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Piao Zhang1#, Chao-Hui Liang1#, Di-ke Qiu1, Yuan Jin1, Cheng-Fei Bi1, Yu-Shi1, Liu-Lin Xiong2, Jia Liu1*
Ibrain 2016;2(4):153-160 Download
Abstract
Backgroud: Spinal cord and cortex with conditioning leison are a kind of neurological trauma which seriously jeopardized the health of human beings. They are devastating for society and individuals, in part owing to the high rates of disability and resulting medical costs. BDNF is a vital molecular, which play a critical roel in the progress of spinal cord or cortex repairment. Interestingly, we found ERK1 pathway was involving in the regulating process. But regretfully, the possible mechanism is ambiguous. Methods: Hence, in order to illuminate the theory, we established the model with sciatic nerve and spinal cord transection. And then spinal cords and cortexes were harvested from rats with sciatic nerve and spinal cord transection for performing RT-PCR and Western Blot, which aimed to detect the level of BDNF and ERK1. Resluts: The results manifested that the expression of BDNF and ERK1 was higher in sciatic nerve transection and spinal cord transection group (RSNTASCT/LD) than sciatic nerve transection one. Conclusion: Here, we may draw a conclusion that spinal cord will restrain the level of BDNF, and sciatic nerve transection can promote ERK1 expression. Moreover, sciatic nerve transection and spinal cord transection will promote ERK1 expression. Nevertheless, sciatic nerve transection and spinal cord transection will promote BDNF and ERK1 expression, whilst sciatic nerve transection can restrain ERK1 expression in cortex. In our data, we are the first time to expound the role of endogenous BDNF relating to the regeneration of spinal cord in the condition of peripheral nerve injury, and reveal the possible underlying mechanism of ERK1 pathway, which may provide certain theoretical basis and experimental basis for the treatment of spinal cord injury and prognosis in clinic.
Feng Wang1, Rui-Ze Niu1, Ya-Xin Tan2, Lu-Lu Xue2,Yuan Peng1, Shan Li2, Jia Liu1*.Ibrain  2019;4(2):53-64
Abstract
Shuai-jie Huang1, Rui-Ze Niu 2,Feng Wang 2,Ting-Hua Wang2,3*.Ibrian  2019;4(2):40-52
Abstract
Lan-Lan Shi1,Jia Liu2,Ting-Hua Wang2.Ibrain 2019; 4(2):65-71
Abstract
Lu-Lu Xue1*.Ibrain 2019;4(1):36-39
Abstract
Jing-Yuan He1, Ke Xiao 2,Lan-Chun Zhang1*.Ibrain 2019;4(1):28-35
Abstract
Shan li1, Ya-Xin Tan1, Lu-Lu Xue1, Feng-Wang4,Ruo-Lan Lan4,Liu-Lin Xiong2, Xiu-Ya Zhou3, Xiao Zhang3, Jia -Liu2* .Ibrain 2019; 4(1):15-27
Abstract
Rui-Ze Niu1, Ke Xiao 2,Ting-Hua Wang1,3,4 *.Ibrain 2019;4(1):1-14
Abstract
Ping Dai1#, Lin Qin2,3#, Yuan Jin1, Yu Zhao1, Rong-Ping Zhang2*, Jin-Tao Li1*
Ibrain 2015;1(6):172-178 Download
Abstract
Objective: Traumatic brain injury (TBI), a common neurosurgical disease, usually induces cognitive impairments, motor deficits, and neuropsychiatric deficits. Effective treatments are still lacking.  breviscapine shows broad pharmacological effects and facilitates functional recovery from cardiovascular and cerebrovascular insults, such as brain ischemia and myocardial ischemia. However,  the role of breviscapine in TBI remains vague. In this study, . we aimed to investigate whether breviscapine can improve functional deficits in rats with TBI. Method: Thirty adult female Sprague–Dawley (SD) rats were employed and randomly divided into three groups: sham group, TBI group, Breviscapine treatment group (Breviscapine+TBI). TBI was initiated using an electromagnetic-controlled cortical impact device. Breviscapine (0.375mg/kg) were administrated into lateral ventricles one time after TBI induction. Behavioral evaluation was conducted on days 2, 4, 6, 8,10, 12and 14 after TBI using mNSS tests,. At 14 days after operation, western blotting analysis, immunofluorescent staining and real-time RT-PCR were performed to evaluate the protein and mRNA level of netrin-1 in the brain tissues, respectively. Results: Compared with the sham rats, TBI deteriorated behavioral function indicated by increased mNSS (P<0.05). Breviscapine administration showed a significant decrease in mNSS compared to TBI group (P<0.05). Quantitative Real-time PCR showed the mRNA levels of netrin-1 in the TBI group were significantly decreased compared with the sham group, moreover, breviscapine treatment up-regulated netrin-1 mRNA in the brain when compared with the TBI group at day 8 post-injury (P<0.05). In addition,western blot analyses also showed breviscapine treatment up-regulated the protein level of netrin-1 in the brain when compared with the TBI group at day 8 post-injury (P<0.05).. Immunofluorescent staining of netrin-1 showed the same variation trend as the western blot. Conclusion: Breviscapine improves neurological function in rats with TBI probably by up-regulating netrin expression. This study would provide a potential therapeutical target for clinical therapy of TBI.
