ABSTRACT
Objective To explore the impact of puerarin treatment on autophagy in rats with traumatic brain injury (TBⅠ) and the underlying mechanism.Methods Seventy five Sprague-Dawley (SD) rats were randomized into 5 groups:sham group (S group,n =15),traumatic brain injury group (TBⅠ group,n =15),TBⅠ + puerarin treatment group (TBⅠ + Pue group,n =15),TBⅠ + JNK inhibitor group (TBⅠ + SP group,n =15),and TBⅠ + JNK activator + Pue (TBⅠ + An + Pue group,n =15).Feeney method was applied to make rats with TBⅠ model.Mter that,head water content and neurological deficit score (NDS) were measured and recorded at day 1,3 and 7 in each group.Western blot was used to measure the JNK activity and autophagic marker proteins,including LC3B and Beclin1.Results Compared to S group,the head water content and NDS were decreased significantly among the others (P ＜ 0.05).The head water content and NDS in TBⅠ + Pue and TBⅠ + SP groups was decreased remarkably compared with TBⅠ group.Combined with puerarin and animycin treatments failed to reduce head water content and NDS compared to the TBⅠ + Pue group.Activated autophagy could be observed in TBⅠ group compared to S group.Compared to group S,LC3Ⅱ,Beclin1 and P-JNK1 were increased significantly.Pue and SP could reduce their expressions,respectively.Combined with puerarin and animycin treatments failed to reduce LC3Ⅱ,Beclin1 and P-JNK1 compared to TBⅠ + Pue group.Conclusions Puerarin could protect rats with TBⅠ via inhibiting autophagy,JNK signal pathway could involve the process of puerarin regulating autophagy.
ABSTRACT
The objective of this paper is to study the expression of caveolin-1 in the traumatic brain injury patients and its relationship with disease prognosis. Caveolin-1 was measured in 52 patients with ventricular hemorrhage within 8h, 24h, 48h, 72h and 1 week after onset by enzyme-linked immunosorbent assay [ELISA], to observe the changes of cerebrospinal fluid caveolin-1. The level of caveolin-1 in the brain of all patients was higher than that of the control group at 8 h, 24h, 48 h, 72h and 1 weeks after the onset [P<0.05] and the level of caveolin-1 in cerebrospinal fluid [CSF] of the severe group was higher than that of the light-medium group within 8h, 24h, 48 h and 72h after the onset [P<0.05]. The level of caveolin-1 in CSF was significantly increased in patients with ventricular hemorrhage within 8h, 24h, 48h, 72h and 1 weeks after onset, and the expression of caveolin-1 in brain was related to the severity of craniocerebral injury. Therefore, the expression of caveolin-1 can be used as an indicator of the prognosis of traumatic brain injury disease