Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, China.
School of Life Sciences and Engineering, Southwest University of Science and Technology, Mianyang, China.
J Neurochem. 2022 Jan;160(1):88-99. doi: 10.1111/jnc.15361. Epub 2021 Apr 18.
The mechanisms of brain injury after intracerebral hemorrhage (ICH) involve mass effect-induced primary injury and secondary injury caused by a pathologic response to the hematoma. Considerable attentions have recently been paid to the mechanisms and therapeutic strategy for secondary brain injury due to no overall benefit from early surgery compared with initial conservative treatment. However, it is unclear whether there is a causal relationship between mass effect and secondary brain injury. Here, the role of mass effect on early erythrolysis after experimental ICH was investigated based on the poly(N-isopropylacrylamide) (PNIPAM) ICH model. Autologous blood and PNIPAM hydrogel were co-injected into the right basal ganglia of rats to induce different degrees of mass effect, but with a constant hematoma. The influences of different mass effect and time courses on erythrolysis and brain damages after ICH were investigated. Furthermore, the protective effect of trehalose against erythrolysis after ICH was evaluated. The results showed that mass effect caused erythrocyte morphological change at 24 hr after ICH. The released hemoglobin was quantitatively evaluated by a polynomial concerning with the mass effect, the volume of hematoma, and the time of ICH. An obvious increase in heme oxygenase-1 (HO-1) and ionized calcium binding adaptor molecule-1 (Iba-1) expression, iron deposition, cell death, and neurological deficits was observed with increasing mass effect. Moreover, trehalose alleviated brain injury by inhibiting erythrolysis after ICH. These data demonstrated that mass effect accelerated the erythrolysis and brain damages after ICH, which could be relieved through trehalose therapy.
脑出血（ICH）后脑损伤的机制涉及由血肿的病理反应引起的质量效应诱导的原发性损伤和继发性损伤。由于与初始保守治疗相比，早期手术没有总体获益，因此最近人们对继发性脑损伤的机制和治疗策略给予了相当多的关注。然而，目前尚不清楚质量效应与继发性脑损伤之间是否存在因果关系。在这里，基于聚（N-异丙基丙烯酰胺）（PNIPAM）ICH 模型，研究了质量效应对实验性 ICH 后早期红细胞溶解的作用。将自体血液和 PNIPAM 水凝胶共同注入大鼠右侧基底节，以诱导不同程度的质量效应，但保持血肿恒定。研究了不同质量效应和时间过程对 ICH 后红细胞溶解和脑损伤的影响。此外，还评估了海藻糖对 ICH 后红细胞溶解的保护作用。结果表明，质量效应在 ICH 后 24 小时引起红细胞形态变化。通过与质量效应、血肿体积和 ICH 时间有关的多项式来定量评估释放的血红蛋白。随着质量效应的增加，血红素加氧酶-1（HO-1）和离子钙结合适应蛋白-1（Iba-1）表达、铁沉积、细胞死亡和神经功能缺损明显增加。此外，海藻糖通过抑制 ICH 后红细胞溶解来减轻脑损伤。这些数据表明，质量效应加速了 ICH 后红细胞溶解和脑损伤，通过海藻糖治疗可以缓解。
