Effects of L-tetrahydropalmatine on the expressions of bcl-2 and bax in rat after acute global cerebral ischemia and reperfusion.
- Author:
Bin LIU
1
;
Guangtian YANG
Author Information
1. Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
drug effects;
Berberine Alkaloids;
pharmacology;
Brain Ischemia;
metabolism;
pathology;
Neurons;
pathology;
Proto-Oncogene Proteins c-bcl-2;
biosynthesis;
genetics;
RNA, Messenger;
biosynthesis;
genetics;
Random Allocation;
Rats;
Rats, Wistar;
Reperfusion Injury;
metabolism;
pathology;
bcl-2-Associated X Protein;
biosynthesis;
genetics
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2004;24(5):445-448
- CountryChina
- Language:English
-
Abstract:
To investigate the effects of L-Tetrahydropalmatine (L-THP) on the expressions of bcl-2, bax and neuronal apoptosis after cerebral ischemia and reperfusion, 60 Wistars rats were randomly divided into 3 groups: sham-operation group (group S, n = 20), ischemic-reperfusion group treated with saline (group I, n = 20) and ischemia-reperfusion group treated with L-THP (group T, n = 20). The rat model of global cerebral ischemia and reperfusion was induced by Pulsinelli's four-vessel occlusion method. The expression of bcl-2 and bax mRNA was detected by in situ hybridization and reverse transcriptional polymerase chain reaction (RT-PCR). The number of apoptotic neurons was examined by terminal deoxynucleotidyl-transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) method. Compared with group S, the expression of bcl-2 and bax mRNA in group I was increased significantly (P<0.01), and the number of apoptotic neurons increased either (P< 0.01). After L-THP treatment, the expression of bcl-2 mRNA was up-regulated (P< 0.01) and that of bax mRNA was down-regulated (P<0.01); the number of apoptotic neurons was decreased (P<0.01). Our results indicated that bcl-2 may suppress apoptosis and bax promote apoptosis after cerebral ischemia and reperfusion. L-THP could ameliorate cerebral ischemia and reperfusion damage by reducing the apoptosis through regulating bcl-2 and bax.
