Quercetin attenuates hypoxia-ischemia induced brain injury in neonatal rats by inhibiting TLR4/NF-κB signaling pathway.

Neonatal hypoxic ischemia (HI) is a kind of brain damage that occurs when an infant's brain does not receive enough oxygen and blood. The unrepairable damage leads to newborn death and short/long term brain dysfunctions. Due to the complicated causes and the variety of brain damages, there is no definitive treatment of neonatal HI. In this study, we set up a HI injury model of newborn rat and administrated Quercetin (Que) to treat rat pups before and after HI injury. We performed immunohistochemistry, quantitative PCR and immunoblot experiments to examine whether Que. has a role in attenuating brain injury after HI. We found that Que. treatment could clearly attenuate cortical cell apoptosis, as well as suppress apoptosis marker Bax, and activate anti-apoptosis marker Bcl-2. Moreover, Que. treatment decreased the number of cortical cells microgliosis and astrogliosis induced by HI injury. Furthermore, Que. treatment decreased cortical inflammation. Finally, it is suggested that Que. played a neuroprotective function on HI brain injury via inhibiting the TLR4/NF-κB signaling pathway. From these results, we conclude that Que. treatment may be a used as a therapeutic drug to prevent and decrease the newborn brain damage caused by HI.