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ÈòÁãÀÇ Áö¿¬¼º ±¹¼Ò ³ú°æ»ö°ú À½¿µºÎ¿¡¼­ÀÇ ¼¼Æ÷ °í»ç¿Í p53, Bcl-2ÀÇ ¹ßÇö ¾ç»ó Apoptosis and the Expression of p53, Bcl-2 in Very Delayed Focal Cerebral Infarction and Penumbra

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Á¤Âù/Chan Chung ¹Ú½Â¿ø/±è¿µ¹é/Ȳ¼º³²/±è¹Ì°æ/±ÇÁ¤ÅÃ/¹Îº´±¹/¼®Á¾½Ä/ÃÖ´ö¿µ/Seung Won Park/Young Baeg Kim/Sung Nam Hwang/Mi Kyung Kim/Jeong Taik Kwon/Byung Kook Min/Jong Sik Suk/Duck Young Choi

Abstract

°á·Ð
ÈòÁã¿¡¼­ ÀÏ°ú¼º Ç÷°ü Æлö°ú Àç°ü·ù¸¦ ÀÌ¿ëÇÑ Áö¿¬¼º ±¹¼ÒÀû ³ú°æ»öÀ» À¯¹ßÇÑ ÈÄ ³ú°æ»ö
Áß½ÉºÎ¿Í ÁÖº¯ ³úÁ¶Á÷¿¡¼­ ¸é¿ªÁ¶Á÷È­Çп°»öÀ¸·Î ¼¼Æ÷ °í»ç¿Í p53 ¹× Bcl-2 ´Ü¹éÁú ¹ßÇö
¾ç»óÀ» Á¶»çÇÑ °á°ú ´ÙÀ½°ú °°Àº °á·ÐÀ» ¾òÀ» ¼ö ÀÖ¾ú´Ù.
1) ³ú°æ»öÈÄ ¼¼Æ÷ »ç¸Á¿¡ ¼¼Æ÷ °í»ç °úÁ¤°ú p53°ú Bcl-2 À¯ÀüÀÚ°¡ °ü¿©ÇÏ´Â °ÍÀ¸·Î º¸ÀÎ
´Ù.
2) ³ú°æ»ö½Ã ¼¼Æ÷ °í»ç´Â ³ú°æ»ö Á߽ɺÎÁß¿¡¼­ ¿Ü°ûºÎ¿¡ °¡Àå ½ÉÇÏ°Ô ÁýÁߵǾî ÀÖ¾ú´Ù.
3) ³ú°æ»ö°ú À½¿µºÎ¿¡¼­ÀÇ p53 ´Ü¹éÁú°ú Bcl-2 ´Ü¹éÁúÀÇ ¹ßÇö ¾ç»óÀ» °üÂûÇÑ °á°ú ³ú°æ»ö
½Ã p53ÀÇ ¼¼Æ÷ °í»ç À¯¹ßÀÛ¿ë¿¡ ¹ÝÇÏ¿© Bcl-2°¡ ±æÇ×Àû ¿ªÇÒÀ» ÇÏ´Â °ÍÀ¸·Î º¸À̸ç p53
Bcl-2ºñÀ²ÀÌ ³ú°æ»öÈÄ ¼¼Æ÷ °í»çÀÇ ¹ßÇö ¿©ºÎ¿Í À¯°üÇÔÀ» ¾Ë ¼ö ÀÖ¾ú´Ù.
3) ³ú°æ»ö½Ã p53 ´Ü¹éÁú ¹ßÇö ¿µ¿ªÀÇ ³ú°æ»ö Á߽ɺΠ¸éÀû¿¡ ´ëÇÑ ºñ´Â 2.3¡¾0.2·Î DWI¿Í
ATP ÃøÁ¤ ¹æ¹ýÀ¸·Î È®ÀÎÇÒ ¼ö ÀÖ´Â À½¿µºÎ¿Í ºñ½ÁÇÑ ¸éÀûºñ¸¦ º¸À̸ç p53 ¹ßÇöÀÇ ³úÇ÷·ù
·®°úÀÇ ¹Ýºñ·Ê °ü°è, p53´Ü¹éÁú ¾ç¼º¼¼Æ÷ÀÇ »ýÁ¸°¡´É¼º, ±×¸®°í p53 ´Ü¹éÁúÀÌ ³úÇ÷·ù·® Àú
ÇÏÀÇ Ãʱ⿡ ¹ßÇöµÈ´Ù´Â Á¡ µîÀ» °í·ÁÇÒ ¶§ ³ú°æ»öÈÄ p53 ´Ü¹éÁú ¹ßÇö ¿µ¿ªÀº À½¿µºÎÀÇ Á¶
°ÇÀ» °®Ãß°í ÀÖ´Â °ÍÀ¸·Î »ç·áµÈ´Ù.
³ú°æ»ö½Ã ¼¼Æ÷ °í»ç¿Í À¯ÀüÀÚ ¹ßÇö ¿µ¿ªÀÇ ¼öÄ¡Àû Á¢±ÙÀº ³ú°æ»ö À½¿µºÎ¿¡ ´ëÇÏ¿© ÃÖÃÊ·Î
½ÃµµµÇ´Â Á¤·®ÀûÀÎ °³³äÀ̸ç, °¢Á¾ ¾àÁ¦ ¹× ȯ°æ Á¶°Ç µîÀÌ ³ú°æ»ö¿¡ ¹ÌÄ¡´Â ¿µÇâÀ» ºñ±³ÇÒ
¼ö ÀÖ´Â ±âÃÊ ÀÚ·á·Î À¯¿ëÇÏ°Ô »ç¿ëÇÒ ¼ö ÀÖÀ» °ÍÀ¸·Î »ç·áµÈ´Ù. ±×·¯³ª ÇâÈÄ ºÎÀ§º° ³úÇ÷
·ù·® ¹× ¼¼Æ÷ °í»ç °ü·Ã À¯ÀüÀÚ ¹ßÇö ¿µ¿ª°úÀÇ ºñ±³¿Í p53À̳ª Bcl-2´Ü¹éÁú ÀÌ¿Ü¿¡ ¼¼Æ÷
°í»ç¿¡ ¿µÇâÀ» ÁÙ ¼ö ÀÖ´Â ´Ù¸¥ À¯ÀüÀÚ³ª Á¶Àý ÀÎÀÚ¿¡ ´ëÇÑ Á¶»ç°¡ ÇÊ¿äÇÒ °ÍÀ¸·Î »ç·áµÈ
´Ù.
#ÃÊ·Ï#
Apoptosis is a physiological or programmed cell death process controlled by genes,
