Abstract
An overarching consequence of traumatic brain injury (TBI) is the cognitive impairment. It may hinder individual performance of daily tasks and determine people's subjective well-being. The damage to synaptic plasticity, one of the key mechanisms of cognitive dysfunction, becomes the potential therapeutic strategy of TBI. In this study, we aimed to investigate whether Xuefu Zhuyu Decoction (XFZYD), a traditional Chinese medicine, provided a synaptic regulation to improve cognitive disorder following TBI. Morris water maze and modified neurological severity scores were performed to assess the neurological and cognitive abilities. The PubChem Compound IDs of the major compounds of XFZYD were submitted into BATMAN-TCM, an online bioinformatics analysis tool, to predict the druggable targets related to synaptic function. Furthermore, we validated the prediction through immunohistochemical, RT-PCR and western blot analyses. We found that XFZYD enhanced neuroprotection, simultaneously improved learning and memory performances in controlled cortical impact rats. Bioinformatics analysis revealed that the improvements of XFZYD implied the Long-term potentiation relative proteins including NMDAR1, CaMKII and GAP-43. The further confirmation of molecular biological studies confirmed that XFZYD upregulated the mRNA and protein levels of NMDAR1, CaMKII and GAP-43. Pharmacological synaptic regulation of XFZYD could provide a novel therapeutic strategy for cognitive impairment following TBI.
Highlights
Traumatic brain injury (TBI) becomes an enormous socioeconomic burden worldwide [1, 2]
Percentage of time staying in the target quadrant in the probe trial was significantly shorter after cortical impact (CCI) (Figure 1C), Xuefu Zhuyu Decoction (XFZYD) (9 g/kg and 18 g/ kg) treatment significantly increased the percentage on the 21st day compared with the Vehicle group (Figure 1C)
Bioinformatics combined with molecular biology methods revealed that XFZYD improves cognitive impairment of traumatic brain injury (TBI) via synaptic regulation
Summary
Traumatic brain injury (TBI) becomes an enormous socioeconomic burden worldwide [1, 2]. It is the leading cause of disability in the under 40 s [3]. The reason is that the cognitive impairment with TBI involves complicated pathological mechanisms, “one-compound, one-target” based modern drugs are not available [9]. TBI can trigger cellular dysfunction/loss, neurotransmission impairments, synaptic connections disruption occur, and lead to the cognitive dysfunction [10,11,12,13]. Neuroscientists hope to identify new therapies for improvement of cognitive deficit after TBI
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