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The Korean Journal of Pathology 2000;34(1): 1-10.
Gender Differences in Expression of Apoptosis, p53, and Bcl-2 in Delayed Focal Cerebral Infarction in Rats.
Hee Suk Jung, Seung Won Park, Sung Nam Hwang, Young Bak Kim, Mi Kyung Kim, Byung Kuk Min, Jung Taik Kwon, Duck Young Choi, Jong Sik Suk
1Departments of Neurosurgery , Chung-Ang University Hospital, Seoul 140-757, Korea.
2Departments of Pathology, Chung-Ang University Hospital, Seoul 140-757, Korea.
ABSTRACT
Apoptosis is a normal physiological process. Morphological studies have shown that cells die by physiological mechanisms after undergoing characteristic changes termed 'apoptosis' or 'programmed cell death'. Several genes were known to participate in the apoptotic process including p53 as a proapoptic gene and Bcl-2 as an antiapoptic gene. It was also known that there are certain gender differences in the cerebrovascular accidents and their effect on tissue damage. The purpose of this study is to evaluate how the apoptotic genes are expressed in delayed focal cerebral infarction and peri-infarct area in male and female adult rats by comparing the immunoexpression of p53 and Bcl-2 and p53:Bcl-2 ratio at delayed focal cerebral infarction between both sexes. In sixteen adult Spraugue-Dawley rats (nine males and seven females), the right MCA and both CCA were ligated for thirty minutes to make a delayed focal cerebral infarction in right frontal lobe. Their brains were taken at seventy two hours after the operation. And then the brains were prepared for immunohistochemical stains for apoptosis, p53 and Bcl-2 proteins. The infarction volume of male rats (11.3 mm3) was larger than that of female rats (7.3 mm3) (p<0.01). In male group, the width (micrometer2) of the apoptotic area (46.4 micrometer2) was significantly larger than those in female group (38.9 micrometer2) (p<0.005). The p53 : Bcl-2 ratio was significantly higher in male group (3.23) compared with female group (2.18) (p<0.01). As a result, the p53:Bcl-2 ratio seemed to be related to the gender differences in neuronal apoptosis after delayed focal cerebral infarction.
Key Words: Delayed focal infarction; Apoptosis; Bcl-2; p53