Early Treatment of AICAR Protects Hypoxia-ischemia Brain Injury in Neonatal Rats
10.3870/j.issn.1004-0781.2016.09.008
- VernacularTitle:早期应用 AICAR 对缺氧缺血性脑病新生大鼠的保护作用
- Author:
Zhihui RONG
;
Wei LIU
;
Wenbin LI
;
Baohuan CAI
;
Dong LIU
- Publication Type:Journal Article
- Keywords:
5-Aminoimidazole-4-carboxamide ribonucleotide formyltransferase/ IMP cyclohydrolase;
Adenosine monophosphate activated protein kinase;
Encephalopathy,hypoxia-ischemia;
Neuron
- From:
Herald of Medicine
2016;35(9):943-946
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the neuroprotective effects and mechanisms of 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/ IMP cyclohydrolase(AICAR) supplement (AMPK activator) in different stages of neonatal rats sufferring from hypoxia-ischemia encephalopathy ( HIE). Methods Neonatal rat hypoxia-ischemia brain injury model was employed in this study. A total of 160 neonatal rats were distributed into five groups: sham, model control,AICAR30 min, AICAR24 h and AICAR72 h. The neuroprotective effects of AICAR supplement (30 min, 24 h, 72 h post operation) were compared by cresyl violet staining; Expressions of P-AMPK,AMPK in the brain tissue were measured by Western blotting.Foot-faults method was used to evaluate the long-term prognosis of the rats. Results Compared with the sham group, the survival of rats brain in model control group was significantly decreased [(100.0± 0.1)% and (45.3± 6.3)%, P< 0.05]. AICAR had neuroprotective effects when treated at 30 min and 24 h post operation,while the protective effects disappeared when treated later (72 h post operation) (P>0.05). Compared with the sham group, the expression of P-AMPK significantly increased about three times, while ATP level decreased close to the same. Conclusion Early AICAR treatment can protect hypoxia-ischemia brain injury by increasing AMPK-ATP level.
