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Abstract

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Ãé°üÀÇ °áÂûÈÄ¿¡ »ý±â´Â ÃéÀåÀ§ÃàÀÇ ±âÀüÀ» ±Ô¸íÇÏ°íÀÚ ¿µ¾ç»óÅ°¡ ¾çÈ£ÇÑ Æò±ÕüÁß 200
gmÁ¤µµÀÇ Sprague-DawleyÁ¾ ¹é¼­ 57¸¶¸®¸¦ ½ÇÇè¿¡ »ç¿ëÇÏ¿´´Ù. ½ÇÇ赿¹°µéÀº Ãé°üÀÇ ºÎºÐ
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1) ±¤ÇÐÇö¹Ì°æÀû ¼Ò°ßÀ¸·Î´Â, Ãʱâ¼Ò°ßÀ¸·Î °£Áú¼º ºÎÁ¾ ¹× ±¹¼ÒÀû ±«»ç°¡ 2ÀÏ°±îÁö °ü
ÂûµÇ°í, ¶Ç ÀÌ ½Ã±â¿¡ ¼±¹æ¼¼Æ÷³»ÀÇ zymogen granuleÀÇ °¨¼Ò, ¼¼Æ÷Áú³»ÀÇ °øÆ÷Çü¼º ¹× ÇÙ³ó
Ãà°ú ºÐÀýÀ» º¸ÀÌ°í, ¼±¹æ¼¼Æ÷ÀÇ ¼ö°¡ °¨¼ÒµÇ°í, ±×¸®°í ¼±¹æ¼¼Æ÷Áú³»¿¡ apoptoticbody°¡ Ãâ
ÇöÇÏ¿´´Ù. 5ÀÏ°¿¡´Â ¼±¹æ¼¼Æ÷°¡ ¼Ò½ÇµÇ°í ±× ÀÌÈÄ¿¡´Â °³Àç¼Ò°üµé (intercalated ducts)¸¸
³²¾Ò´Ù.
2) Åõ°ú ¹× ÁÖ»ç ÀüÀÚÇö¹Ì°æÀû ¼Ò°ßÀ¸·Î´Â, ¼±¹æ¼¼Æ÷ ³»¿¡ membrane-bounded apoptotic
body°¡ Ãé°ü°áÂûÈÄ 1ÀÏ° ºÎÅÍ ÃâÇöÇÏ¿© 3ÀÏ°¿¡ °¡Àå ÇöÀúÇÑ Áõ°¡¸¦ º¸¿´´Ù. À̵é
apoptotic body´Â ´ëºÎºÐ ÀÎÁ¢ÇÑ ´ë½Ä¼¼Æ÷³ª ȤÀº »óÇǼ¼Æ÷¿¡ ÀÇÇØ Å½½ÄµÇ¾î ÀÖ¾ú´Ù.
ÀÌ»óÀÇ ¼ºÀûÀ¸·Î ¹Ì·ç¾îº¸¾Æ Ãé°ü°áÂû ÈÄ¿¡ ¿À´Â ¼±¹æ¼¼Æ÷ÀÇ À§ÃàÀº apoptosis·Î ÀÎÇÑ ¼±
¹æ¼¼Æ÷ÀÇ °á½Ç(deletion)¿¡ ÀÇÇÑ °ÍÀ¸·Î »ç·áµÈ´Ù.
#ÃÊ·Ï#
This study was carried out to investigate the mechanisms of acinar cell deletion,
leading to the pancreatic atrophy of rat pancreas after experimental duct ligation.
Fifty-seven male Sprague-Dawley rats, maintained on a stock diet, weighing 200 gm, in
average, were divided into 2 experimental groups.
Group 1. Control group. Six rats. Abdominal cavity was opened and closed without
further treatment.
Group 2. Fifty-one rats. Animals were treated with partial ligation of the pancreatic
ducts according to the procedure developed by Hultquist followed by sequential sacrifices
at: 1 hour (3 rats), 3 hours (3 rats), 6 hours (6 rats), 12 hours (3 rats) and 24 hours (8
rats); 2 days (8 rats), 3 days (3 rats), 4 days (3 rats) and 5 days (5 rats); 1 week (3
rats), 2 weeks (3 rats) and 8 weeks (3 rats); after ligation. Distal part of the pancreas
of the animals after partial ligation was extirpated and examined by both light and
electron michoscopy.
The results obtained were as follows:
Light microscopically, noted were an interstitial edema and focal necrosis of the
pancreatic tissue along with fine vacuolization and depletion of the zymogen granules in
the acinar cell cytoplasms and condensation of the acinar cell nucleus. These changes
were observed by 2 days after ligation. At about the same time, one can observe the
dense body, identified to be apoptotic body, in the acinar cells which were found to be
decreased in quantity. By 5 days after ligation, no recognizable acinar cells left in the
collagenous stroma except intercalated ducts. Conspicuous stroma except intercalated
ducts. Conspicuous stromal hyalinization, thereafter
Electron microscopically (TEM and SEM), nuclear condensation and margination
toward the nuclear membrane was noted by 6 hours after duct ligation. By 24 hours
sporadic membrane-bounded apoptotic bodies appeared in the acinar cells, the number of
which reach. ins to the peak by 3 days after ligation. These apoptotic bodies were found
to be phagocytes by either intraepithelial mononuclear phagocytes or adjoining acinar
cells.
It can be concluded, therefore:
That orderly remodeling of pancreatic exocrine tissue during atrophy is effected by
rapid deletion of acinar cells by apoptosis.

Å°¿öµå

Apoptosis; Atrophy; Pancreatic duct ligation;

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