Influence of fenofibrate on tissue NF-KB, IL-6 and cell apoptosis in secondary brain injury after traumatic brain injury in rats
10.3760/cma.j.issn.1008-1372.2015.03.015
- VernacularTitle:非诺贝特对大鼠颅脑损伤后核转录因子、白细胞介素－6和细胞凋亡的影响
- Author:
Changzhong SUN
;
Yongqing WANG
;
Yujiang PENG
;
Bo SHAO
;
Zhi YU
- Publication Type:Journal Article
- Keywords:
Procetofen/PD;
Craniocerebral trauma/DT/ME/PA;
NF-kappa B/ME;
Interleukin-6/ME;
Apoptosis
- From:
Journal of Chinese Physician
2015;(3):372-375
- CountryChina
- Language:Chinese
-
Abstract:
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.
