Abstract
BackgroundPrenatal maternal lipopolysaccharide (LPS) exposure leads to behavioral deficits such as depression, anxiety, and schizophrenia in the adult lives. LPS-exposure resulted in the production of cytokines and oxidative damage. On the contrary, astaxanthin is a carotenoid compound, showed neuroprotective properties via its antioxidant capacity. This study examines the effect of astaxanthin on the prenatal maternal LPS-induced postnatal behavioral deficit in mice.ResultsWe found that prenatal LPS-exposed mice showed extensive immobile phase in the tail suspension test, higher frequent head dipping in the hole-board test and greater hypolocomotion in the open field test. All these values were statistically significant (p < 0.05). In addition, a marked elevation of the level of lipid peroxidation, advanced protein oxidation product, nitric oxide, while a pronounced depletion of antioxidant enzymes (superoxide dismutase, catalase and glutathione) were observed in the adult offspring mice that were prenatally exposed to LPS. To the contrary, 6-weeks long treatment with astaxanthin significantly improved all behavioral deficits (p < 0.05) and diminished prenatal LPS-induced oxidative stress markers in the brain and liver.ConclusionsTaken together, these results suggest that prenatal maternal LPS-exposure leads to behavioral deficits in the adults, while astaxanthin ameliorates the behavioral deficits presumably via its antioxidant property.
Highlights
Prenatal maternal lipopolysaccharide (LPS) exposure leads to behavioral deficits such as depression, anxiety, and schizophrenia in the adult lives
Behavioral studies Open field test A significant main effect of treatment on the number of entry into the periphery [F(3,36) = 6.34, p < 0.01] (Fig. 2a), time spent in periphery [F(3,33) = 6.95, p < 0.001] (Fig. 2b) and total distance travelled [F(3,34) = 4.49, p < 0.01] (Fig. 2c) was observed for four conditions
The result of the present study showed that astaxanthin treatment reduces a prominent marker of lipid peroxidation (MDA) which is observed in the ischemic brain injury in adult rats [78]
Summary
Prenatal maternal lipopolysaccharide (LPS) exposure leads to behavioral deficits such as depression, anxiety, and schizophrenia in the adult lives. Prenatal LPS-induced maternal immune activation model has been used to develop animal model of depression [8], anxiety [9,10,11], impairment in learning and memory [12, 13], schizophrenia [14,15,16] and autism [17, 18]. A specific time window is critical in inducing neurodevelopmental disorder and impaired behavioral deficits in the rodent’s offspring [6] In this window, LPS-exposure leads to produce cytokines that crosses the placental barrier, which in turn interrupts the processes of fetal brain development [20]. Prenatal LPS-exposure has shown to enhance the level of nitric oxide (NO), lipid peroxidation
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