| 霍艳慧.基于SIRT6/Nrf2/GPX4信号通路探讨依达拉奉对间歇低氧大鼠海马损伤和神经功能的改善作用[J].安徽医药,待发表. |
| 基于SIRT6/Nrf2/GPX4信号通路探讨依达拉奉对间歇低氧大鼠海马损伤和神经功能的改善作用 |
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| 投稿时间：2025-03-14 录用日期：2025-04-15 |
| DOI： |
| 中文关键词: SIRT6/Nrf2/GPX4 依达拉奉 间歇性低氧 海马损伤 神经功能 |
| 英文关键词: |
| 基金项目:河北省卫生健康委员会项目(编号:20201244) |
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| 中文摘要: |
| 目的:基于SIRT6/Nrf2/GPX4信号通路,探究依达拉奉(EDA)对间歇性低氧大鼠海马损伤和神经功能的影响。方法:将96只Wistar雄性大鼠随机分为对照组、间歇低氧组、EDA组,每组32只。Morris水迷宫进行学习记忆功能评估,HE染色检测海马组织CA1区的病理学损伤情况,试剂盒测量海马组织CA1区中铁死亡标志物(包括ROS、MDA、亚铁离子、GSH)水平,Western blot检测海马组织CA1区SIRT6、Nrf2、GPX4、SLC7A11蛋白的表达水平。结果:与对照组相比,间歇低氧组大鼠在7 d、14 d、21 d、28 d四个时间点的逃避潜伏期显著延长(P<0.05),停留在原平台所在象限的时间显著缩短(P<0.05),CA1区海马组织呈现病理学损伤,CA1区海马组织中ROS、MDA、亚铁离子的水平显著升高(P<0.05),CA1区海马组织中GSH的水平显著降低(P<0.05),CA1区海马组织中SIRT6、Nrf2、GPX4、SLC7A11蛋白的表达显著下调(P<0.05)；与间歇低氧组相比,EDA组大鼠在7 d、14 d、21 d、28 d四个时间点的逃避潜伏期显著缩短(P<0.05),停留在原平台所在象限的时间显著延长(P<0.05),CA1区海马组织的病理学损伤减轻,CA1区海马组织中ROS、MDA、亚铁离子的水平显著降低(P<0.05),CA1区海马组织中GSH的水平显著升高(P<0.05),CA1区海马组织中SIRT6、Nrf2、GPX4、SLC7A11蛋白的表达显著上调(P<0.05)。结论:EDA能够改善间歇性低氧大鼠的海马损伤和神经功能,其机制可能与激活SIRT6/Nrf2/GPX4信号通路相关。 |
| 英文摘要: |
| Objective: Based on SIRT6/Nrf2/GPX4 signaling pathway, the effect of edaravone (EDA) on hippocampal injury and neurological function in rats with intermittent hypoxia was investigated. Methods: Ninety-six Wistar male rats were randomly divided into control group, intermittent hypoxia group and EDA group, and each group was divided into four time subgroups: 7 d, 14 d, 21 d and 28 d, with 8 rats in each subgroup. Morris water maze for assessment of learning memory function. HE staining was used to detect the pathological damage of CA1 in hippocampal tissue. The levels of ferroptosis markers (including ROS, MDA, ferrous ions, GSH) in the CA1 region of hippocampal tissue were measured by kits. The expression levels of SIRT6, Nrf2, GPX4 and SLC7A11 proteins in CA1 region of hippocampus were detected by Western blot. Results: Compared with the control group, the escape latency of the rats in the intermittent hypoxia group was significantly prolonged at the four time points of 7 d, 14 d, 21 d and 28 d (P<0.05), the time spent in the quadrant of the original platform was significantly shortened (P<0.05), the hippocampal tissue in the CA1 area showed pathological damage, the levels of ROS, MDA, ferrous ion in hippocampus of CA1 area were significantly increased (P<0.05), the level of GSH in the hippocampus of CA1 area was significantly decreased (P<0.05), the expression of SIRT6, Nrf2, GPX4, SLC7A11 proteins in hippocampus of CA1 area were significantly down-regulated (P<0.05). Compared with the intermittent hypoxia group, the escape latency of the EDA group was significantly shortened at the four time points of 7 d, 14 d, 21 d and 28 d (P<0.05), the time spent in the quadrant of the original platform was significantly prolonged (P<0.05), pathological damage to hippocampal tissue in CA1 region was reduced, the levels of ROS, MDA, ferrous ion in hippocampus of CA1 area were significantly decreased (P<0.05), the level of GSH in the hippocampus of CA1 area was significantly increased (P<0.05), the expression of SIRT6, Nrf2, GPX4, SLC7A11 proteins in hippocampus of CA1 area were significantly up-regulated (P<0.05). Conclusion: EDA can improve hippocampal injury and neurological function in rats with intermittent hypoxia, and the mechanism may be related to the activation of SIRT6/Nrf2/GPX4 signaling pathway. |
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