Background Neuregulin receptor degradation protein-1 (Nrdp1) is an E3 ubiquitin ligase that plays an important role in regulating cell growth, apoptosis and oxidative stress. However, the data regarding its expression and exact mechanism in neuronal injury following ICH has not been well identified. Methods In this study, primary cortical neurons from C57BL/6 mice were subjected to erythrocyte lysates. Nrdp1 expression, cell apoptosis, caspase-3 and BRUCE levels were detected. In addition, inflammatory response, brain edema, and neurological injury in ICH mice were also assessed. Results We found that the expression of Nrdp1 was significantly increased in neuron cells accompanied by up-regulation of active caspase-3 and decreased expression of BRUCE (an inhibitor of apoptosis protein). However, inhibiting Nrdp1 levels of neurons reduced caspase-3 activity but induced up-regulation of BRUCE. In vivo, inhibiting Nrdp1 levels increased pro-inflammatory cytokines, brain edema, and neurological injury following ICH. Conclusions Taken together, the data suggested that Nrdp1 might play a crucial role in neuronal apoptosis via inhibiting BRUCE following ICH.

中文翻译：

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Nrdp1 通过脑出血后布鲁斯的下调增加神经元凋亡。

背景神经调节蛋白受体降解蛋白-1（Nrdp1）是一种E3泛素连接酶，在调节细胞生长、凋亡和氧化应激中起重要作用。然而，关于其在 ICH 后神经元损伤中的表达和确切机制的数据尚未得到很好的确定。方法 在这项研究中，对来自 C57BL/6 小鼠的原代皮层神经元进行红细胞裂解物处理。检测Nrdp1表达、细胞凋亡、caspase-3和BRUCE水平。此外，还评估了 ICH 小鼠的炎症反应、脑水肿和神经损伤。结果我们发现神经元细胞中Nrdp1的表达显着增加，伴随着活性caspase-3的上调和BRUCE（一种凋亡蛋白抑制剂）的表达降低。然而，抑制神经元的 Nrdp1 水平会降低 caspase-3 的活性，但会诱导 BRUCE 的上调。在体内，抑制 Nrdp1 水平会增加 ICH 后的促炎细胞因子、脑水肿和神经损伤。结论 综上所述，数据表明 Nrdp1 可能通过抑制 ICH 后的 BRUCE 在神经元凋亡中起关键作用。