Abstract
Traumatic brain injury (TBI) is one of the most common diseases in clinical neurosurgery characterized with high incidence rate, mortality and many complications. Objectives: The purpose of this study is to explore the roles of Xuesaitong in the therapeutic effect of brain trauma and alteration of expression in Bax, a kind of promoting apoptosis factor. Methods: The rat traumatic brain injury models were established by using modified free falling body impact method. Thereafter, Xuesaitong was employed to be administered to TBI rats, and NSS Score Rating Scale was used to evaluate the effect of Xuesaitong. Moreover, real-time PCR was used to detect the Bax expression changes before and after the Xuesaitong administration. Results: Xuesaitong could accelerate the neurofunctional recovery of TBI rats, accompanied by NSS Scores significant decrease. Simultaneously, it also could inhibit the expression of Bax factor. Conclusions: Xusaitong could markedly ameliorate TBI restoration, in which it promotes the neurofunctional recovery, and at the same time it inhibits the expression of Bax.
Highlights
Traumatic Brain Injury (TBI) is one of the most common diseases in neurosurgery with high incidence rate, mortality and muti-complications
As there was obvious difference in Neurological Severity Scores (NSS) Scores between TBI and sham operative group, it was indicative that the injury resulted from TBI could not recover completely, that is, the rats of TBI had functional defect to a certain extent
The third, our results in NSS Score evaluation found that there existed a step-up trend in NSS Scores in TBI and Xuesaitong treated group when compared with sham group respectively, and the NSS scores in Xuesaitong treated group had no marked difference between those of TBI group, suggesting that Xuesaitong did not exhibited active role in the Neural functional recovery in TBI rats in this study
Summary
Traumatic Brain Injury (TBI) is one of the most common diseases in neurosurgery with high incidence rate, mortality and muti-complications. It could result in movement defect, cognition disorder, impairment of language function. The lesion of TBI includes direct injury occurring at the injury site and secondary injury induced by the pathological process including ischemia, anoxia, calcium channel dysfunction and lipid peroxidation [1]. Cognition disorder is the most sustained and serious symptom, which expressed as juries or loss of attention and memory [1] [2]. While local brain ischemia is one of the main causes of secondary craniocerebral injury, 90% among which is the direct cause to death [3]. To our knowledge, there are several following methods dedicated to clinical therapy for TBI: cryotherapy, hormonal therapy, neurotrophic factors and growth factors therapies, cellular transplanting therapies (such as Bone Marrow Stem cells (BMSC) and Neural Stem Cells (NSCs)) [2]
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