The regulation of apoptosis by Bcl-2, bcl-X(L), Bcl-2alpha and Bax in chronic liver disease]

OBJECTIVE: To analyse the expression of Fas and Fas ligand (FasL) in patients of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma and to study the regulation of apotosis by Bax and Bcl-2 subfamilies. METHODS: The subfamily of Bcl-2 in the liver tissue was studied by immunohistochemistry. RESULTS: In 156 cases of chronic liver disease the expression levels of Fas and FasL in the chronic hepatitis group were significantly higher than that in hepatocellular carcinoma group(P < 0.01). The expression level of Bax subfamily in the chronic hepatitis group was significantly higher than that of Bcl-2 subfamily. CONCLUSION: It is suggested that Bcl-2 family is involved in the regulation of apoptosis in the chronic liver diseases.     

慢性肝病中凋亡蛋白Bcl-2、Bcl-XL、Bcl-2α、Bax的调节作用

目的 探讨凋亡蛋白Ｂｃｌ－２家族中Ｂａｘ及Ｂａｘ－２两个亚族各在慢性肝炎、肝硬化及肝癌发生、发展中对凋亡的调节作用。方法 １５６例慢性肝病患者中,慢性肝炎７２例,肝硬化２９例,肝癌５５例,采用免疫组化染色检测以上两亚族凋亡蛋白在其肝组织中的表达。结果 慢性肝炎组Ｆａｓ及Ｆａｓ配体（ＦａｓＬ）阳性表达率（８７．５％,９４．４％）明显高于肝癌组（５４．５％,５２．７％）,Ｐ〈０．０１,Ｆａｓ（＋）、（     

乙型肝炎患者肝组织中Bcl-2、Bax、Bak的表达及意义

目的研究Ｂｃｌ－２、Ｂａｘ、Ｂａｋ蛋白在乙型肝炎（乙肝）肝细胞凋亡及坏死中的作用。方法用免疫组织化学法、原位未端标记技术（ＴＵＮＥＬ）检测８９例各型乙肝患者肝组织Ｂｃｌ－２、Ｂａｘ、Ｂａｋ表达和肝细胞凋亡的情况。结果肝硬化组（１０例）、急性肝炎组（８例）、慢性肝炎组（５５例）和重型肝炎组（１６例）的ＴＵＮＥＬ实验中度以上阳性率分别为３０．０％，２５．０％，６１．８％和９３８％；Ｂｃｌ－２蛋白表达中度以上阳性率分别为３０．０％，２５．０％，３８．２％和１２．５％；Ｂａｘ表达中度以上阳性率分别为２０．０％，２５．０％，４７．３％和８７．５％；Ｂａｋ表达中度以上阳性率分别为１０．０％，１２．５％，２５．５％和７５．０％。ＴＵＮＥＬ反应及Ｂａｘ、ＢａＫ表达阳性程度在各型乙型肝炎中的分布差异均有显著性（Ｐ＜０．０５），两蛋白的阳性程度随坏死程度的增加而增强。Ｂｃｌ－２在增生区的表达显著高于坏死区。结论Ｂａｘ、Ｂａｋ的加强表达有促进肝细胞死亡的作用，两者的表达水平可反映肝组织损伤和炎症活动程度。     

The Role of Fas/Fas Ligand System in the Pathogenesis of Liver Cirrhosis and Hepatocellular Carcinoma

Background

The Fas receptor/ligand system including soluble forms is the most important apoptotic initiator in the liver. Dysregulation of this pathway may contribute to abnormal cell proliferation and cell death and is regarded as one of the mechanisms preventing the immune system from rejecting the tumor cells.

Objectives

To analyze the role of Fas system Fas/ Fas ligand (Fas/ FasL) in the multi-step process of hepatic fibrosis/carcinogenesis, and to use of the serum markers as possible candidate biomarkers for early detection of hepatocellular carcinoma (HCC).

Patients and Methods

Ninety patients were enrolled: 30 cases of chronic hepatitis C (CHC) without cirrhosis, 30 cases of CHC with liver cirrhosis, and 30 cases of HCC and hepatitis V virus (HCV) infection. Ten wedge liver biopsies, taken during laparoscopic cholecystectomy, were served as normal controls. Serum soluble Fas (sFas) levels were measured using ELISA technique; Fas and FasL proteins were detected in hepatic tissue by indirect Immuno-histochemical technique (IHC); electron microscopic (EM) and immune electron microscopic examinations were performed for detection of Fas expression on lymphocytes.

