The expression and modulation of Bax in brain tissue of neonatal rats with hyperbilirubinemia
10.3760/cma.j.issn.2096-2932.2018.02.016
- VernacularTitle:高胆红素血症新生大鼠脑组织Bax表达及干预研究
- Author:
Shirun WU
1
;
Huaiqing YIN
;
Weiwei LI
;
Dan BAI
;
Li XIA
;
Yiyang DU
;
Rong LIU
;
Shan ZHU
Author Information
1. 030001太原,山西医科大学第一医院儿科
- Keywords:
Hyperbilirubinemia;
Gangliosides;
Apoptosis;
Bax
- From:Chinese Journal of Neonatology
2018;33(2):142-146
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the influence of GM1 on hyperbilirubinemia-induced brain injury in neonatal rats and its possible mechanism.Method A total of 120 7-day-old Sprague-Dawley (SD) rats were randomly assigned into normal control group (n =40),hyperbilirubinemia group (n =40) and GM1 group (n =40).According to the different duration of hyperbilirubinemia,each group was further assigned into 5 subgroups,6 h,12 h,24 h,48 h and 72 h group (n =8).The model of neonatal rat with hyperbilirubinemia was established injecting bilirubin solution (100 μg/g) intraperitoneally.GM1 (10 mg/kg) was injected intraperitoneally immediately after the model was established in GM1 group.Immunohistochemical method was used to determine the expression of Bax in hippocampus.TUNEL method was used to measure the neural cell apoptosis index (AI) in the brain.Result Six hours after the hyperbilirubinemia model was set up,the expression of Bax and AI in hyperbilirubinemia group and GM1 group were examined.The median of AI were 33.5％ and 15.4％ respectively and the average grey value of Bax positive cells were 157.4 ± 2.8 and 162.9 ± 2.3.Both apoptosis cells and the expression of Bax were gradually increasing,and peaked at 72 h after the model was established.The median of AI were 55.5％ and 35.5％ respectively,and the average grey value of Bax positive cells were 127.8 ± 3.6 and 141.5 ±2.7 in hyperbilirubinemia group and GM1 group.And the expressions of Bax and AI in the control group were nearly undetectable.The expression of Bax and AI in GM1 group were lower than hyperbilirubinemia group,but higher than the control group,the differences were statistically significant (P ＜ 0.001).Conclusion Brain cells apoptosis is influenced by hyperbilirubinemia-induced brain injury and Bax may be involved in the process.GM1 may reduce the brain damage by inhibiting the expression of Bax to reduce the apoptosis of the brain cells.
