天麻素经P53/SLC7A11/GPX4信号轴抑制神经元铁死亡减轻高原低压缺氧性脑损伤

doi:10.12122/j.issn.1673-4254.2026.07.04

南方医科大学学报 ›› 2026, Vol. 46 ›› Issue (7): 1498-1508.doi: 10.12122/j.issn.1673-4254.2026.07.04

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天麻素经P53/SLC7A11/GPX4信号轴抑制神经元铁死亡减轻高原低压缺氧性脑损伤

杨继苹¹(), 顾永增¹, 傅振燚², 董乐馨², 邓仪昊², 李正¹, 刘良丽³(), 郭涛¹^,²()

^1.昆明卫生职业学院基础医学院，云南昆明 650600
^2.昆明理工大学基础医学院，云南昆明 650500
^3.云南省疾病预防控制中心，云南昆明 650022

收稿日期:2025-12-01 出版日期:2026-07-20 发布日期:2026-07-20
通讯作者: 刘良丽,郭涛 E-mail:604416816@qq.com;879004657@qq.com;475612496@qq.com
作者简介:杨继苹，副教授，E-mail: 604416816@qq.com
基金资助:
国家自然科学基金(82160240);云南省教育厅科学研究基金(2024J2099);省级大学生创新训练计划基金(S202410674118);省级大学生创新训练计划基金(S202510674161)

Gastrodin alleviates hypobaric hypoxia-induced brain injury in rats by reducing neuronal ferroptosis via the P53/SLC7A11/GPX4 signaling axis

Jiping YANG¹(), Yongzeng GU¹, Zhenyi FU², Yuexin DONG², Yihao DENG², Zheng LI¹, Liangli LIU³(), Tao GUO¹^,²()

^1.College of Basic Medicine, Kunming Health Vocational College, Kunming 650600, China
^2.College of Basic Medicine, Kunming University of Science and Technology, Kunming 650500, China
^3.Yunnan Provincial Center for Disease Control and Prevention, Kunming 650022, China

Received:2025-12-01 Online:2026-07-20 Published:2026-07-20
Contact: Liangli LIU, Tao GUO E-mail:604416816@qq.com;879004657@qq.com;475612496@qq.com
Supported by:
National Natural Science Foundation of China(82160240)

摘要/Abstract

摘要：

目的研究天麻素（GAS）对高原低压缺氧（HH）性脑损伤的神经保护作用，并探讨其机制是否与调节P53/SLC7A11/GPX4信号通路、抑制神经元铁死亡相关。方法体内实验选取24只成年SD大鼠，随机分为4组（n=6）：常压常氧对照组（Nor）、低压缺氧模型组（HH）、天麻素低剂量组（HH+GAS-L，100 mg/kg）、天麻素高剂量组（HH+GAS-H，200 mg/kg）。除对照组外，其余各组大鼠置于模拟海拔6000 m的低压氧舱中持续暴露24 h以建立HH模型。天麻素于造模后腹腔给药，1次/d。取第7天的脑皮层进行Western blotting检测P53、SLC7A11及GPX4蛋白表达，同时测定组织内活性氧标志物（DHE）、丙二醛（MDA）、谷胱甘肽（GSH）及亚铁离子（Fe²⁺）的含量。体外培养HT22神经元，分为：对照组（Control）、模型组（OGD）、天麻素干预组（OGD+GAS，500 μmol/L）、P53激动剂组（OGD+Nutlin-3，10 μmol/L）及联合处理组（OGD+GAS+Nutlin-3）。检测指标包括铁死亡相关蛋白表达、细胞内活性氧（DCFH-DA）、脂质过氧化（BODIPY-C11）、MDA、GSH、细胞存活率（CCK-8）、线粒体膜电位（JC-1）及亚铁离子（FerroOrange）。结果动物实验显示，与HH组相比，天麻素显著抑制P53表达，上调SLC7A11与GPX4蛋白水平（P<0.05），并显著降低脑皮层组织Fe²⁺、ROS和MDA含量，提高GSH水平（P<0.05）。细胞实验结果一致，天麻素有效减轻低压缺氧诱导的铁死亡，表现为P53表达下降，SLC7A11与GPX4表达升高（P<0.05），细胞内ROS生成、脂质过氧化和Fe²⁺蓄积被抑制，同时GSH含量、细胞活性和线粒体膜电位显著恢复（P<0.05）。而使用Nutlin-3激活P53信号通路后，天麻素的保护作用被明显逆转（P<0.05）。结论天麻素可能通过调控P53/SLC7A11/GPX4信号通路抑制神经元铁死亡，从而对高原低压缺氧性脑损伤发挥神经保护作用。

