| 马忠英,张 迪,孙 金,牛 静,任 茜,吴倩雯,王婧雯.连翘酯苷A通过Akt/Nrf2信号通路发挥抗脑缺血氧化损伤作用研究[J].,2021,(2):214-218 |
| 连翘酯苷A通过Akt/Nrf2信号通路发挥抗脑缺血氧化损伤作用研究 |
| Forsythiaside A Inhibited Cerebral Ischemic Induced Oxidative Damage through Akt/Nrf2 Signaling Pathway |
| 投稿时间：2020-05-25 修订日期：2020-06-21 |
| DOI：10.13241/j.cnki.pmb.2021.02.004 |
| 中文关键词: 连翘酯苷A 脑缺血 氧化损伤 Akt/Nrf2 |
| 英文关键词: Forsythiaside A Cerebral ischemia Oxidative damage Akt / Nrf2 |
| 基金项目:国家自然科学基金项目（81774190） |
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| 中文摘要: |
| 摘要 目的：研究连翘酯苷A（Forsythiaside A，FA）对缺血再灌注引起的脑细胞损伤的保护作用及机制。方法：采用PC12细胞缺氧再复氧模型（OGD/R），细胞分组为正常组，模型组，FA处理组（1.25, 2.5和5μmol/L），测定细胞存活率、凋亡率、ROS、MDA以及抗氧化酶水平。采用Western blotting测定对Akt和Nrf2蛋白的影响，采用Akt抑制LY294002验证FA的调节作用。结果：FA能够有效抑制OGD/R引起的存活率下降和凋亡率增加，同时可以抑制细胞内ROS和MDA水平，升高细胞内抗氧化酶（SOD、GSH、GSH-Px和CAT）水平。FA处理能够增加Akt磷酸化水平以及Nrf2和其下游蛋白HO-1蛋白表达。进一步采用LY294002验证发现FA通过Akt调控Nrf2发挥抗氧化作用从而抑制脑细胞损伤。结论：FA能够抑制缺血再灌注引起的脑细胞损伤，其作用机制可能是通过促进Akt磷酸化，调控Nrf2下游抗氧蛋白酶表达，抑制氧化应激，从而保护脑细胞。 |
| 英文摘要: |
| ABSTRACT Objective: To study the protective effect and mechanism of forsythiaside A (FA) on brain cell damage caused by ischemia/reperfusion. Methods: Oxygen Glucose Deprivation/reoxygenation (OGD/R)model was induced in PC12 cell and divided into normal group, model group, and FA treatment group (1.25, 2.5, and 5 μmol/L). Cell survival rate, apoptosis rate, ROS, MDA and antioxidant enzyme levels were measured. Western blotting was used to determine the effect of FA on Akt and Nrf2, and Akt inhibition of LY294002 was used to verify the regulation effects of FA. Results: FA inhibited the decline of survival rate and the increase of apoptosis rate caused by OGD/R. We also found that FA inhibited the levels of ROS and MDA, and increased the antioxidant proteins (SOD, GSH, GSH-Px and CAT). FA treatment increased the phosphorylation level of Akt and the expression of Nrf2 and its downstream protein HO-1. Further verification using LY294002 found that FA regulated Nrf2 through Akt to inhibit oxidative induced brain cell damages. Conclusion: FA can inhibit brain cell damage caused by ischemia/reperfusion, and its mechanism may be through promotingAkt phosphorylation, regulating the expression of Nrf2 and its downstream antioxidant enzymes, thus inhibits oxidative stress and protects brain cells. |
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