Document Detail

Effects of SAC on oxidative stress and NO availability in placenta: Potential benefits to preeclampsia.
MedLine Citation:
PMID:  22405339     Owner:  NLM     Status:  Publisher    
Preeclampsia (PE) is a major cause of fetal growth restriction and perinatal mortality, which involves oxidative stress and vasodilator signaling disorder. S-allyl-l-cysteine (SAC) is one of the most abundant compounds in garlic extracts, and possesses several biological activities. This research was designed to investigate the protective effects of SAC against H(2)O(2)-induced oxidative insults, as well as the effects on NO/cGMP signaling pathway in placenta. We used TEV-1 cells and placental explants to detect the effects of SAC. TEV-1 cells and human placental explants were separately exposed to SAC, H(2)O(2), or a combination of H(2)O(2) and SAC. Intracellular ROS was detected by flow cytometry; the NO level was detected by an NO metabolites (NOx) assay; the cGMP level was simultaneously measured by the method of radioimmunoassay; the expression of eNOS in TEV-1 cells was measured by immunochemistry and Western blot. Our findings showed that H(2)O(2) treatment increased ROS productions in TEV-1 cells and significantly decreased cGMP and NO level either in TEV-1 cells or explants compared to the control groups (p < 0.05). The expression of eNOS in TEV-1 cells also significantly decreased in H(2)O(2) treated group compared to the control group (p < 0.05). Co-treatment of H(2)O(2) and SAC significantly decreased ROS productions, and increased NO, cGMP and eNOS level compared to the H(2)O(2) treated alone groups (p < 0.05), which were all reverted back to near control levels. Further more, SAC treatment increased NO and cGMP level of TEV-1 cells and explants in a dose-dependent manner even at non-oxidative stress status (p < 0.05). However, when the TEV-1 cells were cultured in the presence of NOS inhibitor (L-NAME) and NO donor (SNP), additional SAC treatment still significantly increased the NO level in comparison with SAC non-treated group (p < 0.05). In conclusion, these results demonstrate that ROS (H(2)O(2)-mediated) can induce insults to NO/cGMP pathway, while SAC could antagonize this insult. And SAC also possesses the ability to increase NO and cGMP level at non-oxidative stress status in TEV-1 cells and placenta explants. SAC is therefore hypothesized to be a potential drug for PE treatment.
J Yu; L Feng; Y Hu; Y Zhou
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-3-7
Journal Detail:
Title:  Placenta     Volume:  -     ISSN:  1532-3102     ISO Abbreviation:  -     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-3-12     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8006349     Medline TA:  Placenta     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012 Elsevier Ltd. All rights reserved.
Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China.
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