Brain ischaemia, which can cause severe nerve injury, is a global health challenge. Long non-coding RNA (lncRNA) growth-arrest specific 5 (Gas5) has been documented to exert tumour suppressive effects in several cancers. However, its role in cerebrovascular disease still requires further investigation. Therefore, in this study, we focused on the role of lncRNA regulatory signalling related to lncRNA Gas5 in ischaemic brain injury. Middle cerebral artery occlusion (MCAO) was employed as a model of ischaemic brain injury in rats. The expression of lncRNA Gas5 and microRNA-21 (miR-21) was altered in neurons to elucidate their effects in ischaemic brain injury and to identify the interactions among lncRNA Gas5, miR-21 and Pten. The neuronal survival rate, apoptosis and the expression of phosphatidyl inositol 3-kinase (PI3K)/Akt signalling pathway-related genes were also evaluated in vitro to determine the effects of lncRNA Gas5. In the brains of rats subjected to MCAO, the expression of lncRNA Gas5 and Pten was upregulated, while miR-21 was downregulated. LncRNA Gas5 inhibited miR-21 expression, leading to elevated levels of Pten. In vitro experiments revealed that lncRNA Gas5 depletion and miR-21 elevation resulted in the suppression of neuronal apoptosis, thus promoting neuronal survival via the PI3K/Akt signalling pathway. These findings demonstrate that lncRNA Gas5 increases miR-21 and activates Pten, contributing to the development of ischaemic brain injury, supporting the silencing of lncRNA Gas5 as a possible therapeutic target for the treatment of ischaemic brain injury.

中文翻译：

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长链非编码 RNA Gas5 增强 microRNA-21 下调对缺血性脑损伤的影响。

可导致严重神经损伤的脑缺血是一项全球性的健康挑战。长链非编码 RNA (lncRNA) 生长阻滞特异性 5 (Gas5) 已被证明在几种癌症中发挥肿瘤抑制作用。然而，其在脑血管疾病中的作用仍需进一步研究。因此，在本研究中，我们重点研究了与 lncRNA Gas5 相关的 lncRNA 调控信号在缺血性脑损伤中的作用。大脑中动脉闭塞（MCAO）被用作大鼠缺血性脑损伤的模型。lncRNA Gas5 和 microRNA-21 (miR-21) 在神经元中的表达被改变，以阐明它们在缺血性脑损伤中的作用，并确定 lncRNA Gas5、miR-21 和 Pten 之间的相互作用。神经元存活率，还在体外评估细胞凋亡和磷脂酰肌醇 3 激酶 (PI3K)/Akt 信号通路相关基因的表达，以确定 lncRNA Gas5 的作用。在接受 MCAO 的大鼠大脑中，lncRNA Gas5 和 Pten 的表达上调，而 miR-21 的表达下调。LncRNA Gas5 抑制 miR-21 表达，导致 Pten 水平升高。体外实验表明，lncRNA Gas5 消耗和 miR-21 升高导致神经元凋亡的抑制，从而通过 PI3K/Akt 信号通路促进神经元存活。这些发现表明，lncRNA Gas5 增加 miR-21 并激活 Pten，有助于缺血性脑损伤的发展，支持沉默 lncRNA Gas5 作为治疗缺血性脑损伤的可能治疗靶点。