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首页> 外文期刊>Frontiers in Neuroscience >MicroRNA Let-7i Is a Promising Serum Biomarker for Post-stroke Cognitive Impairment and Alleviated OGD-Induced Cell Damage in vitro by Regulating Bcl-2
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MicroRNA Let-7i Is a Promising Serum Biomarker for Post-stroke Cognitive Impairment and Alleviated OGD-Induced Cell Damage in vitro by Regulating Bcl-2

机译：MicroRNA Let-7i是一种有前途的血清生物标志物，用于缓冲后认知障碍，并且通过调节BCL-2来缓解OGD诱导的细胞损伤<斜体>斜体>

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Background The mechanism of post-stroke cognitive impairment (PSCI) has not been explained. We aimed to investigate whether miR-let-7i participates in the PSCI and illuminates its underlying role in oxygen–glucose deprivation (OGD)-induced cell apoptosis. Methods Blood samples from 36 subjects with PSCI and 38 with post-stroke cognitive normality (Non-PSCI) were collected to evaluate the differential expression of miR-let-7 family members, using qRT-PCT analysis. Spearman correlation was performed to estimate the correlation between the miR-1et-7i level and Montreal Cognitive Assessment (MoCA) score. Treatment of SH-SY5Y cells with OGD was used to induce cell apoptosis in vitro . Effects of miR-let-7i on OGD-induced cell apoptosis was estimated after transfection. The target gene of miR-let-7i was analyzed by dual luciferase reporter gene assay. Results The expression of miR-let-7i was up-regulated in PSCI patients compared with Non-PSCI ( p & 0.001) and negatively correlated with MoCA score ( r = ?0.643, p & 0.001). When exposed to OGD, SH-SY5Y cells showed significant apoptosis accompanied by miR-let-7i up-regulation. In OGD-treated cells, miR-let-7i up-regulation was accompanied by cell apoptosis, while down-regulation showed the opposite effect. Luciferase reporter assay showed that Bcl-2 was a target gene of miR-let-7i. Western blot showed that miR-let-7i up-regulation promoted Bcl-2 expression, while qRT-PCR showed that miR-let-7i had no effect on Bcl-2 expression. Conclusion miR-let-7i was overexpressed in PSCI patients and it could be used as a diagnostic biomarker for PSCI. We illuminated the potential mechanism that miR-let-7i alleviated OGD-induced cell damage by targeting Bcl-2 at the post-transcriptional level.
机译：背景技术尚未解释冲程后认知障碍（PSCI）的机制。我们旨在调查miR-let-7i是否参与PSCI并在氧血糖剥夺（OGD）诱导的细胞凋亡中照亮其潜在作用。方法收集来自36种受试者的血液样品和38带有后冲程认知认知正常性（非PSCI），以评估MIR-Let-7家族成员的差异表达，使用QRT-PCT分析。进行了矛盾的相关性以估计miR-1et-7i水平与蒙特利尔认知评估（MoCA）评分之间的相关性。用OGD处理SH-SY5Y细胞在体外诱导细胞凋亡。 miR-let-7i对转染后估计MIR-Let-7i对OGD诱导的细胞凋亡的影响。通过双荧光素酶报告基因测定分析miR-Let-7i的靶基因。结果与非PSCI（P <0.001）相比，PSCI患者MiR-Let-7i的表达上调，与MoCA得分（R = 0.643，P <0.001）负相关。当暴露于OGD时，SH-SY5Y细胞显示出显着的细胞凋亡，伴随着MIR-Let-7i上调。在OGD处理的细胞中，MIR-Let-7i上调伴有细胞凋亡，而下调表现出相反的效果。荧光素酶报告器测定显示Bcl-2是miR-let-7i的靶基因。 Western印迹显示MiR-Let-7i上调促进了Bcl-2表达，而QRT-PCR显示MIR-Let-7i对Bcl-2表达没有影响。结论MIR-Let-7i在PSCI患者中过表达，它可以用作PSCI的诊断生物标志物。我们照亮了MIR-Let-7i通过在转录后水平靶向Bcl-2来减轻OGD诱导的细胞损伤的潜在机制。

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