| 汤丽萍,闫 瑾,范 芳,王 浩,任丽芬.香草醛对新生大鼠缺氧缺血性脑损伤的神经保护作用研究[J].,2021,(20):3833-3840 |
| 香草醛对新生大鼠缺氧缺血性脑损伤的神经保护作用研究 |
| The Neuroprotective Effect of Vanillin on Hypoxic-ischemic Brain Injury in Neonatal Rats |
| 投稿时间：2021-03-04 修订日期：2021-03-28 |
| DOI：10.13241/j.cnki.pmb.2021.20.007 |
| 中文关键词: 新生儿缺氧缺血性脑病 香草醛 缺氧缺血性脑损伤 神经炎症 高迁移率族蛋白-1 |
| 英文关键词: Neonatal hypoxic-ischemic encephalopathy Vanillin Hypoxic-ischemic brain injury Neuroinflammation High mobility group protein-1 |
| 基金项目:陕西省自然科学基础研究计划项目（2019JM-514） |
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| 中文摘要: |
| 摘要 目的：探讨香草醛对新生大鼠缺氧缺血性脑损伤(HIBI)的神经保护作用及机制。方法：参考Rice-Vannucci方法建立HIBI大鼠模型。HIBI大鼠建模后立即腹腔注射20 mg/kg（HIBI+20Van组）或40 mg/kg（HIBI+40Van组）的香草醛，每隔12 h给药，连续7 d。然后评估大鼠的神经行为及脑组织中IL-1β、IL-6和TNF-α的水平。对BV2小胶质细胞进行氧糖剥夺/复氧(OGD/R)处理，并用20 μM香草醛培养。通过Western blot及免疫荧光检测HMGB1、NF-κB p65、SIRT1、MyD88和TLR4的表达水平。通过乳酸脱氢酶（LDH）释放测定试剂盒测定用不同BV2细胞培养基处理的原代神经元的LDH释放。结果：与HIBI组比较，HIBI+20Van组和HIBI+50Van组新生大鼠的前肢悬吊时间和旷场得分均升高，脑组织中的IL-1β、IL-6和TNF-α的水平均降低。香草醛均升高了HIBI大鼠和OGD/R处理的BV2细胞质中的SIRT1的表达水平，降低了TLR4、MyD88和HMGB1的表达水平及细胞核中NF-κB p65的表达水平（P<0.05）。香草醛降低了原代神经元的LDH释放量（P<0.05）。结论：香草醛通过调节SIRT1/HMGB1/TLR4/MyD88/NF-κB信号通路抑制HIBI引起的神经炎症，从而提高HIBI大鼠的神经功能。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the neuroprotective effect and mechanism of vanillin on hypoxic-ischemic brain injury (HIBI) in neonatal rats. Methods: The HIBI model was established by referring to the Rice-Vannucci method. HIBI rats were injected intraperitoneally with 20 mg/kg (HIBI+20Van group) or 40 mg/kg (HIBI+40Van group) of vanillin immediately after modeling. The drug was administered once every 12 h for 7 consecutive days. Neurological behavior and the levels of IL-1β, IL-6 and TNF-α in the brain tissue of the rats were assessed. BV2 microglia were treated with oxygen glucose deprivation/reoxygenation (OGD/R), and cultured with 20 μM vanillin. The expression of HMGB1, NF-κBp65, SIRT1, MyD88 and TLR4 was detected by Western blot and immunofluorescence. The LDH release of primary neurons treated with different BV2 cell culture media was measured by a lactate dehydrogenase (LDH) release assay kit. Results: Compared with the HIBI group, the forelimb suspension time and open field scores of neonatal rats in the HIBI+20Van group and HIBI+50Van group were increased, and the levels of IL-1β, IL-6 and TNF-α in the brain tissue decreased (P<0.05). Vanillin increased the expression of SIRT1 in the cytoplasm of HIBI rats and BV2 treated with OGD/R, while decreased the expression of TLR4, MyD88 and HMGB1, and the expression of NF-κ Bp65 in the nucleus. Vanillin decreased the release of LDH from primary neurons(P<0.05). Conclusion: Vanillin inhibits the neuroinflammation caused by HIBI by regulating the SIRT1/HMGB1/ TLR4/MyD88/NF-κB signaling pathway, thereby improving the nerve function of HIBI rats. |
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