The Effect of Duration of Ischemia and Body Temperature on the Expression of Bax/Bcl-2 in Transient Global Ischemia

Lee, Yong Seok; Park, Seong Ho; Yoon, Byung Woo; Roh, Jae Kyu

Abstract

BACKGROUND: Transient global ischemia causes delayed neuronal death (DND) in the CA1 area, of which the mecha-nism is controversial. Induction of apoptosis-regulating proteins during the process of DND has been reported, howev-er ,the exact role of Bcl-2/Bax is not well understood. We tried to reveal the pattern of the Bax/Bcl-2 expression modi-fied by the duration of ischemia and hypothermia.
METHODS
Global ischemia was induced in Mongolian gerbils for 2, 5, and 10 minutes under the temperature of 36 degrees C and 32 degrees C. Hippocampal sections were evaluated 48 hours after ischemia with H&E and immunohistochemical staining to Bcl-2/Bax. Viable neuronal density and semi-quantitative grading were compared.
RESULTS
In the CA1 area, neurons were intact in 2 min ischemia, while partial or significant ischemic changes were observed in 5-10 min ischemia of 36 degrees C setting, which were less severe in 32 degrees C . Bcl-2 was posi-tive in 2 min ischemia, while negative in 5~10 min ischemia of 36 degrees C . Bax was negative in 2 and 10 min ischemia, while positive in 5 min ischemia. In 32 degrees C setting, Bcl-2 was also positive in 2 min ischemia and partially positive in 5- 10 min ischemia, although Bax expression was not different from 36 degrees C.
CONCLUSIONS
The complex mechanism of DND, which is in the spectrum of apoptosis and necrosis, seems to be determined by the severity of ischemia. The bal-ance between Bcl-2 and Bax may determine the survival of neurons in mild to moderate ischemia. Further evidence remains to be determined by morphological and molecular biological methods.