Modulatory Mechanism of Polyphenols and Nrf2 Signaling Pathway in LPS Challenged Pregnancy Disorders.
Tarique HussainBi-E TanGang LiuGhulam MurtazaNajma RahuMuhammad SaleemYu-Long YinPublished in: Oxidative medicine and cellular longevity (2017)
Early embryonic loss and adverse birth outcomes are the major reproductive disorders that affect both human and animals. The LPS induces inflammation by interacting with robust cellular mechanism which was considered as a plethora of numerous reproductive disorders such as fetal resorption, preterm birth, teratogenicity, intrauterine growth restriction, abortion, neural tube defects, fetal demise, and skeletal development retardation. LPS-triggered overproduction of free radicals leads to oxidative stress which mediates inflammation via stimulation of NF-κB and PPARγ transcription factors. Flavonoids, which exist in copious amounts in nature, possess a wide array of functions; their supplementation during pregnancy activates Nrf2 signaling pathway which encounters pregnancy disorders. It was further presumed that the development of strong antioxidant uterine environment during gestation can alleviate diseases which appear at adult stages. The purpose of this review is to focus on modulatory properties of flavonoids on oxidative stress-mediated pregnancy insult and abnormal outcomes and role of Nrf2 activation in pregnancy disorders. These findings would be helpful for providing new insights in ameliorating oxidative stress-induced pregnancy disorders.
Keyphrases
- oxidative stress
- preterm birth
- signaling pathway
- gestational age
- induced apoptosis
- pregnancy outcomes
- ischemia reperfusion injury
- dna damage
- diabetic rats
- low birth weight
- endothelial cells
- emergency department
- transcription factor
- epithelial mesenchymal transition
- type diabetes
- immune response
- adipose tissue
- preterm infants
- electronic health record
- endoplasmic reticulum stress
- glycemic control
- skeletal muscle
- young adults
- heat shock protein