JNK3Gene Participates Apoptosis Of Nerve Cells And Neural Functional Recover After Traumatic Brain Injury

Objective:Increasing evidence revealed that the activation of c-Jun amino-terminal kinase (JNK) pathway participated the apoptosis of nerve cells and the neural functional recovery after traumatic brain injury (TBI). However, what genes in JNK family were activated in JNK’s roles of above mentioned is still unknown. Therefore, in this study, in situ end labeling (TUNEL), reverse transcription-polymerase chain action (RT-PCR) and neurologic functional assessment (NSS) were adopted to investigate the alteration of gene expression of JNK1, JNK2and JNK3in cerebral injured rats and their roles in neuronal apoptosis and neurological function restoration.Methods:Sprague-dawly(SD) male healthy rats of SPF grade were6month old, weighing200-260g. A total of100rats were randomized into sham operated group (n=30) and TBI group (n=70)(established the rat cerebral injury models by using weight dropping impacter). A total of10rats from the sham operated group and10rats in1h,6h,1d and7d post of injury respectively from TBI group were subjected to’ RT-PCR test. Tissues in the peripheral area of injured cerebral cortex in10rats from sham operated group and10rats from6h and7d sub-group of cerebral injury respectively were harvested and subjected to TUNEL staining. NSS evaluation was used to assess the neurological functional change in10rats from sham operated group and TBI group respectively.Results:We found that expression of JNK3markedly down regulated at1h,6h and on1d and7d post of TBl(P＜0.05). However, the JNK1and JNK2expression did not exhibit significant change(P>0.05). TUNEL staining showed that the number of apoptotic cells surrounding the area of brain injury significantly increased6h after injury(P＜0.05), while in7d post injury, the number of apoptotic cells was less than 6h post injury(P＜0.05), this showed that the number of apoptosis of nerve cells surrounding the injured cerebral cortex gradually reduced over time after TBI. The Scores reflecting neurological functional deficit gradually decrease over time from1,3,5,7,14to28d post of injury, there was significant difference in NSS Scores among different time spots post operation (P＜0.05); NSS Scores were markedly increased in TBI group when compared with the sham operated group (P＜0.05).Conclusion:These suggested that JNK3expression down regulated after TBI, which may associated with apoptosis of nerve cells. Down regulation of JNK3may promote the neurological functional recovery following TBI.