Effect of ulinastatin on isoflurane-induced neuronal apoptosis in the hippocampus of rats.
10.12122/j.issn.1673-4254.2019.07.16
- Author:
Yuanbo GUO
1
;
Yan WANG
2
;
Dengwen ZHANG
1
;
Can CUI
1
;
Tao LI
3
;
Sheng WANG
1
Author Information
1. Department of Anesthesiology of Medical Sciences, Guangzhou 510080, China.
2. Department of Science and Education, Guangdong Provincial People's Hospital/Guangdong Academy of Medical Sciences, Guangzhou 510080, China.
3. Department of Critical Care Medicine, Chenzhou First People's Hospital, Chenzhou 423000, China.
- Publication Type:Journal Article
- Keywords:
apoptosis;
hippocampus;
isoflurane;
mitochondria;
ulinastatin
- MeSH:
Animals;
Apoptosis;
Glycoproteins;
Hippocampus;
Isoflurane;
Male;
Rats;
Rats, Sprague-Dawley
- From:
Journal of Southern Medical University
2019;39(7):850-854
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect of ulinastatin pretreatment on isoflurane-induced mitochondria-dependent neuronal apoptosis in the hippocampus of rats.
METHODS:Thirty-six male SD rats were randomly assigned into control group, isoflurane group and ulinastatin group. In the latter two groups, the rats were subjected to acute exposure to 0.75% isoflurane for 6 h and pretreated with 50 000 U/kg of ulinastatin before isoflurane exposure, respectively. After the treatments, apoptosis of the hippocampal neurons was detected using TUNEL assay, and the mitochondrial membrane potential (△ ψm) was measured using JC-1 mitochondrial membrane potential kit; cytochrome C release and caspase-3 activity were examined with Western blotting, and intracellular reactive oxygen species (ROS) was detected using the fluorescent probe H2DCFDA.
RESULTS:Compared with those in the control group, the rats with acute exposure to isoflurane showed markedly increased TUNEL-positive cells in the hippocampus ( < 0.05), which were obviously reduced by ulinastatin pretreatment ( < 0.05). The △ψm of the hippocampal neurons was significantly reduced after isoflurane exposure ( < 0.05), and was partly recovered by ulinastatin pretreatment ( < 0.05). Acute exposure to isoflurane resulted in obviously increased cellular ROS, cytochrome C release and caspase-3 activity in the hippocampal neurons ( < 0.05), and these changes were significantly inhibited by ulinastatin pretreatment ( < 0.05).
CONCLUSIONS:Ulinastatin pretreatment provides neuroprotection against isoflurane-induced apoptosis of the hippocampal neurons in rats possibly by inhibiting mitochondria-dependent apoptosis pathway.
