Rohadi Rohadi, Bambang Priyanto, Lale Maulin Prihatina, D. Zulkarnaen, Januarman Januarman, Bayu Putra Wibowo, Muzzaki Hasnan Ali, Gibran Ihza Sukma
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摘要

机械上,创伤性脑损伤之后会出现导致周围神经元损伤的病理机制,如细胞和组织坏死、炎症、脑水肿、血脑屏障破裂和高热。脑损伤越严重,对炎症反应的影响越大。因此,本研究旨在确定创伤性脑损伤后大鼠脑细胞水肿的组织病理学描述,分析创伤负荷差异与创伤性脑损伤后小鼠脑细胞炎症、血肿、水肿的组织病理学特征之间的关系。本研究采用实验观察分析研究设计。Sprague-Dawley小鼠作为研究对象,被分为四组(和一个对照组),采用不同的创伤负荷干预措施。创伤负荷分别为20g, 40g, 60g和80g。在创伤负荷作用后1小时,对小鼠进行脑组织活检,观察炎症标志物(synaptophysin)和脑细胞水肿的组织病理学特征。然后使用SPSS程序对数据进行分析。本研究共选取20只小鼠。研究结果表明,平均负荷为50克,平均突触素百分比为23.5%。创伤负荷差异与脑损伤后大鼠脑细胞水肿百分比之间存在显著相关(p <0.001)。创伤负荷的差异与synaptophysin百分比之间有较强的相关性(p=0.926)。研究发现,随着创伤负荷的增加,小鼠大脑组织病理特征中水肿和炎症的比例越来越大。小鼠脑损伤1小时后,损伤程度与脑细胞炎症、水肿比例有显著性差异。创伤程度越严重,大鼠脑细胞中出现炎症和水肿的比例就越高。由于炎症和水肿是在受伤一小时内发现的,因此效果尤其显著。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Gambaran Imunohistokimia Synaptophisin pada Neuron Otak Tikus Pasca Mengalami Cedera Otak Traumatik
TBI is mechanically followed by pathomechanisms that cause damage to surrounding neurons, such as cell and tissue necrosis, inflammation, cerebral edema, breakdown of the blood-brain barrier, and hyperthermia. The more severe the brain injury, the greater the impact on the inflammatory response. Therefore, this study aims to determine the histopathological description of edema in rat brain cells after TBI and to analyze the relationship between differences in trauma burden and histopathological features of brain cell inflammation, hematoma, and edema in mice after traumatic brain injury. This study uses an experimental observational-analytical research design. Sprague-Dawley mice were used as research subjects and divided into four cluster groups (and one control group) with varying trauma-loading interventions. The trauma loads given were 20 grams, 40 grams, 60 grams, and 80 grams. Following the trauma load application, the mice's brains were biopsied one hour after the intervention to observe histopathological features of inflammatory markers (synaptophysin) and brain cell edema. The data were then analyzed using the SPSS program. Twenty mice were included in this study. The results of the study showed that there was a mean load of 50 grams, and there is a mean synaptophysin percentage of 23.5%. There was a significant relationship between differences in trauma load and the percentage of post-TBI rat brain cell edema (p <0.001). There is a perfect and strong correlation between differences in trauma load and the percentage of synaptophysin (p=0.926). It was discovered that as the trauma load increased, there was a growing percentage of edema and inflammation in the histopathological features of the mice’s brains. There was a significant difference between the severity of trauma and the percentage of brain cell inflammation and edema one hour after brain injury in mice. The more severe the level of trauma given, the higher the percentage of inflammation and edema that occurs in rat brain cells. The result is especially notable since the inflammation and edema is found one hour within injury.
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