Natural Compound S-allyl-L-cysteine Possesses Potential Benefits To Preeclampsia

ObjectivePreeclampsia (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 effects of SAC on the NO/cGMP signaling pathway in placenta, as well as the protective effects of SAC against H2O2-induced oxidative insults to the pathway.MethodTEV-1cells and placental explants were used to detect the effects of SAC. TEV-1cells and human placental explants were separately exposed to SAC, H2O2, or a combination of H2O2and SAC. Intracellular ROS was detected by flow cytometry; the NO level was detected, and the cGMP level was simultaneously measured by the method of radioimmunoassay; the expression of eNOS in TEV-1cells was measured by immunochemistry and Western blot.ResultThe results showed that H2O2treatment increased ROS production in TEV-1cells and significantly decreased NO and cGMP levels either in TEV-1cells or placental explants compared to the control groups (p<0.05). The expression of eNOS in TEV-1cells also significantly decreased in H2O2treated group compared to the control group (p<0.05). Co-treatment of H2O2and SAC significantly decreased ROS productions, and increased NO, cGMP and eNOS levels compared to the H2O2treated alone groups (p<0.05), which were all reverted back to near control levels. Further more, SAC treatment increased NO and cGMP levels of TEV-1cells and placental explants in a dose-dependent manner even at non-oxidative stress status (p<0.05). However, when the TEV-1cells were cultured in the presence of eNOS 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). ConclusionIn conclusion, these results demonstrate that oxidative stress (H2O2-mediated) can induce insults to NO/cGMP pathway, while SAC could antagonize these insults. And SAC also possesses the ability to increase NO and cGMP levels at non-oxidative stress status in TEV-1cells and placenta explants. SAC is therefore hypothesized to be a potential drug for PE treatment.