中国地方病学杂志
中國地方病學雜誌
중국지방병학잡지
CHINESE JOURNAL OF ENDEMIOLOGY
2011年
4期
368-370
,共3页
张晓丽%董云霞%韩甦%答嵘%李懿宏%舒晶%张凤民
張曉麗%董雲霞%韓甦%答嶸%李懿宏%舒晶%張鳳民
장효려%동운하%한소%답영%리의굉%서정%장봉민
肝吸虫%感染%凋亡%肝细胞
肝吸蟲%感染%凋亡%肝細胞
간흡충%감염%조망%간세포
Clonorchis sinensis%Infection%Apoptosis%Hepatoeyte
目的 分析肝吸虫感染大鼠和肝吸虫病患者肝组织的病理改变及损伤情况,探讨细胞凋亡在肝吸虫感染所致肝损伤中的作用.方法 将Wistar大鼠分为2组:感染组60只,对照组20只.感染组大鼠经口饲感染囊蚴法建立肝吸虫感染模型,对照组大鼠采用生理盐水灌胃.于感染后第4、6、8、12周时处死动物.同时收集尸检获得的肝吸虫病患者及健康对照人体肝组织标本各4例.光镜下观察大鼠和人体肝吸虫感染情况以及肝组织的病理学改变;并用TUNEL法检测肝细胞的凋亡率.结果 光镜下各时间点感染组大鼠和肝吸虫病患者胆管壁增厚,胆管黏膜呈乳头状和腺瘤样增生,管腔内可见虫体及虫卵,胆管周围可见炎细胞浸润和少量纤维组织增生,汇管区周围有一些肝细胞出现核固缩,呈现细胞凋亡的形态特征.感染组大鼠第4、6、8、12周时肝细胞凋亡率分别为(7.15±1.50)%、(11.61±3.09)%、(13.21±3.47)%、(11.26±4.06)%,均明显高于对照组[(2.57±0.72)%、(3.17±0.77)%、(3.67±0.96)%、(2.84±0.87)%,t值分别为4.45、5.49、5.95、4.74,P均<0.01].肝吸虫病患者肝组织细胞凋亡率为(12.02±1.78)%,明显高于对照组[(2.03±0.68)%,t=15.13,P<0.01].结论 肝吸虫感染可以引起宿主肝细胞凋亡,后者可能与感染者肝损伤有关.
目的 分析肝吸蟲感染大鼠和肝吸蟲病患者肝組織的病理改變及損傷情況,探討細胞凋亡在肝吸蟲感染所緻肝損傷中的作用.方法 將Wistar大鼠分為2組:感染組60隻,對照組20隻.感染組大鼠經口飼感染囊蚴法建立肝吸蟲感染模型,對照組大鼠採用生理鹽水灌胃.于感染後第4、6、8、12週時處死動物.同時收集尸檢穫得的肝吸蟲病患者及健康對照人體肝組織標本各4例.光鏡下觀察大鼠和人體肝吸蟲感染情況以及肝組織的病理學改變;併用TUNEL法檢測肝細胞的凋亡率.結果 光鏡下各時間點感染組大鼠和肝吸蟲病患者膽管壁增厚,膽管黏膜呈乳頭狀和腺瘤樣增生,管腔內可見蟲體及蟲卵,膽管週圍可見炎細胞浸潤和少量纖維組織增生,彙管區週圍有一些肝細胞齣現覈固縮,呈現細胞凋亡的形態特徵.感染組大鼠第4、6、8、12週時肝細胞凋亡率分彆為(7.15±1.50)%、(11.61±3.09)%、(13.21±3.47)%、(11.26±4.06)%,均明顯高于對照組[(2.57±0.72)%、(3.17±0.77)%、(3.67±0.96)%、(2.84±0.87)%,t值分彆為4.45、5.49、5.95、4.74,P均<0.01].肝吸蟲病患者肝組織細胞凋亡率為(12.02±1.78)%,明顯高于對照組[(2.03±0.68)%,t=15.13,P<0.01].結論 肝吸蟲感染可以引起宿主肝細胞凋亡,後者可能與感染者肝損傷有關.
목적 분석간흡충감염대서화간흡충병환자간조직적병리개변급손상정황,탐토세포조망재간흡충감염소치간손상중적작용.방법 장Wistar대서분위2조:감염조60지,대조조20지.감염조대서경구사감염낭유법건립간흡충감염모형,대조조대서채용생리염수관위.우감염후제4、6、8、12주시처사동물.동시수집시검획득적간흡충병환자급건강대조인체간조직표본각4례.광경하관찰대서화인체간흡충감염정황이급간조직적병이학개변;병용TUNEL법검측간세포적조망솔.결과 광경하각시간점감염조대서화간흡충병환자담관벽증후,담관점막정유두상화선류양증생,관강내가견충체급충란,담관주위가견염세포침윤화소량섬유조직증생,회관구주위유일사간세포출현핵고축,정현세포조망적형태특정.감염조대서제4、6、8、12주시간세포조망솔분별위(7.15±1.50)%、(11.61±3.09)%、(13.21±3.47)%、(11.26±4.06)%,균명현고우대조조[(2.57±0.72)%、(3.17±0.77)%、(3.67±0.96)%、(2.84±0.87)%,t치분별위4.45、5.49、5.95、4.74,P균<0.01].간흡충병환자간조직세포조망솔위(12.02±1.78)%,명현고우대조조[(2.03±0.68)%,t=15.13,P<0.01].결론 간흡충감염가이인기숙주간세포조망,후자가능여감염자간손상유관.
Objective To investigate the liver injury and pathological changes of rat and patients with Clonorchis sinensis(C, sinensis) infection, and to clarify the role of apoptosis in the injury induced by C. sinensis.Methods Wistar rats were divided into two group: 60 in infection group and 20 in control. The rats in infection group were infected with C. sinensis via oral feeding encysted cercaria;rats in control group were fed with normal saline. The rats were sacrificed 4, 6, 8 and 12 weeks after infection, respectively. Liver tissue specimens of the patients infected with C. sinensis were collected. The pathological changes of liver tissue were observed by light microscopy and the apoptofic rate of hepatocyte was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling(TUNEL) assay. Results Parasites and eggs could he seen around the bile duct, and the duct was associated with mucosa and adenoma papillary hyperplasia, wall thickening, inflammatory cell infiltration, a small amount of fibrous tissue hyperplasia, and periportal liver cells surrounded by a number of nuclear condensation, all these changes meant morphological characteristics of apoptosis. Apoptotic rates of liver cells in infection group 4, 6,8 and 12 weeks after infection were (7.15 ± 1.50)%,(11.61 ± 3.09)%,(13.21 ± 3.47)% and (11.26 ± 4.06)%,respectively, which was significantly higher than that in control group [(2.57 ± 0.72)%, (3.17 + 0.77)%, (3.67 ±0.96)% and (2.84 ± 0.87)%, t values were 4.45, 5.49, 5.95 and 4.74, respectively, all P < 0.01]. Conclusions These findings indicate that C, sinensis can stimulate both hepatoeytic apoptosis and degeneration which may he related to clinical manifestations and liver lesions in patients with clonorchiasis.
