| 鲍 和,王 晨,张源源,杨 珊,郭 琪,王志刚.NOX2在黄连素减轻Aβ所致神经元氧化应激损伤中的作用[J].,2019,19(14):2632-2637 |
| NOX2在黄连素减轻Aβ所致神经元氧化应激损伤中的作用 |
| NOX2 Mediates Berberine-induced Neuroprotection on HT22 Neuronal Cells Exposed to β Amyloid |
| 投稿时间：2018-12-28 修订日期：2019-01-23 |
| DOI：10.13241/j.cnki.pmb.2019.14.006 |
| 中文关键词: 黄连素 阿尔兹海默症 β淀粉样蛋白 还原型辅酶氧化酶Ⅱ 神经保护 |
| 英文关键词: Berberine Alzheimer's disease β Amyloid NOX2 Neuroprotection |
| 基金项目:国家自然科学基金项目(81700644) |
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| 中文摘要: |
| 摘要 目的：探讨还原型辅酶氧化酶Ⅱ(NADPH oxidase II，NOX2)是否参与了黄连素(Berberine，BBR)对β淀粉样蛋白(β Amyloid，Aβ)诱导的神经元损伤的保护作用。方法：将HT22神经元细胞分为5组，分别为正常培养的Control组、10 μM的Aβ损伤组(Aβ)、1 μM的BBR保护组(BBR+Aβ)、NOX2-siRNA干扰组(NOX2-siRNA+BBR+Aβ)和乱序siRNA处理组(SC-siRNA+BBR+Aβ)，孵育24 h后，采用噻唑蓝法(Methylthiazolyldiphenyl-tetrazolium, MTT)检测细胞活力，试剂盒检测培养基内乳酸脱氢酶(Lactic Dehydogenase，LDH)水平，Western blot检测细胞凋亡相关蛋白Cleaved caspase-3和NOX2蛋白表达、试剂盒检测细胞内活性氧(Reactive Oxygen Species，ROS)和戊二醛(Malondialdehyde，MDA)水平。结果：与Control组相比，10 μM的Aβ可显著下调HT22细胞活力，增加LDH释放和细胞内ROS及MDA水平，上调Cleaved caspase-3和NOX2蛋白表达(P<0.05)；1 μM的BBR可显著抑制Aβ对神经元细胞产生的上述氧化损伤作用(P<0.05)，而NOX2-siRNA显著逆转了BBR对Aβ诱导的HT22神经元细胞的保护作用(P<0.05)，而SC-siRNA未对BBR的上述细胞保护作用产生显著影响(P>0.05)。结论：NOX2蛋白介导了BBR对暴露于Aβ中的神经元细胞的保护作用。 |
| 英文摘要: |
| ABSTRACT Objective: To determine whether NADPH oxidase II (NOX2) is associated in berberine (BBR)-induced protection on HT22 neuronal cells exposed to β amyloid (Aβ). Methods: HT22 neuronal cells were divided into five groups, including the normal cultured Control group, 10 μM Aβ exposure group (Aβ), 1 μM BBR plus 10 μM Aβ treatment group (BBR+Aβ), NOX2-siRNA treatment group (NOX2-siRNA+BBR+Aβ) and scrambled (SC)-siRNA group (SC-siRNA+BBR+Aβ), after an incubation for 24 h, methylthiazolyldiphenyl-tetrazolium (MTT) was used to assess cell viability, lactic dehydrogenase (LDH) reagent kit was used to evaluate the LDH release in the medium, Western blot was taken to evaluate the apoptosis-associated protein Cleaved caspase-3 and NOX2 expressions, reactive oxygen species (ROS) and malondialdehyde (MDA) reagent kits were used to assess the intracellular ROS and MDA levels respectively. Results: Compared with the control group, 10 μM Aβ reduced the viability of HT22 cells, increased LDH activity, intracellular ROS and MDA levels, upregulated cleaved caspase-3 and NOX2 expressions(P<0.05), and 1 μM BBR treatment significantly inhibited the Aβ-induced injury and oxidative effects mentioned above(P<0.05). However, NOX2-siRNA treatment obviously abrogated BBR-induced neuroprotection and anti-oxidative effects(P<0.05), and SC-siRNA showed no significant effect on BBR-mediated neuroprotective effects(P>0.05). Conclusion: NOX2 may mediate BBR-induced neuroprotective effects on the HT22 neuronal cells exposed to Aβ. |
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