Fig. 9From: Exercise attenuates neurological deficits by stimulating a critical HSP70/NF-κB/IL-6/synapsin I axis in traumatic brain injury ratsSynapsin I expression was higher in a the frontal cortex, b the hippocampus, c the striatum, or d the hypothalamus. Illustration of synapsin I protein levels in (EP− + sham + siRNA-vector) rats, (EP+ + sham + siRNA-vector) rats, (EP+ + sham + siRNA-HSP70) rats, (EP− + TBI + siRNA-vector) rats, (EP+ + TBI + siRNA-vector) rats, and (EP+ + TBI + siRNA-HSP70) rats 3 days after TBI determined by Western blot. The level of synapsin I is significantly (P < 0.05) elevated in (EP+ + sham + siRNA-vector) group or (EP+ + TBI + siRNA-vector) group over control. The increased levels of synapsin I caused by EP+ are significantly (P < 0.05) attenuated by depleting HSP70 levels with shHSP70 gene silence. Values are expressed as means ± SEM (n = 8 for each group) and relative to β-actin. *P < 0.05 for EP+ + siRNA-vector vs. EP− + siRNA-vector and † P < 0.05 for EP+ + siRNA-vector vs. EP+ + siRNA-HSP70Back to article page