Results

Hepatic expression of both Fas and FasL as well as expression of Fas on separated lymphocytes were significantly increased in the diseased groups (P < 0. 01) compared to the control specimens. The highest expression was noticed in CHC specimens, particularly with the necro-inflammatory activity and advancement of the fibrosis. The sFas in cirrhotic patients and HCC were significantly higher than that in normal controls and CHC without cirrhosis group (P < 0.01).

Conclusions

Apoptosis and the Fas system were significantly involved in the process of converting liver cirrhosis into hepatocellular carcinoma. Down-regulation of Fas expression, up regulation of FasL expression in hepatocytes, and elevation of serum sFas levels were important in tumor evasion from immune surveillance, and in hepatic carcinogenesis.     

抗独特型抗体NP30诱导虫卵肉芽肿细胞凋亡的分子机制

目的研究抗独特型抗体NP30诱导虫卵肉芽肿细胞凋亡的分子机制.方法 BALB/c 小鼠随机分为两组,实验组腹腔注射NP30 10 μg/次,连续3次,对照组腹腔注射生理盐水,分别在尾蚴攻击感染后第39、49、64、108、112天处死,应用免疫组化S-P法检测凋亡相关基因Bax、Bcl-2、Fas、FasL和c-Fos的表达,原位分子杂交检测Bax与Fas mRNA.结果虫卵肉芽肿细胞均表达Bax、Fas、FasL和c-Fos蛋白,其中实验组Bax和FasL蛋白表达均高于对照组(P<0.05);实验组Fas和c-Fos蛋白表达在第64天和第112天低于对照组,其余各时间点均高于对照组(P<0.05);Bcl-2蛋白在实验组和对照组均无表达.实验组Bax和fas mRNA表达均高于对照组.结论死亡受体Fas和FasL途径启动了NP30诱导肉芽肿细胞凋亡的信号,NP30通过凋亡相关基因Bax和c-Fos表达增强来诱导肉芽肿的细胞凋亡.     

In situ investigation of Fas/FasL expression in chronic hepatitis B infection and related liver diseases

To evaluate Fas/FasL expression in hepatitis B virus-related chronic liver disease, liver biopsies from 44 such cases were studied immunohistochemically. FasL was detected in the infiltrating lymphocytes and both FasL and Fas were found in the hepatocytes. The Fas and FasL-positive cells were mostly found at the advancing edges of interphase hepatitis, and Fas/FasL expression was closely correlated with the inflammatory activity. Unexpectedly, FasL was also expressed in liver cirrhotic nodules, particularly in those with hepatocellular carcinoma with or without inflammation. These results suggest that the factors which induce hepatocyte transformation might also trigger FasL expression and promote FasL/Fas-mediated apoptosis.     

弓形虫感染对妊娠中期小鼠胎盘组织中细胞凋亡相关蛋白表达的影响

目的观察弓形虫感染妊娠中期的BALB/c小鼠后,对胎盘组织中细胞凋亡相关蛋白Bax、Bcl-2、Fas、FasL及TNF-α表达的影响,探讨弓形虫感染导致细胞凋亡增加的可能机制。方法在妊娠第8d,实验组经腹腔无菌接种纯化的弓形虫速殖子100个,溶于0.2mL PBS;对照组注射等量无菌PBS(0.01mol/L,pH=7.4)。于妊娠第12、14、16、18d,随机处死实验组和对照组孕鼠各5只,采用免疫组织化学法(i mmunohistochemistry)检测胎盘组织中细胞凋亡相关蛋白Bax、Bcl-2、Fas、FasL及TNF-α的表达水平。结果免疫组化显示,细胞凋亡相关蛋白在胎盘绒毛和蜕膜组织中均有表达,以胎盘合体滋养细胞表达较多。Bax、Fas、FasL及TNF-α的表达量实验组和对照组均随着妊娠期的延长而增加,相同妊娠天数实验组的表达量均比对照组多。Bcl-2的表达量均随着妊娠期的延长而减少,相同妊娠天数实验组的表达量均比对照组少。结论弓形虫感染妊娠中期的小鼠,可引起胎盘组织中细胞凋亡相关蛋白表达量的改变,进而启动内、外源性的细胞凋亡途径,导致胎盘细胞凋亡增加。     

