Format

Send to

Choose Destination
Toxicol In Vitro. 2009 Feb;23(1):47-52. doi: 10.1016/j.tiv.2008.10.001. Epub 2008 Oct 17.

Black ginseng inhibits ethanol-induced teratogenesis in cultured mouse embryos through its effects on antioxidant activity.

Author information

1
Laboratory of Veterinary Anatomy, College of Veterinary Medicine and Research Institute of Veterinary Medicine, Core Research Institute, Chungbuk National University, Cheongju, Chungbuk 361-763, Republic of Korea.

Abstract

Fetal alcohol syndrome is caused by excessive ethanol consumption during pregnancy. We investigated the effect of black ginseng (red ginseng that is subjected to 9 cycles of 95-100 degrees C for 2-3h) on ethanol-induced teratogenesis using an in vitro whole embryo culture system. Postimplantational mouse embryos at embryonic day 8.5 were exposed to ethanol (1 microl/ml) in the presence or absence of black ginseng (1, 10, and 100 microg/ml) for 2 days, and then morphological scoring and real-time PCR analysis were carried out. In ethanol-treated embryos, the total morphological score and individual scores for flexion, heart, fore-, mid-, and hindbrains, otic, optic, and olfactory systems, branchial bars, maxillary and mandibular processes, caudal neural tube, and somites were significantly lower than the control group (p<0.05). Treatment with black ginseng improved most of the morphological scores significantly as compared to ethanol-treated embryos (p<0.05). The mRNA levels of the antioxidant enzymes cytosolic glutathione peroxidase (GPx), phospholipid hydroperoxide GPx, and selenoprotein P were significantly decreased in ethanol-treated embryos, but co-treatment with black ginseng restored the mRNA levels to those of control embryos. These results indicate that black ginseng has a protective effect on ethanol-induced teratogenesis through the augmentation of antioxidative activity in embryos.

PMID:
18992320
DOI:
10.1016/j.tiv.2008.10.001
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center