The protective effect of astaxanthin on fetal alcohol spectrum disorder in mice.
Astaxanthin is a strong antioxidant with the ability of reducing the markers of inflammation. To explore the protective effect of astaxanthin on maternal ethanol induced embryonic deficiency, and to investigate the underlying mechanisms, we detected the morphology, expression of neural marker genes, oxidative stress indexes, and inflammatory factors in mice model of fetal alcohol spectrum disorder with or without astaxanthin pretreatment. Our results showed that astaxanthin blocked maternal ethanol induced retardation of embryonic growth, and the down-regulation of neural marker genes, Otx1 and Sox2. Moreover, astaxanthin also reversed the increases of malondialdehyde (MDA), hydrogen peroxide (H2O2), and the decrease of glutathione peroxidase (GPx) in fetal alcohol spectrum disorder. In addition, maternal ethanol induced up-regulation of toll-like receptor 4 (TLR4), and the down-streaming myeloid differentiation factor 88 (MyD88), NF-κB, TNF-α, and IL-1β in embryos, and this was inhibited by astaxanthin pretreatment. These results demonstrated a protective effect of astaxanthin on fetal alcohol spectrum disorder, and suggested that oxidative stress and TLR4 signaling associated inflammatory reaction are involved in this process.
Department of Neurology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou 510120, China; Department of Neurology, Guangzhou Brain Hospital, Guangzhou 510170, China.
Dong
D
Zheng
Department of Neurology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou 510120, China.
Yi
Y
Li
Department of Neurology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou 510120, China.
Lei
L
He
Department of Neurology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou 510120, China.
Yamei
Y
Tang
Department of Neurology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou 510120, China.
Xiangpen
X
Li
Department of Neurology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou 510120, China.
Qingyu
Q
Shen
Department of Internal Medicine, College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA.
Deling
D
Yin
Department of Neurology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou 510120, China. Electronic address: 2353352460@qq.com.
Ying
Y
Peng
D000818:Animals; D002492:Central Nervous System Depressants / Q000009:adverse effects; D004195:Disease Models, Animal; D000431:Ethanol / Q000009:adverse effects; D005260:Female; D063647:Fetal Alcohol Spectrum Disorders / Q000517:prevention & control*; D047109:Fetal Development / Q000187:drug effects / Q000502:physiology; D005979:Glutathione Peroxidase / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D008810:Mice, Inbred C57BL; D053594:Myeloid Differentiation Factor 88 / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology*; D051857:Otx Transcription Factors / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D011247:Pregnancy; D011897:Random Allocation; D055748:SOXB1 Transcription Factors / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D024341:Xanthophylls / Q000494:pharmacology
D002492:Central Nervous System Depressants; C587672:IL1B protein, mouse; D053583:Interleukin-1beta; C507780:Myd88 protein, mouse; D053594:Myeloid Differentiation Factor 88; D016328:NF-kappa B; D018696:Neuroprotective Agents; D051857:Otx Transcription Factors; C497656:Otx1 protein, mouse; D055748:SOXB1 Transcription Factors; C527783:Sox2 protein, mouse; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D024341:Xanthophylls; D000431:Ethanol; D008315:Malondialdehyde; C005948:astaxanthine; D006861:Hydrogen Peroxide; D005979:Glutathione Peroxidase
Astaxanthin; Embryo; Ethanol