凋亡相关基因Fas、Fas配体及bax在慢性病毒肝炎组织中的表达及意义

为探讨凋亡相关基因Ｆａｓ、Ｆａｓ配体及ｂａｘ在慢性病毒性肝炎中表达的意义。采用免疫组化技术研究４８例慢性肝炎（乙型肝炎３３例,丙型肝炎１５例）组织中Ｆａｓ、ＦａｓＬ及ｂａｘ的表达。结果：慢性乙型肝炎和丙型肝炎组织中Ｆａｓ、ＦａｓＬ及ｂａｘ表达均较正常肝增加,以细胞坏死和炎细胞浸润区域增加明显。结论：凋亡相关基因Ｆａｓ、Ｆａｓ及ｂａｘ可能参与了肝炎病毒致肝细胞的损伤过程。     

Possible mechanism for hepatitis B virus X gene to induce apoptosis of hepatocytes

AIM: To investigate the possible mechanism for HBV X gene to induce apoptosis of hepatocyte HL-7702 cells. METHODS: HBV X gene eukaryon expression vector pcDNA3-X was established and transfected into HL-7702 cells by Iipid-mediated transfection, including transient and stable transfection. Positive clones were screened by incubating in the selective medium with 600 μg/mL G418 and named HL-7702/HBV-encoded X protein (HBx) cells. The expressions of Fas/FasL, Bax/Bcl-2, and c-myc mRNA were measured by semi-quantitative RT-PCR in HL-7702/HBx and control group, respectively. RESULTS: RT-PCR analysis confirmed that HBV X gene was transfected into HL-7702 cells successfully. By semi-quantitative RT-PCR analysis, Bax and c-myc mRNA levels in HL-7702/HBx cells of transient transfection were significantly higher than those in control, FasL and c-myc mRNA levels in HL-7702/HBx cells of stable transfection were significantly higher than those in control, whereas the Bcl-2 mRNA levels in HL-7702/HBx cells of transient and stable transfection were significantly lower than those in control. CONCLUSION: HBV X gene may promote the apoptosis of hepatocytes by regulating the expressions of Fas/FasL, Bax/Bcl-2, and c-myc gene in a dose-dependent manner.     

Transfection of apoptosis related gene Fas ligand in human hepatocellular carcinoma cells and its significance in apoptosis

AIM: To evaluate the expression of apoptosis related gene Fas ligand (FasL) in human hepatocellular carcinoma (HCC) cells HepG2 and its significance in apoptosis. METHODS: Levels of soluble Fas ligand (sFasL) in a group of patients with hepatitis B virus (HBV)-induced chronic hepatitis, HBV-positive liver cirrhosis and HCC were evaluated. In a further study, the recombinant eukaryotic expression plasmid pcDNA3.1hisB-FasL was transfected into HCC cells HepG2 by lipofection, and then soluble FasL was examined in the supernatant of culture cells by EIA, FasL expression in HepG2 cells was detected by immuohistochemistry. After being stained by annexin V and propidium iodine, cells were passed through a flow cytometer and examined by a fluorescence microscope and a laser scanning microscope. RESULTS: The sFasL levels were significantly lower in patients with HCC when compared to the patients with hepatitis or liver cirrhosis. In comparison with untransfected cells, the soluble FasL could be detected in the supernatant of transfected cells. FasL was expressed on the membranes and cytoplasm of transfected cells. The apoptotic cell rate was 36.30% in transfected cells, and was 11.53% in untransfected cells. Moreover, the different stage of apoptotic cells could be distinguished by annexin V and propidium iodine staining. CONCLUSION: Fas ligand is an apoptotic pathway of HCC cells.     

