Protective effects of quercetin against brain injury in a rat model of lipopolysaccharide-induced fetal brain injury.

Maternal exposure to lipopolysaccharide (LPS), a bacterial endotoxin produced during infection, leads to disruption in fetal brain development and causes newborn brain injury. Quercetin (QR) is a multipotent flavonoid that functions as an antioxidant and protects against inflammation and neurodegeneration. In this study, we explored the potential functions of QR in alleviating maternal LPS exposure induced fetal brain damage. Pregnant rats at late gestational stages were treated with saline, LPS, QR, LPS and QR. Brain injury biomarker TGF-1β was assessed in cerebrospinal fluid (CSF) and brain tissue of newborn rats. Pro-inflammatory cytokines, apoptosis markers and oxidative stress indicators were evaluated. We found that LPS treatment induced an increased production of TGF-1β which was suppressed by QR administration. LPS enhanced pro-apoptotic Bax and inhibited anti-apoptotic Bcl-2 expression. QR reduced that ratio of Bax and Bcl-2 that was high in LPS treated brain tissue. Additionally, QR suppressed oxidative stress induced by LPS. Finally, QR reduced the levels of pro-inflammatory cytokines that were produced as a result of LPS exposure. In summary, our study indicates that QR potently alleviates maternal LPS exposure induced fetal brain injury in rats, making it a potential therapeutic for suppressing infant brain damage as a result of maternal infection.