MiR-145-5p靶向成纤维细胞生长因子-5参与神经元缺血再灌注损伤

IF 0.1 4区 生物学 Q4 GENETICS & HEREDITY International Journal of Human Genetics Pub Date : 2023-10-17 DOI:10.31901/24566330.2024/24.01.809
Lei Xu
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引用次数: 0

摘要

研究人员通过靶向成纤维细胞生长因子-5 (FGF5)阐明了miR-145-5p参与神经元缺血再灌注损伤(I/R)的机制。采用OGD/R法构建神经元损伤模型。OGD/R后,神经细胞氧化应激损伤显著增强,乳酸脱氢酶、活性氧和丙二醛水平升高,超氧化物歧化酶活性降低。miR-145-5p和细胞凋亡率均升高。MiR-145-5p与FGF5具有靶向关系。miR- 145-5p抑制剂转染神经细胞后,观察到氧化应激和细胞凋亡的抑制作用。在OGD/ R模型中,FGF5 siRNA可以逆转mir -145-5p抑制剂对氧化应激、FGF5和细胞凋亡的影响。miR-145-5p作为I/R治疗的潜在靶点,通过靶向结合FGF5诱导HT22细胞氧化应激损伤和凋亡。
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Participation of MiR-145-5p in Neuronal Ischemia/Reperfusion Injury by Targeting Fibroblast Growth Factor-5
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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