关键词: 天麻素, 高原低压缺氧性脑损伤, 氧糖剥夺, 铁死亡, GPX4/SLC7A11/FTH1

Abstract:

Objective To investigate the neuroprotective effect of gastrodin (GAS) against hypobaric hypoxia (HH)-induced brain injury in rats and the underlying mechanism. Methods Twenty-four adult SD rats were randomized equally into normoxic control group, HH model group, low-dose (100 mg/kg) GAS group (HH+GAS-L group), and high-dose (200 mg/kg) GAS group (HH+GAS-H group). In the latter 3 groups, the rats were exposed to HH in a hypobaric oxygen chamber for 24 h to simulate the condition at an altitude of 6000 m, and GAS was administered intraperitoneally once daily for 7 days. Cerebral cortex tissues were collected for analysis of P53, SLC7A11, and GPX4 protein expressions using Western blotting and for determination of the levels of reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), and ferrous ion (Fe²⁺). In cultured HT22 neurons exposed to oxygen-glucose deprivation (OGD), the effects of GAS (500 μmol/L), nutlin-3 (a P53 agonist; 10 μmol/L) or their combination were examined on ferroptosis-related protein expressions, intracellular ROS, lipid peroxidation, MDA, GSH, cell viability, mitochondrial membrane potential, and Fe²⁺ levels. Results In the rat models of HH, GAS treatment significantly inhibited P53 expression, upregulated SLC7A11 and GPX4 proteins, markedly reduced Fe²⁺, ROS, and MDA levels, and increased GSH content in the cerebral cortex. In cultured HT22 neurons, GAS treatment effectively alleviated OGD-induced cell ferroptosis as shown by decreased P53 expression, increased SLC7A11 and GPX4 expressions, and lowered levels of intracellular ROS generation, lipid peroxidation, and Fe²⁺ accumulation, along with obvious restoration of GSH levels, cell viability, and mitochondrial membrane potential. The protective effects of GAS was markedly attenuated by activation of the P53 pathway using nutlin-3. Conclusion GAS produces neuroprotective effects against HH-induced brain injury in rats by inhibiting neuronal ferroptosis via regulating the P53/SLC7A11/GPX4 signaling pathway.

Key words: gastrodin, hypobaric hypoxia-induced brain injury, oxygen-glucose deprivation, ferroptosis, GPX4/SLC7A11/FTH1

杨继苹, 顾永增, 傅振燚, 董乐馨, 邓仪昊, 李正, 刘良丽, 郭涛. 天麻素经P53/SLC7A11/GPX4信号轴抑制神经元铁死亡减轻高原低压缺氧性脑损伤[J]. 南方医科大学学报, 2026, 46(7): 1498-1508.

Jiping YANG, Yongzeng GU, Zhenyi FU, Yuexin DONG, Yihao DENG, Zheng LI, Liangli LIU, Tao GUO. Gastrodin alleviates hypobaric hypoxia-induced brain injury in rats by reducing neuronal ferroptosis via the P53/SLC7A11/GPX4 signaling axis[J]. Journal of Southern Medical University, 2026, 46(7): 1498-1508.

