RESUMO
Objective To investigate the changes of apoptosis-related proteins Fas, Caspase-3 andBd-2 expression in rat brain during morphine addiction. Methods A total of 48 adult male Sprague-Dawley rats, weighing 190-210 g, were randomly divided into 3 groups (n = 16): chronic morphine-dependent group, chronic morphine-abstinent group and control group. The rats in dependent group and abstinent group were chronically treated with morphine for 13 days to establish morphine dependent model. In the abstinent group, the withdrawal syndromes were induced with intraperitoneal injection of naloxone 5 mg/kg for 30 min. The control group was injected with normal saline. Immunohistochemistry and Western blotting analysis were used to examine the expression of Fas, Bcl-2 and Caspase-3 proteins. Results Compared with the control group, the other two groups had significantly increased expression of Fas and Caspase-3 (P<0.01) and significantly decreased expresssion of Bcl-2 (P<0.01) in the hippocampal synapse. Conclusion It is demonstrated that long term use of morphine can promote abnormal neuronal apoptosis in rat brain by enhancing the expression of pro-apoptotic Fas, Caspase-3 and decreasing the expression of anti-apoptotic Bcl-2, which might be one of the mechanisms for opiate-induced neuronal damage.
RESUMO
Objective To investigate the changes of apoptosis-related proteins Fas, Caspase-3 andBd-2 expression in rat brain during morphine addiction. Methods A total of 48 adult male Sprague-Dawley rats, weighing 190-210 g, were randomly divided into 3 groups (n = 16): chronic morphine-dependent group, chronic morphine-abstinent group and control group. The rats in dependent group and abstinent group were chronically treated with morphine for 13 days to establish morphine dependent model. In the abstinent group, the withdrawal syndromes were induced with intraperitoneal injection of naloxone 5 mg/kg for 30 min. The control group was injected with normal saline. Immunohistochemistry and Western blotting analysis were used to examine the expression of Fas, Bcl-2 and Caspase-3 proteins. Results Compared with the control group, the other two groups had significantly increased expression of Fas and Caspase-3 (P<0.01) and significantly decreased expresssion of Bcl-2 (P<0.01) in the hippocampal synapse. Conclusion It is demonstrated that long term use of morphine can promote abnormal neuronal apoptosis in rat brain by enhancing the expression of pro-apoptotic Fas, Caspase-3 and decreasing the expression of anti-apoptotic Bcl-2, which might be one of the mechanisms for opiate-induced neuronal damage.
