Liu Shuang, Yin Feng, Zhang Jianning, Qian Yangming
Department of Neurosurgery, Navy General Hospital of PLA , Beijing , PR China.
Brain Inj. 2014;28(2):133-7. doi: 10.3109/02699052.2013.860479.
This article attempts to provide a framework that will help to illustrate the roles of calpains in the process of traumatic brain injury (TBI).
This review provides meaningful points about the essential role of calpains in the neuropathological changes that follow TBI, identifies useful biomarkers of calpain activation and states the important roles of calpain in the treatment of TBI.
Neuronal calpains can be activated within hours or even minutes following contusive or diffuse brain trauma in animals. It has been suggested that they are early mediators of neuronal damage. Trauma can produce sustained calpain activation. In turn, this may result in axonal degeneration and neuronal death in models of TBI. Calpains can cleave cytoskeletal proteins into stable proteolytic fragments that have been widely used as biomarkers of the activation of calpain. The inhibition of calpains can reduce the functional and behavioural deficits by ameliorating axonal pathology and reducing cell deaths in animal models of TBI.
This review concentrates on the current understanding of the role of calpains in neuropathology that has been induced by TBI and the significance of calpains as a therapeutic target for the treatment of primary and secondary injuries that are associated with brain trauma.
本文试图提供一个框架，以帮助阐明钙蛋白酶在创伤性脑损伤（TBI）过程中的作用。
本综述提供了关于钙蛋白酶在TBI后神经病理变化中的重要作用的有意义观点，确定了钙蛋白酶激活的有用生物标志物，并阐述了钙蛋白酶在TBI治疗中的重要作用。
在动物遭受挫伤性或弥漫性脑外伤后的数小时甚至数分钟内，神经元钙蛋白酶即可被激活。有人认为它们是神经元损伤的早期介质。创伤可导致钙蛋白酶持续激活。反过来，这可能导致TBI模型中的轴突退化和神经元死亡。钙蛋白酶可将细胞骨架蛋白切割成稳定的蛋白水解片段，这些片段已被广泛用作钙蛋白酶激活的生物标志物。在TBI动物模型中，抑制钙蛋白酶可通过改善轴突病理和减少细胞死亡来减轻功能和行为缺陷。
本综述集中于目前对钙蛋白酶在TBI诱导的神经病理学中的作用的理解，以及钙蛋白酶作为治疗与脑外伤相关的原发性和继发性损伤的治疗靶点的意义。
