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RISS 인기검색어
- 검색키워드
- 저자 : 제갈승주 ( Seung Joo Jakal ) (검색결과 3 건)
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샤염화탄소 투여 쥐에서 아연이 간세포의 아포토시스와 TGF-ßl 분바에 미치는 영향
제갈승주 ( Seung Joo Jakal ),김은정 ( Eun Jung Kim ),최영자 ( Young Ja Choi ),곽효일 ( Hyo Il Kwak ),노종섭 ( Jong Sup Rho ),신용섭 ( Yong Sup Shin ),김진경 ( Jin Kyung Kim ) 대한임상검사과학회 2002 대한임상검사과학회지(KJCLS) Vol.34 No.2
Recently zinc has been known as a beneficial agent in the protection against hepatotoxicity and Its effect was supposed due to decreased hepatic cel1 apoptosis by the inhibition of endonuclease activity. Meanwhile, Transfonning growth factor-ßl (TGF-ßl) was considered an important regu1ator in the pathogenesis of early hepatic fibrosis. The aim of this study was to ascertain the effect of zinc on hepatic cell apoptosis and TGF-ß lsecretion in early hepatic fibrosis induced by carbon tetrachloride (CC4). Twenty male Wistar rats were divided into four groups: the control group, control + zinc treated group, CC14 treated group and CC4 +zinc treated group. All the rats were sacrified 8 days later for histological and biochemical assessments. The col1agen content in liver was measured after Masson’s trichrome staining, apoptosis was detected by terminal UDP-nick end labelling (TUNEL) staining and TGF-ßl was quantified by labelled streptavidin biotin (LSAB) immunostaining using a computerized image analysis system. TUNEL-positive cells (apoptotic cel1s) increased in rats with early hepatic fibrosis and oral zinc administration decreased the number of apoptotic cells in the CC14-treated rats. The zinc-mediated decrease of apoptosis in the liver was related to an increase of TGF-ßl positive cel1s and col1agen content. However, AST, ALT levels and the number of fatty changed hepatic cel1s as an index of hepatic cell damage increased in rats with early hepatic fibrosis and two indices decreased by zinc administration. These results suggest that apoptosis may be involved, together with necrosis, in the early hepatic fibrogenesis and was closely related to the increase of TGF-ß 1 secretion and collagen content. Therefore, zinc could play an important role in the inhibition of early hepatic fibrosis induced by CC4
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Helicobacter pylori 위염에서의 비만세포와 염증반응과의 관련성
제갈승주 ( Seung Joo Jakal ) 대한임상검사과학회 2000 대한임상검사과학회지(KJCLS) Vol.32 No.3
Helicobacter pylori(H. pylori) induces severe inflammation and plays a key role in gastric mucosal disease. In general, mast cells are well known as initiators and regu1ators of inflammation, but their role in the gastric mucosal inflammation caused by H. pylori still remains unclear. πlerefore, this study was performed to investigate the differences of number of mast cell and mast cell degranulation in gastritis with and without H. pylori infection. Endoscopic biopsy specimens from 21 H. pylori-positive and 19 H. pylori-negative subjects were examined. The sections were cut from routine1y forma1in-fixed and paraffm embedded tissues, and stained with hematoxylin-eosin(HE), Warthin-Starry(WS) and 0.5% toluidine blue(TB) respective1y. HE-and WS-stained sections were assessed for inflammation and infection, and TB-stained sections were used in mast cell counting. The mast cells were quantificated the numbers per square millimeter using a computerized image analysis system. Mean number of mast cell and degranulated mast cell were significant1y higher in the mucosa with H. pylori infection than in the mucosa of noninfected gasπitis subjects. πlese also correlated significant1y with the inflammatory intensity Thus, mast cells may be important effector cells in the pathogenesis of H. pylori infected gastritis.
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사염화탄소 유도 간섬유증 발생에 었어서 비만세포와 근섬유모세포의 상호 관련성
제갈승주 ( Seung Joo Jakal ) 대한임상검사과학회 2001 대한임상검사과학회지(KJCLS) Vol.33 No.2
Hepatic fibrosis is known to be developed by producing the extracellular matrices from myofibroblasts(a-SMA postive cells) that are transformed from hepatic satellite cells. The development of the fibrotic process is thought to be mediate by various fibrogenic mediators. Recent1y, several studies have suggested that mast cells participate in the development of the hepatic fibrosis in human liver diseases and in rodent models. But The close relation between mast cells and myofibroblasts in the development of hepatic fibrosis remains still llllclear. In this study We have investigated the change of collagen content, the disπibution and density of mast cells and myofibrobalsts during 2, 4, 6-week after carbon tetrachloride treatment in rat. Twenty male Wistar rats were divided into four groupsincluding control. Hepatic fibrosis was induced by intraperitoneal injection of carbon tetrachloride(CC14) in rats. πle degree of fibrosis was evaluated by measuring the hydroxyproline content(ugjg tissue) of the liver as an index of the collagen content and by using a numerical scoring system for grading hepatic fibrosis in the liver sections stained with Masson trichrome and Gomori reticulum, respectively. The density of mast cells (number/mmj was determined by cOllllting mast cells using a computerized image analyser system in liver sections stained with toluidine blue and alcian blue-safranin O, respectively. Also, πle morphological relation between mast cells and myofibloblasts was examined by elecπon microscopy. πle c이lagen content was significant1y increased at 4 to 6week after CC4 treatment compared with control rats. These results showed significant correlations (Spe따man’ s,r=O.76, p<0.001) with those of a numerical scoring system. In control rats, mast cells were found principally in portal areas, and their average density was 4.76 i= 2.23/ MM2 in liver sections stained with alcian blue-safranin O. Whereas in CC4-treated rats mast cells were diffusely distributed in fibrous septa and fibrous capsule on liver surface and were significantly increased at 2(8.86 i= 1.94/mnf), 4(12.26 i= 3.59/mm2 to 6week(28.09 i= 12.74/ mm2)after CC4 treatment compared with control rats. In cαltrol rats, myofibroblasts were not found in portal areas and observed only Q-SMA positive staining on vessel walls in portal areas. In CC4-treated rats, myofibroblasts were occasionally found at 2week after CC4 treatment in portal areas, fibrous septa and liver parencyma, but were statistically not significant compared with control rats. Myofibrobasts were significantly increased at 4 to 6week after CC4 treatment. U1trastructurally, mast cel1s were observed in close contact with myofibroblasts in fibrous septa and showed the various stages of degranulation. πlese results suggested that mast cell may play role in deve10pment of hepatic fibrosis, probably because of the production of extracellular maπix components by myofibroblasts which activate by some mediators released from mast cells.
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