ABSTRACT
Objective To investigate the protective effect of propofol on neurological function in rats after traumatic brain injury (TBI) and its possible mechanism.Methods A total of 96 SD rats were randomly divided into sham operation group,sham operation + propofol group,TBI group and TBI +propofol group,with 24 rats in each group.The TBI model was prepared by modified Feeney method.The sham operation + propofol group and the TBI + propofol group were given 50 mg/kg of propofol once daily.The sham operation group and the TBI group were injected with the same amount of normal saline.Modified neurobehavioral functional scores (mNSS) were evaluated at 1,3,7 and 14 days after injury;dry-wet specific gravity method was used to detect brain water content in injured area;TUNEL staining was used to detect neuronal apoptosis;chemiluminescence was used to detect activity of Oxygen cluster (ROS) content;Western blot was used to determine the expressions of inositol requirement enzyme 1 (IRE-1),enhancer binding protein homolog protein (CHOP),heme oxygenase 1 (HO-1,quinone oxidoreductase 1 (NQO1) and nuclear factor E2 related factor 2 (Nrf2) protein.Results Compared with the sham operation group and the sham operation + propofol group,the mNSS,brain tissue water content,apoptosis number and ROS increased at 1,3,7 and 14 days after TBI in the TBI group and TBI + propofol group (P ＜ 0.05).Compared with TBI group,mNSS in TBI + propofol group decreased significantly [(9.3 ± 1.4) points ∶ (10.9 ± 1.2) points] 7 days after injury (P ＜ 0.05);the brain tissue water content decreased significantly [(81.0 ± 0.8) ％ ∶ (82.1 ± 0.8) ％] 3 days after injury (P ＜ 0.05);the number of apoptotic cells decreased significantly 7 days after injury [(14.1 ± 1.4) ％ ∶ (15.6 ± 1.6) ％],with the most significant decrease at 14 days after injury [(10.4 ± 1.5) ％ ∶ (13.2 ± 1.4) ％ (P ＜ 0.05);and ROS decreased significantly 7 days after injury [(61.5 ± 4.0) RFU∶ (77.3 ± 5.5) RFU] (P ＜ 0.05).Compared with the sham operation group and the sham operation + propofol group,the expressions of IRE-1 and CHOP were significantly up-regulated in the TBI group and the TBI + propofolgroup (P ＜ 0.05);the expressions of HO-1,NQO1 and Nrf2 in the TBI group were significantly decreased (P ＜0.05);the expressions of HO-1 and NQO1 in TBI + propofol group were increased (P ＜0.05) while the expression of Nrf2 were decreased slightly (P ＜ 0.05).Compared with the TBI group,the expressions of IRE-1 and CHOP in TBI + propofol group were decreased (P ＜ 0.05),while the expressions of HO-1,NQO1 and Nrf2 were significantly increased (P ＜ 0.05).Conclusion After TBI in rats,propofol can reduce oxidative stress by activating the Nrf2-antioxidant element (ARE) pathway,reduce brain edema,and inhibit neuronal apoptosis,thus playing a neuro-protective role.
ABSTRACT
Objective@#To investigate the protective effect of propofol on neurological function in rats after traumatic brain injury (TBI) and its possible mechanism.@*Methods@#A total of 96 SD rats were randomly divided into sham operation group, sham operation+ propofol group, TBI group and TBI + propofol group, with 24 rats in each group. The TBI model was prepared by modified Feeney method. The sham operation+ propofol group and the TBI+ propofol group were given 50 mg/kg of propofol once daily. The sham operation group and the TBI group were injected with the same amount of normal saline. Modified neurobehavioral functional scores (mNSS) were evaluated at 1, 3, 7 and 14 days after injury; dry-wet specific gravity method was used to detect brain water content in injured area; TUNEL staining was used to detect neuronal apoptosis; chemiluminescence was used to detect activity of Oxygen cluster (ROS) content; Western blot was used to determine the expressions of inositol requirement enzyme 1 (IRE-1), enhancer binding protein homolog protein (CHOP), heme oxygenase 1 (HO-1), quinone oxidoreductase 1 (NQO1) and nuclear factor E2 related factor 2 (Nrf2) protein.@*Results@#Compared with the sham operation group and the sham operation + propofol group, the mNSS, brain tissue water content, apoptosis number and ROS increased at 1, 3, 7 and 14 days after TBI in the TBI group and TBI + propofol group (P<0.05). Compared with TBI group, mNSS in TBI+ propofol group decreased significantly [(9.3±1.4)points ∶(10.9±1.2)points] 7 days after injury (P<0.05); the brain tissue water content decreased significantly [(81.0±0.8)%∶(82.1±0.8)%] 3 days after injury (P<0.05); the number of apoptotic cells decreased significantly 7 days after injury[(14.1±1.4)%∶(15.6±1.6)%], with the most significant decrease at 14 days after injury [( 10.4±1.5)%∶(13.2±1.4)% (P<0.05); and ROS decreased significantly 7 days after injury [(61.5±4.0)RFU∶(77.3±5.5)RFU](P<0.05). Compared with the sham operation group and the sham operation+ propofol group, the expressions of IRE-1 and CHOP were significantly up-regulated in the TBI group and the TBI+ propofol group (P<0.05); the expressions of HO-1, NQO1 and Nrf2 in the TBI group were significantly decreased (P<0.05); the expressions of HO-1 and NQO1 in TBI+ propofol group were increased (P<0.05) while the expression of Nrf2 were decreased slightly (P<0.05). Compared with the TBI group, the expressions of IRE-1 and CHOP in TBI+ propofol group were decreased (P<0.05), while the expressions of HO-1, NQO1 and Nrf2 were significantly increased (P<0.05).@*Conclusion@#After TBI in rats, propofol can reduce oxidative stress by activating the Nrf2-antioxidant element (ARE) pathway, reduce brain edema, and inhibit neuronal apoptosis, thus playing a neuro-protective role.