[Gly14]-Humanin inhibits oxidative stress levels and controls apoptosis after traumatic brain injury in ;rats
10.3969/j.issn.1002-0152.2016.03.011
- VernacularTitle:[Gly14]-Humanin减轻大鼠颅脑外伤后氧化应激及细胞凋亡
- Author:
Zheng LIN
;
Zhi YU
;
Bo ZENG
;
Kang YIN
- Publication Type:Journal Article
- Keywords:
Traumatic brain injury Secondary brain injury;
[Gly14]-Humanin;
Oxidative stress;
Apoptosis
- From:
Chinese Journal of Nervous and Mental Diseases
2016;42(3):180-183
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of [Gly14]-Humanin(HNG) on SOD, MDA, GSH and cell apopto?sis in a rat model of secondary brain injury. Methods One hundred thirty-five adult and healthy male rats were random?ly divided into 3 groups: sham model group (n=45), vehicle control group (n=45) and HNG group (n=45). Secondary brain injury was induced in the vehicle control and HNG groups using improved Feeney method. Vehicle control received abdominal injections of Sodium Chloride Injection (2 ml/kg) whereas the HNG group received abdominal injections of HNG (2 μL/kg) immediately and 24 h after injury. Each group was divided into three subgroups (n=15 rats per each group) by sacrificed time including 1 h, 3 d, and 7 d after injury. The expression levels of SOD, MDA and GSH of the brain tissue were analyzed and the cell apoptosis was examined using TUNEL method after brain contusion. Results MDA and cell apoptosis around the lesion started to increased at 1h, reached a peak at 3d and then gradually subsided but still remained a higher level at 7 d than 1 h. HNG significantly attenuated brain injury-induced increase in MDA and apopto?sis at all time points (P<0.05). By contrast, SOD started to decrease at 1h, reached the lowest point at 3 d and then gradu? ally recovered but still remained a lower level at 7 d than 1 h. HNG significantly mitigated brain injury-induced increase in MDA and apoptosis at all time points (P<0.05). The time course of GSH expression followed a pattern similar to that of MDA. MDA expression was strongly positive correlated with the number of cell apoptosis (r=0.720, P<0.05), strongly neg?ative correlated with the level of SOD and GSH(r=-0.702, P<0.05;r=-0.674, P<0.05). Conclusions After brain injury, HNG inhibits oxidative stress levels and reduces apoptosis, thereby mitigating secondary brain injury.
