标题：Curcumin attenuates hypoxic-ischemic brain injury in neonatal rats through induction of nuclear factor erythroid-2-related factor 2 and heme oxygenase-1
作者：Cui, Xiaolu; Song, Hongquan; Su, Jie
作者机构：[Cui, Xiaolu] Shandong Prov Qianfoshan Hosp, Dept Rehabil Med, Jinan 250014, Shandong, Peoples R China.; [Song, Hongquan] Shandong Univ TCM, Affilia 更多
通讯作者地址：[Su, J]Shandong Univ TCM, Affiliated Hosp 2, Dept Cadres & Hlth Care, 1 West Qingnian Rd,Cent Rd, Jinan 250001, Shandong, Peoples R China.
来源：EXPERIMENTAL AND THERAPEUTIC MEDICINE
关键词：curcumin; hypoxic-ischemic brain injury; nuclear factor; erythroid-2-related factor 2; heme oxygenase-1
摘要：Curcumin has previously demonstrated anti-inflammatory, anti-infective and immuno-suppressive effects. In the present study, whether the attenuating effects of curcumin against hypoxic-ischemic brain injury in neonatal rats are mediated via nuclear factor erythroid-2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was investigated. A model of hypoxic-ischemic brain injury was created using 1-week-old Sprague Dawley rats (weight, 52 +/- 1 g). The model rats were treated with 150 mg/kg curcumin by gavage for 3 days. Malondialdehyde levels, and superoxide dismutase and caspase-3 activities were assayed using commercial kits and western blot analysis was used to measure inducible nitric oxide synthase (iNOS), Nrf2 and HO-1 expression levels. Treatment with curcumin effectively reduced the brain injury score, increased myelin basic protein (MBP) expression and increased the quantity of neuronal cells in neonatal rats with hypoxic-ischemic brain injury. Furthermore, treatment with curcumin significantly attenuated the changes in SOD activity and MDA levels and suppressed the iNOS protein expression induced in neonatal rats by hypoxic-ischemic brain injury. Treatment with curcumin significantly increased Nrf2 and HO-1 expression in the neonatal rats with hypoxic-ischemic brain injury. The present study indicated that curcumin attenuates hypoxic-ischemic brain injury in neonatal rats through the induction of Nrf2 and HO-1.