MM. Department of Neurosurgery - Wuxi Medical College of Anhui Medical University - 904th Hospital of PLA (101th Hospital of PLA) - Wuxi, and Department of Neurosurgery - The Second People's Hospital of HeFei - Anhui, China.
MM. Department of Neurosurgery - Wuxi Medical College of Anhui Medical University - 904th Hospital of PLA (101th Hospital of PLA) - Wuxi, China.
Acta Cir Bras. 2021 May 28;36(4):e360406. doi: 10.1590/ACB360406. eCollection 2021.
To evaluate the effects of controlled decompression and rapid decompression, explore the potential mechanism, provide the theoretical basis for the clinical application, and explore the new cell death method in intracranial hypertension.
Acute intracranial hypertension was triggered in rabbits by epidural balloon compression. New Zealand white rabbits were randomly put into the sham group, the controlled decompression group, and the rapid decompression group. Brain water content, etc., was used to evaluate early brain injury. Western blotting and double immunofluorescence staining were used to detect necroptosis and apoptosis.
Brain edema, neurological dysfunction, and brain injury appeared after traumatic brain injury (TBI). Compared with rapid decompression, brain water content was significantly decreased, neurological scores were improved by controlled decompression treatment. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and Nissl staining showed neuron death decreased in the controlled decompression group. Compared with rapid decompression, it was also found that apoptosis-related protein caspase-3/ tumor necrosis factor (TNF)-a was reduced markedly in the brain cortex and serum, and the expression levels of necroptosis-related protein, receptor-interacting protein 1 (RIP1)/receptor-interacting protein 1 (RIP3) reduced significantly in the controlled decompression group.
Controlled decompression can effectively reduce neuronal damage and cerebral edema after craniocerebral injury and, thus, protect the brain tissue by alleviating necroptosis and apoptosis.
评估控制性减压和快速减压的效果，探讨潜在机制，为临床应用提供理论依据，并探索颅内高压新的细胞死亡方法。
通过硬膜外球囊压迫法诱发兔急性颅内高压。将新西兰白兔随机分为假手术组、控制性减压组和快速减压组。采用脑水含量等方法评价早期脑损伤。Western blot 和双免疫荧光染色检测坏死性凋亡和细胞凋亡。
创伤性脑损伤（TBI）后出现脑水肿、神经功能障碍和脑损伤。与快速减压相比，控制性减压治疗可显著降低脑水含量，改善神经功能评分。末端脱氧核苷酸转移酶 dUTP 缺口末端标记（TUNEL）染色和尼氏染色显示，控制性减压组神经元死亡减少。与快速减压相比，大脑皮质和血清中凋亡相关蛋白半胱氨酸天冬氨酸蛋白酶-3/肿瘤坏死因子（TNF）-a 明显减少，控制性减压组坏死性凋亡相关蛋白受体相互作用蛋白 1（RIP1）/受体相互作用蛋白 3（RIP3）的表达水平明显降低。
控制性减压可有效减轻颅脑损伤后神经元损伤和脑水肿，从而通过减轻坏死性凋亡和细胞凋亡来保护脑组织。