图/表 6

图1 GAS对HH模型中铁死亡相关蛋白P53、SLC7A11及GPX4表达的影响

Fig.1 Effect of gastrodin (GAS) on expressions of ferroptosis-related proteins P53, SLC7A11, and GPX4 in rat models exposed to hypobaric hypoxia (HH). A: Western blotting for detecting protein expressions of P53, SLC7A11, and GPX4 in cerebral cortical tissues of the rats. B-D: Quantitative analysis of the relative expression levels of the proteins. ***P<0.001 vs normal control (Nor) group; #P<0.05, ##P<0.01, ###P<0.001 vs HH group (n=3).

图2 GAS对HH模型神经元中铁死亡标志物P53及4-HNE的影响

Fig.2 Effect of GAS on ferroptosis markers P53 and 4-HNE in the cortical neurons of rat models of HH. A, C: Expressions of P53 and 4-HNE (red) in the neurons (NeuN, green) detected by double immunofluorescence staining (Scale bar=10 μm). B, D: Quantitative analysis of fluorescence intensity of P53 and 4-HNE. **P<0.001, ***P<0.001 vs Nor group; #P<0.05, ##P<0.01 vs HH group (n=3).

图3 GAS对HH模型中氧化应激及亚铁离子水平的影响

Fig.3 Effects of GAS on oxidative stress and ferrous ion levels in the cortical tissues of rat models of HH. A, B: ROS levels detected by DHE fluorescence staining and quantitative analysis of fluorescence intensity (Scale bar=10 μm). C: Relative MDA content. D: Relative GSH content. E: Relative ferrous ion concentration. ***P<0.001 vs Nor group; #P<0.05, ##P<0.01, ###P<0.001 vs HH group (n=3).

图4 GAS通过P53通路调控OGD模型中SLC7A11/GPX4的表达

Fig.4 GAS regulates expressions of SLC7A11 and GPX4 via the P53 pathway in cultured HT22 neurons exposed to oxygen-glucose deprivation (OGD). A, B: Expression of P53 (red) in the neurons (NeuN, green) detected by immunofluorescence staining and quantitative analysis of fluorescence intensity (Scale bar=50 μm). C: Western blotting for detecting P53, SLC7A11, and GPX4 proteins. D-F: Quantitative analysis of relative expression levels of P53, SLC7A11, and GPX4. ***P<0.001 vs Control group; #P<0.05, ##P<0.01, ###P<0.001 vs OGD group; &P<0.05, &&P<0.01, &&&P<0.001 vs OGD+GAS group (n=3).

图5 GAS通过P53通路调控OGD模型的氧化应激与脂质过氧化

Fig.5 GAS regulates oxidative stress and lipid peroxidation via the P53 pathway in the OGD cell model. A, C: ROS levels detected by DCFH-DA fluorescence staining and quantitative analysis of fluorescence intensity (Scale bar=50 μm). B, D: Lipid peroxidation levels detected by BODIPY-C11 fluorescence staining and quantitative analysis of the oxidized/reduced ratio (Scale bar=50 μm). E: Relative MDA content. F: Relative GSH content. ***P<0.001 vs Control group; #P<0.05, ##P<0.01, ###P<0.001 vs OGD group; &&P<0.01, &&&P<0.001 vs OGD+GAS group (n=3).

图6 GAS通过P53通路调控OGD模型的细胞存活、线粒体膜电位及铁离子水平

Fig.6 GAS regulates cell survival, mitochondrial membrane potential, and Fe2+ levels via the P53 pathway in the OGD cell model. A: Quantitative analysis of cell viability. B, C: Mitochondrial membrane potential detected by JC-1 staining and quantitative analysis of the aggregates/monomers ratio. D, E: Fe2+ levels detected by FerroOrange fluorescent probe staining and quantitative analysis of fluorescence intensity. Scale bar=50 μm. ***P<0.001 vs Control group; #P<0.05, ###P<0.001 vs OGD group; &&P<0.01, &&&P<0.001 vs OGD+GAS group (n=3).

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天麻素经P53/SLC7A11/GPX4信号轴抑制神经元铁死亡减轻高原低压缺氧性脑损伤

Gastrodin alleviates hypobaric hypoxia-induced brain injury in rats by reducing neuronal ferroptosis via the P53/SLC7A11/GPX4 signaling axis

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