氧化应激
丙二醛
细胞凋亡
超氧化物歧化酶
神经生长因子
药理学
转染
化学
活性氧
成纤维细胞
再灌注损伤
细胞生物学
缺血
生物
医学
生物化学
内科学
受体
体外
基因
出处
期刊:International Journal of Human Genetics
[Kamla Raj Enterprises]
日期:2023-10-17
卷期号:24 (01)
标识
DOI:10.31901/24566330.2024/24.01.809
摘要
The researchers made efforts in elucidating the mechanism for miR-145-5p participating in neuronal ischemia/reperfusion injury (I/R) via targeting fibroblast growth factor-5 (FGF5). OGD/R was performed to construct the neuronal injury model. After OGD/R, the oxidative stress injury of nerve cells was enhanced significantly, the levels of lactic dehydrogenase, reactive oxygen species and malondialdehyde rose, while the superoxide dismutase activity decreased. Both miR-145-5p and cell apoptosis rate increased. MiR-145-5p had a targeting relation to FGF5. After miR- 145-5p inhibitor transfection of nerve cells, inhibition of oxidative stress together with apoptosis was observed. FGF5 siRNA could reverse the impact on oxidative stress, FGF5, and apoptosis exerted by miR-145-5p-inhibitor in the OGD/ R model. Being a latent target of I/R treatment, miR-145-5p induces the oxidative stress injury as well as apoptosis of HT22 cells by targeting and binding FGF5.
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