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Objective To explore the therapeutic effect of curcumin on neronal apoptosis, autophagy and neural renovation in cerebral cortex of mice after traumatic brain injury (TBI). Methods A total of 90 mice were randomly divided into 4 groups: blank control group (N=12), sham group (N=26), TBI+NaCl group (N=26, NaCl was pretreated by intraperitoneal injection 30min after TBI) and TBI+ curcumin group (N=26,curcumin was pretreated by intraperitoneal injection 30 min after TBI). Propidium iodide (PI)-labeled cell-counting was used to study the cell protective effect of curcumin. Expression of apoptosis and autophagy related proteins B celllymphoma (Bcl-2),activated Caspase-3, P62, microtubule-associated protein 1 light chain 3 (MAP1LC3-Ⅱ) were detected by Western Blotting. The lesion volume of cortex was tested by Cavalieri mothod. Results PI positive cells significantly increased 48h after TBI (t= 26.000, P=0.000; t=18.520, P=0.000), and reduced after curcumin injection (t=3.686, P=0.014); in cortex lesion area,expression level of apoptosis associated protein Bcl-2 decreased(t=5.656, P=0.000; t= 3.254, P =0.008; t =4.485, P =0.001; t =3.150, P =0.009), expression level of activated Caspase-3 increased (t=8.534, P=0.000; t=3.468, P=0.005; t=8.565, P=0.000; t=2.846, P=0.016), expression level of autophagy associated protein P62 decreased (t=3.574, P=0.004; t=7.612, P=0.000; t=3.465, P= 0.005; t=8.637, P=0.000),expression level of MAP1LC3-Ⅱ increased(t=7.101, P=0.000; t=7.656, P= 0.000; t=6.816, P=0.000; t=9.043, P=0.000),curcumin suppressed apoptotic activity by showing higher expression level of Bcl-2 (t=3.290, P=0.007),lower expression level of activited Caspase-3 (t=3.520, P= 0.005),lower expression level of P62 (t=3.595, P=0.004),and higher expression level of MAP1LC3-Ⅱ (t= 4.954, P=0.000). More tissue damage was seen 28d after TBI (t=34.813, P=0.000; t=11.172, P=0.000) but less tissue damage was seen in TBI+curcumin group (t=4.525, P=0.003). Conclusions Curcumin could inhibit neuronal apoptosis and enhance antophagic activity. Therefore,it may induce neuroprotection and promote nerual renovaion after fraumatic brain injury.