乙型肝炎患者肝组织中Fas及Fas配体的表达

为探讨乙型肝炎肝组织中Ｆａｓ及Ｆａｓ配体（ＦａｓＬ）表达和分布的相互关系，采用免疫组织化学技术，以兔抗－Ｆａｓ及兔抗－ＦａｓＬ多克隆抗体，对６０例急性轻型肝炎、慢性活动性肝炎及活动性肝硬化患者石蜡包埋肝组织中的Ｆａｓ及ＦａｓＬ进行了检测。Ｆａｓ及ＦａｓＬ的检出率分别为７６．７％（４６／６０）及７０．０％（４２／６０），Ｆａｓ于肝细胞胞浆内表达，ＦａｓＬ多在肝组织中浸润的淋巴细胞胞浆内表达（３４／４２，８０．９％），也见于肝细胞胞浆中（２５／４２，５９．５％）。ＦａｓＬ阳性淋巴细胞主要分布于汇管区，肝小叶内很少见，ＦａｓＬ阳性肝细胞的分布类同Ｆａｓ阳性肝细胞；在急性轻型肝炎，阳性细胞多在小叶内弥散分布，在慢性活动性肝炎和活动性肝硬化则更多集聚于碎屑样坏死灶和假小叶的周边。免疫组化双标记染色显示，Ｆａｓ及ＦａｓＬ可在同一或不同肝细胞胞浆内表达，但多分布于同一区域。本研究在正常肝组织中未查见ＦａｓＬ的表达，提示在病理状态下，肝细胞才出现ＦａｓＬ的表达。Ｆａｓ及ＦａｓＬ在肝组织中的分布表明，Ｆａｓ－ＦａｓＬ系统在乙型病毒性肝炎肝细胞损伤中起着重要的作用。     

益母草注射液对糖尿病心肌病大鼠心肌细胞凋亡和增殖活性的作用研究

目的探讨中药益母草注射液(LHS)对链脲佐霉素(STZ)制备的糖尿病心肌病(DCM)大鼠心肌细胞凋亡和增殖活性的作用。方法2004年3月至2004年9月于汕头大学医学院第二附属医院内分泌科建立STZ诱导DCM的大鼠模型,将实验大鼠随机分为未治疗组、LHS治疗组和正常对照组,16周龄时处死,观察心肌细胞的凋亡百分数(TUNEL法)、Fas、FasL、Bax、Bcl-2、增殖细胞核抗原(PCNA)的表达(免疫组化法)、心肌细胞超微结构的改变(电镜)。结果与DCM组相比,DCM给药组大鼠心肌肌节对位仅见少部分错位,肌原纤维无溶解,线粒体结构完整;心肌细胞中促凋亡因子Fas、FasL和Bax的表达降低,抑制凋亡的Bcl-2/Bax比值增加,心肌细胞凋亡百分数降低,差异均有显著性(P<0·05);PCNA阳性细胞数增多,差异有显著性(P<0·05)。结论LHS治疗后,心肌细胞凋亡比未治疗组明显减少,而增殖活性明显增强,LHS能有效防治大鼠DCM,改善超微结构的异常。     

Janus激酶-信号转导子与转录激活子通路介导粒细胞集落刺激因子影响冠状动脉微栓塞后心肌细胞凋亡的实验研究

目的 探讨粒细胞集落刺激因子(G-CSF)对大鼠冠状动脉微栓塞(CME)后心肌细胞凋亡的影响以及Janus激酶-信号转导子与转录激活子(JAK/STAT)通路的介导作用.方法 将92只雄性成年SD大鼠,随机分成CME组(24只)、G-CSF组(24只)、JAK2特异性抑制剂(AG490)组(G-CSF+AG490,24只)和假手术组(20只).CME组、G-CSF组及AG490组升主动脉夹闭后自左室腔内注入自体微血栓,造成CME,假手术组注入等量生理盐水.G-CSF组及AG490组术后2 h起给予皮下注射重组人G-CSF(rhG-CSF)100 μg·kg-1·d-1持续5 d,AG490组同时给予AG490溶液腹腔注射5 mg·kg-1·d-1,其他组给予等量生理盐水.术后3 d、1、2及4周处死动物.各组心肌样品中以实时定量聚合酶链式反应法检测Bcl-2、Bax、Fas及FasL的mRNA表达,并计算Bcl-2/Bax比值;以Western blot法检测Caspase-3、裂解多聚二磷酸腺苷-核糖聚合酶(PARP)、总JAK2(t-JAK2)、磷酸化JAK2(p-JAK2)、t-STAT3以及p-STAT3蛋白的表达;脱氧核糖核苷酸末端转移酶介导的缺口末端标记(TUNEL)法测定凋亡细胞.结果 (1)与假手术组比较,CME组术后Bcl-2、Bax、Fas及FasL的mRNA表达均升高,Bcl-2/Bax比值降低(0.28±0.04比2.98±0.49),Caspase-3(0.762±0.129比0.133±0.027)及PARP蛋白(0.992±0.146比0.386±0.074)表达增强,心肌细胞凋亡指数升高(P＜0.05或P＜0.01);t-JAK2、p-JAK2、t-STAT3以及p-STAT3蛋白表达差异无统计学意义.(2)与CME组比较,G-CSF组术后p-JAK2与p-STAT3蛋白表达明显增强,Bax、Fas及FasL的mRNA表达明显减弱,Bcl-2的mRNA表达增强,Bcl-2/Bax比值升高(2.07±0.29比0.28±0.04),Caspase-3(0.371±0.041比0.762±0.129)及PARP蛋白(0.548±0.093比0.992±0.146)表达减弱;心肌细胞凋亡指数下降(P＜0.05或P＜0.01);t-JAK2及t-STAT3蛋白表达则差异无统计学意义.(3)经AG490干预后,G-CSF引起的基因与蛋白表达的变化均有不同程度减弱(P＜0.05或P＜0.01).结论 G-CSF通过激活JAK2/STAT3细胞内信号通路减轻CME导致的心肌细胞凋亡.     