which is thought to be one of the main mechanisms of cell death in cerebral infarction.
The apoptosis is controlled by several proto-oncogenes including p53 and Bcl-2 genes.
The purpose of this study is to evaluate how the apoptotic genes express in the focal
cerebral infarction and penumbra at very delayed focal cerebral infarction in adult rats.
In twelve adult Sprague-Dawley rats of both sex, the right middle cerebral
artery(MCA) and both common carotid arteries were ligated for thirty minutes and the
rats were killed after seventy-two hours to obtain a focal cerebral infarction.
Immunohistochemical stains for the apoptosis, p53, and Bcl-2 proteins were performed.
The thickness(§­) and the area(mm2) of the infarction core and periinfarct
areas containing apoptotic cells, p53, or Bcl-2 protein were measured. The apoptosis,
p53, and Bcl-2 positive cells were counted, and the p53 : Bcl-2 ratio was calculated at
each sector.
The p53 area was the widest(6.8¡¾2.4mm2) and the apoptosis area was
the narrowest(3.1¡¾2.1mm2). The apoptotic cells were mostly concentrated
in the peripheral portion of the infarction core(6.1¡¾3.7/HPF). The p53 positive cells were
mostly concentrated(26.6¡¾8.0/HPF) in the adjacent periinfarct area with a gradual
decrease peripherally, and it seemed that p53 expression was reversely proportional to
the regional cerebral blood flow(rCBF). The p53 : Bcl-2 ratio was significantly higher at
the apoptosis-positive zone(3.3¡¾2.7) compared with the apoptosis-negative zone(2.2¡¾
1.8)(p<0.05). From these results, it could be postulated that the proapoptotic action of
the p53 protein and the antiapoptotic action of Bcl-2 protein were closely interactive in
the periinfarct area. These data indicate that the p53 protein positive area might be
compatible with the penumbric area of cerebral infarction.

Å°¿öµå

Apoptosis; Cerebral infarction; p53; Bcl-2; Penumbra;

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