Kai Le1, Zhiping Song2, Jie Deng3, Xin Peng4, Jun Zhang1, Liang Wang1, Lu Zhou1, Haidi Bi1, Zhengyu Liao5, Zhen Feng6. 1. Department of Rehabilitation Medicine, The First Affiliated Hospital of Nanchang University, No. 17 Yongwaizheng Street, Nanchang, 330006, Jiangxi Province, China. 2. Department of Anesthesia, The First Affiliated Hospital of Nanchang University, No. 17 Yongwaizheng Street, Nanchang, 330006, Jiangxi Province, China. 3. Department of Neonatology, The Affiliated Children's Hospital of Nanchang University, No. 122 Yangming Road, Nanchang, 330006, Jiangxi Province, China. 4. Department of Otolaryngology, The Affiliated Children's Hospital of Nanchang University, No. 122 Yangming Road, Nanchang, 330006, Jiangxi Province, China. 5. Department of Orthodontics, School of Stomatology, The Key Laboratory of Oral Biomedicine, Affiliated Stomatological Hospital of Nanchang University, No. 49 Fuzhou Road, Nanchang, 330006, Jiangxi Province, China. hello67@163.com. 6. Department of Rehabilitation Medicine, The First Affiliated Hospital of Nanchang University, No. 17 Yongwaizheng Street, Nanchang, 330006, Jiangxi Province, China. fengzhenly@sina.com.
Abstract
OBJECTIVE AND DESIGN: Microglia stimulated by oxygen glucose deprivation (OGD) were treated with quercetin to investigate the effect on oxidative stress and the inflammatory response and to explore whether toll-like receptor 4 (TLR4) signaling was involved. In addition, the effect of quercetin on the neurological functions of neonatal mice with hypoxic-ischemic brain injury (HIBI) was examined. MATERIALS AND SUBJECTS: Mouse BV2 microglial cells and postnatal day 7 neonatal mice were used. TREATMENT: A predetermined concentration of quercetin was used in cell experiments. Quercetin was injected i.p. (50 mg/kg) at three time points after HI insult: 0, 24, and 48 h. METHODS: Cell viability assay, Western blotting, qRT-RCR, ELISA, HIBI model construction and behavioral tests. RESULTS: This study first showed that quercetin protected BV2 cells from OGD-induced damage and reversed the changes in microglial oxidative stress-related molecules. Second, quercetin inhibited OGD-induced expression of inflammatory factors in BV2 cells and suppressed TLR4/MyD88/NF-κB signaling. Finally, quercetin was disclosed to be effective in mitigating cerebral infarct volume and cognitive and motor function deficits in HIBI mice. CONCLUSION: These results suggest that the neuroprotective effect of quercetin in HIBI mice is partially due to the inhibition of oxidative stress and TLR4-mediated inflammatory responses in activated microglia.
OBJECTIVE AND DESIGN: Microglia stimulated by oxygen glucose deprivation (OGD) were treated with quercetin to investigate the effect on oxidative stress and the inflammatory response and to explore whether toll-like receptor 4 (TLR4) signaling was involved. In addition, the effect of quercetin on the neurological functions of neonatal mice with hypoxic-ischemic brain injury (HIBI) was examined. MATERIALS AND SUBJECTS: Mouse BV2 microglial cells and postnatal day 7 neonatal mice were used. TREATMENT: A predetermined concentration of quercetin was used in cell experiments. Quercetin was injected i.p. (50 mg/kg) at three time points after HI insult: 0, 24, and 48 h. METHODS: Cell viability assay, Western blotting, qRT-RCR, ELISA, HIBI model construction and behavioral tests. RESULTS: This study first showed that quercetin protected BV2 cells from OGD-induced damage and reversed the changes in microglial oxidative stress-related molecules. Second, quercetin inhibited OGD-induced expression of inflammatory factors in BV2 cells and suppressed TLR4/MyD88/NF-κB signaling. Finally, quercetin was disclosed to be effective in mitigating cerebral infarct volume and cognitive and motor function deficits in HIBI mice. CONCLUSION: These results suggest that the neuroprotective effect of quercetin in HIBI mice is partially due to the inhibition of oxidative stress and TLR4-mediated inflammatory responses in activated microglia.
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