Fas、FasL在慢性乙型肝炎患者肝细胞和外周血淋巴细胞上的表达

探讨慢性乙型肝炎患者肝细胞及外周血淋巴细胞上Fas、FasL的表达与乙型肝炎病毒（HBV）复制水平及肝组织炎症程度的关系。对30例慢性乙型肝炎患者进行肝穿刺肝组织病理检查及免疫组化SP法检测肝细胞中Fas、FasL表达强度。并采用单克隆抗体经流式细胞仪检测外周血淋巴细胞上Fas、FasL表达阳性百分率;同时,采用荧光实时标记法测定血清中病毒复制指标HBV DNA水平;采用Beckman全自动生化分析仪检测肝功能并研究其相关性。慢性乙型肝炎患者肝细胞中Fas、FasL表达强度随肝组织炎症活动度加重而增强（P均〈0．001）,与白蛋白及丙氨酸转移酶（ALT）呈负相关（P〈0．005,P〈0．001）,与球蛋白、总胆红质无明显相关性（P均〉0．05）。外周血淋巴细胞上Fas、FasL的表达阳性率与血清中肝炎病毒复制指标HBV DNA水平呈正相关;与慢性肝炎分度无明显的相关性。乙型肝炎病毒感染可诱导肝细胞及外周血淋巴细胞上Fas、FasL的表达。肝细胞Fas、FasL的表达随炎症活动度加重而表达增强,但其介导的凋亡并不引起肝细胞炎症损伤即ALT活性并不升高,相反减少;同时在某种程度上影响白蛋白的合成。提示Fas—FasL介导的肝细胞凋亡是以非细胞损伤方式参与慢性乙型肝炎的发病过程。同时,随血清HBV DNA水平增高,外周血淋巴细胞上Fas、FasL的表达亦增强,淋巴细胞的凋亡因而增多,是导致乙型肝炎慢性化的原因之一。由此可见,Fas、FasL介导的凋亡参与了慢性乙型肝炎的发病机制,且在慢性乙型肝炎的发生发展中起重要作用。     

慢性丙型肝炎肝组织CPP32、Fas和Fas配体的表达及其与病毒抗原的关系

目的 探讨慢性丙型病毒性肝炎（ＣＨＣ）中Ｆａｓ－ＦａｓＬ－ＣＰＰ３２介导的细胞凋亡的意义及其与丙型肝炎病毒（ＨＣＶ）抗原表达间的关系。方法 用免疫组织化学和核酸原位杂交法,在连续组织切片上对６５例不同病变程度的ＣＨＣ穿刺活检肝组织中ＣＰＰ３２、Ｆａｓ和ＦａｓＬ蛋白（酶）及其ｍＲＮＡ的表达进行检测。同时用免疫组织化学方法检测ＨＣＶ核心抗原、ＮＳ３和ＮＳ５抗原的表达,原位检测结果用图象分析作定量测定,     

