ABSTRACT
AIM:To study the effects of basic fibroblast growth factor (bFGF) on brain edema, nerve function damage and autophagy related proteins in rats with head injury.METHODS:The rat model of craniocerebral injury (CI) was constructed.The rats were divided into control group, CI group, and low-, middle-and high-dose bFGF groups (n=10).The CI model was established in CI group, while the rats in control group were not given epidural impact.The rats in low-dose, middle-dose and high-dose bFGF groups were given bFGF at 2, 4 and 6μg, respectively, by intraperitoneal injection after 30 min.The neurological function in the rats was evaluated by improved neurological function scoring.The rat brain tissues were taken, and the water content was detected.The levels of tumor necrosis factor-α (TNF-α) , interleukin-6 (IL-6) and IL-1βin the brain tissue were measured by ELISA.The malondialdehyde (MDA) content was analyzed by thiobarbituric acid method.The activity of superoxide dismutase (SOD) was examined by WST-8 assay.The glutathine peroxidase (GSH-Px) activity was detected by colorimetric method.The protein levels of autophagy related proteins LC3-II and beclin-1 in the brain tissues were determined by Western blot.RESULTS:The neurological function score was increased significantly of the rats in CI group.The rat model of craniocerebral injury was successfully constructed.Neurological function scores in the rats in low-dose, middle-dose and high-dose bFGF groups were reduced, the water content of the brain tissue was also reduced (P<0.05).The levels of TNF-α, IL-6 and IL-1βwere decreased in the brain tissues (P<0.05) , the content of MDA was declined (P<0.05) , the activities of SOD and GSH-Px were increased (P<0.05) , the protein levels of LC3-II and beclin-1 were decreased, compared with the untreated rats in CI group (P<0.05).CON-CLUSION:bFGF improves the nerve function of the rats with craniocerebral injury, reduces the water content of the brain tissue, reduces the expression of autophagic protein LC3-II and beclin-1.The mechanism is related to the inhibition of inflammatory reaction and oxidative damage.