Xiong Xin-Gui, Liang Qinghua, Zhang Chunhu, Wang Yang, Huang Wei, Peng Weijun, Wang Zhe, Xia Zi-An
Institute of Integrated Medicine, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
Department of Integrated Traditional Chinese & Western Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Biomed Res Int. 2017;2017:8572509. doi: 10.1155/2017/8572509. Epub 2017 Jan 30.
. Cognitive impairment is the leading cause of traumatic brain injury- (TBI-) related disability; however, the underlying pathogenesis of this dysfunction is not completely understood. . Using an isobaric tagging for relative and absolute quantitation- (iTRAQ-) based quantitative proteomic approach, serum samples from healthy control subjects, TBI patients with cognitive impairment, and TBI patients without cognitive impairment were analysed to identify differentially expressed proteins (DEPs) related to post-TBI cognitive impairment. In addition, DEPs were further analysed using bioinformatic platforms and validated using enzyme-linked immunosorbent assays (ELISA). . A total of 56 DEPs were identified that were specifically related to TBI-induced cognitive impairment. Bioinformatic analysis revealed that a wide variety of cellular and metabolic processes and some signaling pathways were involved in the pathophysiology of cognitive deficits following TBI. Five randomly selected DEPs were validated using ELISA in an additional 105 cases, and the results also supported the experimental findings. . Despite limitations, our findings will facilitate further studies of the pathological mechanisms underlying TBI-induced cognitive impairment and provide new methods for the research and development of neuroprotective agents. However, further investigation on a large cohort is warranted.
认知障碍是创伤性脑损伤(TBI)相关残疾的主要原因;然而,这种功能障碍的潜在发病机制尚未完全明确。采用基于相对和绝对定量的等压标记(iTRAQ)定量蛋白质组学方法,对健康对照受试者、有认知障碍的TBI患者和无认知障碍的TBI患者的血清样本进行分析,以鉴定与TBI后认知障碍相关的差异表达蛋白(DEP)。此外,利用生物信息学平台对DEP进行进一步分析,并通过酶联免疫吸附测定(ELISA)进行验证。共鉴定出56种与TBI诱导的认知障碍特异性相关的DEP。生物信息学分析表明,多种细胞和代谢过程以及一些信号通路参与了TBI后认知缺陷的病理生理过程。另外选取105例病例,采用ELISA对随机选择的5种DEP进行验证,结果也支持实验发现。尽管存在局限性,但我们的研究结果将有助于进一步研究TBI诱导的认知障碍的病理机制,并为神经保护剂的研发提供新方法。然而,有必要对更大的队列进行进一步研究。