肝细胞凋亡与慢性乙型肝炎病毒携带者肝组织病变的关系

目的 观察慢性HBV携带者（ASC）肝组织凋亡指数及Fas、FasL的表达,探讨肝细胞凋亡在ASC肝组织病变中的作用.方法 选取HBV携带者患者120例,并进行肝组织活检.采用原位末端转移酶标技术进行肝细胞凋亡情况检测,采用免疫组织化学技术检测肝组织中的Fas、FasL.结果 120例ASC肝组织完全正常者仅占11％,轻度肝炎组占59％,而中、重度肝炎组占30％.ASC患者的凋亡指数（AI）随着炎症程度加重而升高,正常组为1.50±1.04,而中度组、重度组分别为11.33 ±1.51和17.67 ±6.42,各组间比较差异有统计学意义（P＜0.05）.肝组织免疫组化结果显示,Fas、FasL表达程度随炎症活动度加重而增强,尤其在汇管区周围碎屑状坏死区及周边小叶更明显,正常组基本无表达,而轻度组以无表达或阳性表达为主,仅见于界面炎症区的肝细胞及淋巴细胞上;中、重度肝炎组Fas、FasL则均为阳性及强阳性表达,除界面炎症区外,肝小叶中也弥漫分布.Fas强阳性表达率在中、重度组分别为34.8％和69.2％,FasL的强阳性表达率分别为30.4％和53.8％,均明显高于正常组和轻度组（P＜0.05）,同时中、重度组间比较差异亦有统计学意义,肝组织中Fas、FasL表达程度随炎症活动度加重而增强,两者间明显相关.结论 肝细胞凋亡在ASC肝组织病变的发生发展中可能起到重要作用.     

Immunohistochemical detection of Fas and apoptosis in type-1 autoimmune hepatitis

BACKGROUND/AIMS: Although Fas expression has been reported in liver with chronic viral hepatitis and primary biliary cirrhosis, little is known about Fas expression and apoptosis in type-1 autoimmune hepatitis. The aim of this study was to investigate whether the expression of Fas and apoptosis are found in liver with autoimmune hepatitis. The relationship between Fas expression and clinicopathological findings including the occurrence of apoptosis was also investigated. METHODOLOGY: Fas expression and apoptosis were immunohistochemically examined in liver tissues from 20 patients with autoimmune hepatitis and five control subjects using specific antibodies against Fas and single-stranded DNA. The grade of expression of Fas and apoptosis was evaluated and compared with histological findings and the results of liver function tests in each patient. RESULTS: Fas expression in hepatocytes was detected in all patients with autoimmune hepatitis, while Fas expression was not detected in control livers. The Fas-positive hepatocytes were particularly abundant in those areas facing piecemeal and confluent necrosis. In 30% of autoimmune hepatitis cases, bile-duct cells were faintly stained for Fas. A few hepatocytes positive for single-stranded DNA were found in the areas facing piecemeal necrosis and confluent necrosis. In 95% cases, many bile-duct cells were positive for single-stranded DNA. No relationship between the expression of Fas and single-stranded DNA was found in hepatocytes or bile-duct cells. However, the degree of Fas expression in hepatocytes significantly correlated with serum transaminase concentrations and was increased in parallel with the grade of activity but not with the stage of fibrosis. CONCLUSIONS: We have demonstrated that Fas expression is detected in hepatocytes of the liver with autoimmune hepatitis and that the level of Fas expression reflects the severity of inflammation in autoimmune hepatitis.     

溃疡性结肠炎肠黏膜组织CD8、Fas/FasL和Bcl-2/Bax的表达及关系

目的:研究溃疡性结肠炎(UC)肠黏膜CD8 T细胞Fas／FasL、Bcl-2／Bax蛋白表达以及相互关系,探讨细胞凋亡机制在UC发病中的作用．方法:采用免疫组化SP法检测60例UC肠黏膜组织以及60例正常肠黏膜组织CD8,Fas／FasL, Bcl-2／Bax蛋白表达．结果:CD8阳性细胞在上皮间的浸润在UC 组为52％,正常组为78％,两组相比差异显著 (P<0．01);急性期较缓解期也显著减少(20％ vs 74％,P<0．01)．CD8在UC患者急性期黏膜固有层的表达为80％,高于缓解期的34％(P= 0．0006)．Fas在UC上皮中表达62％,正常组织 30％,两组相比差异显著(P<0．01);急性期高于缓解期(84％ vs 45％,P<0．01)．FasL在固有膜炎性细胞中的表达UC组为62％,正常组7％, 两组相比差异显著(P<0．00;急性期(88％)高于缓解期(43％),而且CD8与FasL在黏膜固有层炎性细胞的表达呈正相关(X2=7．3,P<0．01)． Bcl-2／Bax在UC肠黏膜上皮的表达率与正常组相近,差异无显著性．结论:UC肠黏膜组织Fas／FasL表达增强, Bcl-2／Bax表达无明显变化,CD8细胞与UC急性期Fas／FasL表达相关．