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张玉婷,谢小娟,王彩云,张梦露.灵芝酸A通过激活Nrf2/GPX4信号通路减轻七氟烷诱导的HT22细胞铁死亡[J].湖南中医药大学学报英文版,2022,42(7):1064-1069.[Click to copy
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| 灵芝酸A通过激活Nrf2/GPX4信号通路减轻七氟烷诱导的HT22细胞铁死亡 |
| 张玉婷,谢小娟,王彩云,张梦露 |
| (河南科技大学第一附属医院/河南科技大学临床医学院, 河南 洛阳 471003) |
| 摘要: |
| 目的 研究灵芝酸A（ganoderic acid A,GAA）对七氟烷诱导的HT22细胞铁死亡的影响和机制。方法 采用CCK-8法检测不同浓度GAA对HT22细胞的增殖活性，筛选出合适的GAA处理浓度。将HT22细胞分成对照组、七氟烷诱导组（Sev组）、GAA-25 μmol/L组、GAA-50 μmol/L组、GAA-100 μmol/L组。对照组细胞按照常规方法处理；其他组均利用七氟烷进行诱导处理，同时不同浓度GAA组给予相应浓度的GAA干预。采用Western blot检测氧化应激相关因子（Nrf2、GPX4）与铁死亡相关因子（ACSL4、SLC7A11）的蛋白表达。利用相应的试剂盒检测Fe2+、ROS、MDA、GSH、4-HNE等因子的含量。结果 根据CCK-8实验结果，选择对HT22细胞增殖活性无影响的25、50、100 μmol/L GAA进行后续研究。与对照组比较，Sev组的HT22细胞存活率降低（P<0.05），Nrf2、GPX4、ACSL4、SLC7A11蛋白表达减少（P<0.05），Fe2+、ROS、MDA、4-HNE含量升高（P<0.05），GSH含量降低（P<0.05）。与Sev组比较，随着CAA处理浓度的升高，HT22细胞存活率显著升高（P<0.05），Nrf2、GPX4、ACSL4、SLC7A11蛋白表达增多（P<0.05），Fe2+、ROS、MDA、4-HNE含量降低（P<0.05），GSH含量升高（P<0.05）。结论 GAA通过激活Nrf2/GPX4信号通路减轻七氟烷诱导的HT22细胞铁死亡，从而发挥神经保护作用。GAA可作为治疗七氟烷麻醉神经损伤的潜在药物。 |
| 关键词: 灵芝酸A 七氟烷 铁死亡 神经损伤 Nrf2/GPX4信号通路 HT22细胞 |
| DOI：10.3969/j.issn.1674-070X.2022.07.002 |
| Received:December 30, 2021 |
| 基金项目: |
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| Ganoderic acid A reduces sevoflurane-induced ferroptosis of HT22 cells through activating the Nrf2/GPX4 signaling pathway |
| ZHANG Yuting,XIE Xiaojuan,WANG Caiyun,ZHANG Menglu |
| (The First Affiliated Hospital of Henan University of Science and Technology, College of Clinical Medicine of Henan University of Science and Technology, Luoyang, Henan 471003, China) |
| Abstract: |
| Objective To study the effect and mechanism of ganoderic acid A (GAA) on the ferroptosis of HT22 cells induced by sevoflurane. Methods The proliferation activity of HT22 cells was detected by CCK-8 assay to selecte the appropriate concentration. HT22 cells were divided into control group, Sev group, and CAA-25 μmol/L group, CAA-50 μmol/L group and CAA-100 μmol/L group. Cells in the control group were treated with conventional methods. The other groups were treated with sevoflurane induction, and the GAA groups with different concentrations were given corresponding concentrations of GAA intervention. Western blot was used to detect the protein expression of oxidative stress related factors (Nrf2, GPX4) and ferroptosis related factors (ACSL4, SLC7A11). The content of Fe2+, ROS, MDA, GSH, 4-HNE was detected by using the corresponding concentration detection kits. Results According to the results of CCK-8 experiment, 25, 50, 100 μmol/L GAA which had no effect on the proliferation activity of HT22 cells were selected for follow-up study. Compared with control group, HT22 cells survival rate decreased (P<0.05), Nrf2, GPX4, ACSL4, SLC7A11 protein expression decreased (P<0.05), Fe2+ level and ROS, MDA, 4-HNE content increased (P<0.05), and GSH content decreased in Sev group (P<0.05). Compared with Sev group, with the increase of CAA concentration, the survival rate of HT22 cells was increased (P<0.05), the protein expression of Nrf2, Gpx4, ACSL4, SLC7A11 increased (P<0.05), Fe2+ level and ROS, MDA, 4-HNE content decreased (P<0.05), and the content of GSH increased (P<0.05). Conclusion GAA plays a neuroprotective role by activating Nrf2/GPX4 signaling pathway to reduce sevoflurane-induced ferroptosis in HT22 cells. GAA has great potential as a therapeutic agent for sevoflurane anesthetic nerve injury. |
| Key words: ganoderic acid A sevoflurane ferroptosis nerve injury Nrf2/GPX4 signaling pathway HT22 cells |
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