摘要
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.
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.
