Editor: Muh-Shi Lin

                Author information
                https://orcid.org/0000-0003-0978-5775
                Article
                10.1155/2021/5549638
                8195670
                cebef9bf-08ba-4877-833a-1b9318f234cf
                Copyright © 2021 Aziza Rashed Al-Rafiah and Khlood Mohammed Mehdar.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 21 January 2021
                : 13 April 2021
                : 24 May 2021
                Funding
                Funded by: Najran University
                Award ID: NU/MRC/10/297
                Categories
                Research Article

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