Résumé
Objective To investigate the changes of NF-κB p65, IL-6 and cell apoptosis in sec-ondary brain injury after traumatic brain injury and the influence of fenofibrate on these parameters in rats. Methods Ninety-eight male Sprague-Dawley ( SD) rats were randomly divided into two groups:fenofibrate group ( n =49) and control group ( n =49) .The fenofibrate group was induced with the improved Feeney method and received intragastrica of lipanthyl 60 mg/(kg? d) immediately after injury.The control group were received intragastrica of sodium chloride injection 2 ml/( kg? d) immediately after injury and twice everyday until rats were killed.Each group was divided into seven subgroups by sacrificed time after injury, those were 1 h, 3 h, 6 h, 12 h, 24 h, 3 d, and 7 d, and each subgroup got 7 rats.Each subgroup was ran-domly selected three rats after being killed to detect expressions of NF-κB p65 and IL-6 of rat contusion peri tissues brain tissues with immunohistochemical method.While using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling ( TUNEL) method was used to observe the peri cell apoptosis after brain contusion.Results The expressions of NF-κB p65 and the IL-6 in each fenofibrate group were significantly decreased relative to the control group ( P <0.05),and a significant positive correlation between both pa-rameters in two groups ( P <0.01) .At the same time, the number of apoptotic cells was decreased ( P <0.05).Conclusions Fenofibrate was probably through the route of relieving inflammation response to re-duce the change of secondary brain injury after traumatic brain injury and decrease neural cell apoptosis, and then provide protection of neurocytes.
Résumé
Objective To examine the effects and mechanisms of simvastatin and fenofibrate, and combination of the two drugs on the expression of apolipoprotein M (apoM). Methods The male C57BL/6N mice ( n =32) were random divided into four groups, including control group (with no special treatment), statin group (with simvastatin [10mg/( kg · d) for 4 weeks], fibrate group (with fenofibrate [100mg/( kg · d) for 4 weeks] and combination group ( with simvastatin [10mg/( kg· d)] and fenofibrate [100mg/( kg · d) for 4 weeks]. The levels of apoMmRNA and protein, hepatic nuclear factor (HNF-1α)mRNA, liver X receptor-α (LXRα) mRNA in mouse liver were measured. Results Both of simvastatin and fenofibrate can increase the expression of apolipoprotein M ( 1.97 ± 0. 04,2. 02 ± 0. 02 ) and HNF-1αmRNA ( 1.74 ± 0. 05,1.71 ± 0. 04). Combination group obtained more effects than either single agent ( P < 0. 05 ). Simvastatin could decrease the expression of LXRα mRNA ( 1.00 ± 0. 02 ) ( P < 0. 05 ). Fenofibrate could increase the expression of LXRα mRNA(2. 80 ±0. 04) ( P <0. 05). No significant difference in LXRα expression was seen between combination( 1.56 ±0. 03 ) and control group( 1.53 ±0. 03 )( P >0. 05). Conclusions Simvastatin and fenofibrate can increase apoM expression. Treatment with combination of the two drugs is more effective, and the mechanism might be related to the regulation of HNF-1α and LXRα.