Abstract

In this study, the potential effects of astaxanthin (AST) were investigated on preventing the prenatal LPS-induced injures in mothers and adult male offspring of NMRI mice.Pregnant mice were randomly divided into four groups: 1. Saline + vehicle; 2. Saline + AST: received astaxanthin (4 mg/kg for 3 days, ip) on 11–13 gestation days; 3. LPS + vehicle (LPS-treated group): injected with LPS (20 µg/kg, sc) on gestation day 11; 4. LPS + AST: administrated LPS and astaxanthin on gestation days 11 and 11–13, respectively. In each group, maternal care behaviors and TNF-α serum levels were examined until weaning of male offspring at 23 days. At 60 days old, male pups underwent analysis of body weight and length, serum gonadotropins and testosterone hormone levels, sperm quality, gonadal and brain tissues morphologies, and the expression of SOX9 and GnRH genes by real-time PCR.Serum TNF-α level increased significantly in mothers treated with LPS, while AST reduced it. In adult male offspring, serum hormone levels, sperm quality, and the number of spermatocytes and Leydig cells in the testes improved when AST was administrated. According to histological studies of the brain, neurons in the LPS-treated group were smaller and less active, whereas neurons in the LPS + AST group were larger, more numerous, and more active. LPS significantly reduced GnRH expression, while AST induction improved its expression.AST administration during pregnancy prevented the adverse effects of prenatal exposure to LPS, presumably through its genomic and non-genomic effects, in adult male offspring.

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