Ru-Xin Xing1#, Jing Liu2#, Liang-Liang Zhu1, Min Yang1, Liu-Lin Xiong2*, Yong-Jian Zhu1*
Ibrain 2015;1(5):141-149 Download
Abstract
Background/aim: spinal cord injury (SCI), as leading causes of death and disability in worldwide, commonly threatens human health, and brings heavy burden to the family and the society, which is needing to develop new technique for the treatment of this diseases. Gene therapy, as conventional approaches to target certain pathophysiological process, has well been considered for biological therapy, but the efficiency is waiting to be improved. Here, we explore the effect of HSV BDNF releasing in local region in spinal cord injury condition. Methods: Adult Sprague–Dawley rats were randomly divided into sham group, SCT group, SCT-BDNF administrated group and SCT empty-vector group. After constructed the HSV-BDNF recombinant, they were transfected the motor neurons in the injured site of spinal cord. Moreover, stereology was used to determine the expression of BDNF in motor neurons. Meanwhile, the number of CD68 positive staining was detected to evaluate the inflammatory reaction in injected area. Lastly, BBB scores were utilized for assessing the motor function of hindlimbs. Results: HSV-BDNF recombinant was successfully constructed and transfected into neurons. BBB scores showed that HSV-BDNF administration could promote the improvement of hindlimb function, and HSV-BDNF injection can induce an inflammatory reaction, partly. These suggested that HSV-BDNF administration improve motor function and induce inflammation in injured spinal cord. Conclusions: The present results indicate that HSV-BDNF injection can promote the recovery of motor function and induce a slight inflammatory reaction in SCT rats. The mechanism may relate to the improvement of neuronal activity. The present findings therefore provides a novel therapeutic strategy for clinical treatment of SCI by releasing BDNF in local region.
Ru-Xin Xing1*, Liang-Liang Zhu1, Min Yang1, Fei Liu2*
Ibrain 2015;1(5):136-140 Download
Abstract
Spinal cord injury is a prevalent disease in surgical clinic with a high morbidity and mortality. Due to its complex pathological process, there is no satisfied strategies for its repair. BDNF, an important member of neurotrophin family, is crucial in supporting survival and differentiation of neurons. However, the concentration of BDNF in CNS is very low, so as to not reach an effective level for the treatment. It therefore needs to develop new strategy to increase BDNF release in injury region. Human simple herpes virus(HSV), a neural invasion virus, has been developed as a vector to carry bio-factors into organism. Here, adult SD rats are divided into sham, SCT, and SCT with HSV-BDNF administrated group. The effect of HSV-BDNF recombinant infection on motor function recovery evaluated by BBB scale was detected, and labeled cells of HSV is observed under fluorescence microscope, as well as the BDNF expression level is evaluated using Western Blot and IHC. As the result, HSV-BDNF recombinant is detected in motor neurons from spinal cord tissue, and the level of BDNF substantially is increased. Finally, motor function recovery of rats in HSV-BDNF group is significantly improved, compared with the SCT group, which confirmed HSV-BDNF releasing in skeleton muscle could be as an effective strategy for the treatment of SCI.
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