Heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1) is the most abundant and expressed widely member of the hnRNP family. It has been extensively studied in developmental biology, oncology, and neurodegenerative diseases, which has not been reported on in intracerebral hemorrhage (ICH) induced-secondary brain injury (SBI). The purpose of this study was to explore the role of hnRNPA1 exerts and its underlying mechanism in ICH-induced SBI. Experimental ICH models were established by injecting autologous heart blood into the basal ganglia region of rats and increased or inhibited hnRNPA1 expression through the hnRNPA1 plasmid and small interfering RNA. The results illustrated that the protein levels of hnRNPA1 are significantly elevated after ICH, and hnRNPA1 is transported from the nucleus to the cytoplasm. Upregulated hnRNPA1 could improve neurological function and the learning and memory ability decline after ICH-induced injury. Furthermore, TUNEL and FJB staining indicated that hnRNPA1 overexpression could reduce neuronal cell death and injury induced by ICH. However, downregulated hnRNPA1 damages neurological function and learning and memory abilities and aggravates neuronal cell degeneration and apoptosis. Consistently, the levels of Bcl-xl mRNA and Bcl-xl are elevated or decreased depending on the levels of hnRNPA1, which could be one of the mechanisms through which hnRNPA1 participates in ICH-induced neuronal cell death. In summary, hnRNPA1 plays a protective role in ICH-induced SBI via upregulating Bcl-xl expression, indicating that hnRNPA1 could be a potential target for ICH therapy.

异质核核糖核蛋白 A1 (hnRNPA1) 是 hnRNP 家族中最丰富和表达最广泛的成员。它已在发育生物学、肿瘤学和神经退行性疾病中得到广泛研究，但尚未在脑出血 (ICH) 诱导的继发性脑损伤 (SBI) 中报道。本研究的目的是探讨 hnRNPA1 在 ICH 诱导的 SBI 中发挥的作用及其潜在机制。通过将自体心脏血注入大鼠基底神经节区建立实验性脑出血模型，并通过hnRNPA1质粒和小干扰RNA增加或抑制hnRNPA1的表达。结果表明，脑出血后hnRNPA1蛋白水平显着升高，hnRNPA1从细胞核转运至细胞质。上调hnRNPA1可以改善脑出血损伤后的神经功能和学习记忆能力下降。此外，TUNEL 和 FJB 染色表明 hnRNPA1 过表达可以减少 ICH 诱导的神经元细胞死亡和损伤。然而，下调的 hnRNPA1 会损害神经功能和学习记忆能力，并加剧神经元细胞的变性和凋亡。一致地，Bcl-xl mRNA 和 Bcl-xl 的水平根据 hnRNPA1 的水平升高或降低，这可能是 hnRNPA1 参与 ICH 诱导的神经元细胞死亡的机制之一。总之，hnRNPA1 通过上调 Bcl-xl 表达在 ICH 诱导的 SBI 中发挥保护作用，表明 hnRNPA1 可能是 ICH 治疗的潜在靶点。