Carotenoids from Marine Sources as a New Approach in Neuroplasticity Enhancement

Abstract

An increasing number of people experience disorders related to the central nervous system (CNS). Thus, new forms of therapy, which may be helpful in repairing processes’ enhancement and restoring declined brain functions, are constantly being sought. One of the most relevant physiological processes occurring in the brain for its entire life is neuroplasticity. It has tremendous significance concerning CNS disorders since neurological recovery mainly depends on restoring its structural and functional organization. The main factors contributing to nerve tissue damage are oxidative stress and inflammation. Hence, marine carotenoids, abundantly occurring in the aquatic environment, being potent antioxidant compounds, may play a pivotal role in nerve cell protection. Furthermore, recent results revealed another valuable characteristic of these compounds in CNS therapy. By inhibiting oxidative stress and neuroinflammation, carotenoids promote synaptogenesis and neurogenesis, consequently presenting neuroprotective activity. Therefore, this paper focuses on the carotenoids obtained from marine sources and their impact on neuroplasticity enhancement.

Anti-Inflammatory Effects of Marine Bioactive Compounds and Their Potential as Functional Food Ingredients in the Prevention and Treatment of Neuroinflammatory Disorders

“…In another study, Aslankoc et al [168] observed that treatment with astaxanthin at a dose of 100 mg/kg for one week provided protection against methotrexate-induced damage in the cerebellar cortex, cerebral cortex, and hippocampus in rat models. In contrast, in the control group, there was an elevated level of oxidative damage in the blood, hippocampus, and cerebral cortex, as demonstrated by a reduction in total antioxidant status and an elevated total oxidative state, while astaxanthin decreased oxidative damage in the study group [135].…”

“…In the transfected human monocytic cell line, it was observed that treatment with siphonaxanthin at a concentration of 1.0 µM for 24 hours exhibited an anti-inflammatory effect, as demonstrated by the marked suppression of TNF-α-and LPS-induced NF-κB activation. Furthermore, siphonaxanthin pretreatment at a concentration of 1.0 µM markedly inhibited the IL-1β-mediated activation of NF-κB [134,135].…”

“…Moreover, astaxanthin decreased microglial activation and the expression of various pro-inflammatory cytokines, which further resulted in the suppression of neuroinflammation. The anti-inflammatory activity of astaxanthin was demonstrated by the nuclear translocation of NFκB p65, as well as by the suppression of p38 and Erk1/2 phosphorylation [135,137].…”

“…Fucoxanthin also inhibited neuroinflammation by regulating NLRP3 inflammasome. It has been demonstrated that fucoxanthin might regulate the initiation step of inflammasome signaling cascades since it has the potential to decrease the expression of phosphorylated IκBα and pro-IL-1β [135,173].…”

“…Siphonaxanthin (Figure 6) is a keto-carotenoid found in various edible green algae, including Umbraulva japonica, Caulerpa lentillifera, and Codium fragile [135]. In the transfected human monocytic cell line, it was observed that treatment with siphonaxanthin at a concentration of 1.0 µM for 24 hours exhibited an anti-inflammatory effect, as demonstrated by the marked suppression of TNF-α-and LPS-induced NF-κB activation.…”