| Objection: To investigate the contribution of NF-κB pathway to the autophagic progression after traumatic brain injury in rat model.Methods: Traumatic brain injury model was induced by a modified weight-drop device that was allowed a free-fall until the silicone tip (diameter 5 mm) hit the exposed skull on the left cerebral hemisphere,1mm lateral to the midline in the mid-coronal plane. SN50 (10μg) was injected intracerebroventricularly (icv) 10min before the onset of strike. Western blot was employed to determine alternations in Beclin1, Bcl-2, cathepsin D and LC3 in impaired cortex and hippocampus at different time points after TBI, as well as parallel groups of mice.Results: The expression of Beclin1, Bcl-2, cathepsin D and LC3 are significantly increased in impaired cortex and hippocampus on 1h, 3h, 6h, 12h, 24h, and 48h time point after TBI. At every post-injury time, Beclin1, cathepsinD and LC3Ⅱexpression in SN50 group is lower, while Bcl-2 is higher than Saline group.Conclusions: 1. Autophagy was activated by TBI. 2. NF-κB pathway contributes to the regulation of autophagosome after TBI. 3. The expression of lysomal enzyme cathepsin D was accommodated by NF-κB pathway after TBI. |