Lu Zhanhua, Huang Kun
Department of Emergency, Nantong Haimen District People's Hospital, No. 1201 Peking Road, Haimen District, Nantong, 226100, China.
BMC Neurosci. 2025 Jan 8;26(1):2. doi: 10.1186/s12868-024-00923-7.
Intracerebral hemorrhage (ICH) is a common subtype of stroke, characterized by a high mortality rate and a tendency to cause neurological damage. This study aims to investigate the role and mechanisms of lncRNA HCP5 in ICH.
We simulated ICH in vivo by injecting collagenase into rats and established an in vitro model using hemoglobin-treated BV2 cells. HCP5 and miR-195-5p levels were quantified by RT-qPCR. mNSS score was used to evaluate neurological deficits in the rats. The dry-wet weight method assessed the degree of brain edema. Cell viability and apoptosis rates were determined using the CCK-8 assay and flow cytometry, respectively. The targeting relationship between HCP5 and miR-195-5p was confirmed using dual-luciferase reporter assays and RNA immunoprecipitation. ELISA was utilized to measure inflammatory factors, and commercial kits were used to detect MDA and ROS levels.
In the ICH model rats, HCP5 levels were significantly elevated. It was also found that silencing HCP5 significantly alleviated brain edema and neurological deficits in the ICH rats, and there was a marked improvement in ICH-induced neuroinflammation and oxidative stress. Moreover, HCP5 was found to sponge miR-195-5p, and inhibiting miR-195-5p could counteract the neuroprotective effects of silencing HCP5. Similar results were obtained in the in vitro experiments with BV2 cells.
Silencing HCP5 can alleviate brain edema, neurological dysfunction, neuroinflammation, and oxidative stress caused by ICH via miR-195-5p.
脑出血（ICH）是中风的一种常见亚型，其特征是死亡率高且易导致神经损伤。本研究旨在探讨长链非编码RNA HCP5在脑出血中的作用及机制。
通过向大鼠注射胶原酶在体内模拟脑出血，并使用经血红蛋白处理的BV2细胞建立体外模型。采用RT-qPCR定量检测HCP5和miR-195-5p水平。用mNSS评分评估大鼠神经功能缺损情况。采用干湿重法评估脑水肿程度。分别使用CCK-8法和流式细胞术测定细胞活力和凋亡率。通过双荧光素酶报告基因检测和RNA免疫沉淀法确认HCP5与miR-195-5p之间的靶向关系。利用ELISA检测炎症因子，使用商业试剂盒检测丙二醛（MDA）和活性氧（ROS）水平。
在脑出血模型大鼠中，HCP5水平显著升高。还发现沉默HCP5可显著减轻脑出血大鼠的脑水肿和神经功能缺损，且脑出血诱导的神经炎症和氧化应激有明显改善。此外，发现HCP5可吸附miR-195-5p，抑制miR-195-5p可抵消沉默HCP5的神经保护作用。在BV2细胞的体外实验中也获得了类似结果。
沉默HCP5可通过miR-195-5p减轻脑出血引起的脑水肿、神经功能障碍、神经炎症和氧化应激。
