NGR1 reduces neuronal apoptosis through regulation of ITGA11 following subarachnoid hemorrhage

Subarachnoid hemorrhage (SAH), a prevalent cerebrovascular condition associated with a high mortality rate, frequently results in neuronal apoptosis and an unfavorable prognosis. Recent research has indicated that the adjunctive use of Traditional Chinese medicine (TCM) with surgical interventions exerts a therapeutic impact on SAH. Nevertheless, the mechanism by which TCM mediates apoptosis following SAH remains unclear. In the present study, HT22 mouse neuronal cells were exposed to Oxyhemoglobin (OxyHb) to establish an in vitro model of SAH. The results indicated that treatment with Notoginsenoside R1 (NGR1) alleviated the short-term neurological deficits, reduced the expression of apoptosis-related proteins, and mitigated brain edema in mice. Similarly, it attenuated OxyHb-induced apoptosis of HT22 neurons. Furthermore, RNA-seq analysis was used to examine the transcriptomic changes between HT22 cells stimulated with OxyHb alone and those treated with NGR1 concurrently or independently. The RNA-seq results revealed significant alterations in the expression levels of apoptosis-related genes in OxyHb-stimulated HT22 cells upon administration of NGR1. This study explored the potential mechanism by which NGR1 mitigates neuronal apoptosis, presenting a novel therapeutic approach for treating SAH through the use of a single TCM ingredient. Overall design: The total RNA was extracted through the culture of neuron cell HT22. Each group was divided into three replicates. There were three groups in total, namely, the experimental group, the control group and the intervention group. Subsequently, RNA isolation, quantification and quality assessment were carried out. Then, the mRNA sequencing library was prepared, and then the library quality analysis was carried out. Finally, the high-throughput Transcriptome was sequenced on Illumina NovaSeq.