病毒性肝炎患者血清γ-IFN与肝纤维化关系的研究

目的 :研究病毒性肝炎患者γ IFN与肝纤维化指标HA、LN、PCⅢ血清水平的变化 ,探讨其在肝纤维化机制中的作用。方法 :对 80例各种类型病毒性肝炎检测血清γ IFN、HA、LN、PCⅢ ,并与肝组织病理学变化进行对照研究。结果 :γ IFN在AH、CH、LC组中依次降低 ,γ IFN与HA、PCⅢ血清水平负相关 ,并且γ IFN血清水平降低与肝脏病理学纤维组织增生程度有关。结论 :γ IFN是病毒性肝炎发病及肝纤维化进展过程中重要的细胞因子 。

混合稀土“常乐”对大鼠脾细胞IL-2和γ-IFN的影响

应用脾体比、常规组织学染色观察、淋巴细胞转化率试验及脾细胞IL 2与γ IFN水平的检测研究了不同剂量混合稀土"常乐"灌胃不同时间对大鼠脾脏形态及机能的影响。各剂量组"常乐"灌胃1个月后,大鼠脾体比、脾脏形态结构及免疫功能与对照组无明显差别。"常乐"灌胃6个月后,2,0.2mg·kg-1剂量组可使大鼠脾淋巴细胞转化率升高,2,0.2,0.1mg·kg-1剂量组分泌IL 2水平上升。20,10mg·kg-1剂量组淋巴细胞转化率及IL 2活性与对照组比较无明显差别。

不同光照条件下褪黑素对鸡鸭外周血白细胞和γ-IFN含量变化的影响

为探讨不同褪黑素水平对禽类机体免疫系统的调节作用,通过控制不同光照条件分三组(分别是短光照组6h,对照组12h,长光照组18h)饲养鸡45只、鸭45只,采用翼下静脉采血,用经典血细胞计数法(WBC)测定鸡、鸭外周血白细胞数;用放射免疫法(RIA)测定褪黑素水平,用酶联免疫分析法(ELISA)测定血清中干扰素(γ-IFN)含量变化,研究不同褪黑素水平对鸡、鸭外周血白细胞消长规律和γ-IFN含量变化的影响。结果表明:短光照组的鸡、鸭血中褪黑素水平明显升高,长光照组的血中褪黑素水平明显降低,且与对照组相比,差异显著;短光照组的鸡、鸭血中白细胞数、γ-IFN含量由于褪黑素水平的升高而明显升高,长光照组的则明显下降,分别与对照组相比,差异显著。结论:由于控制光照时间使内源性褪黑素水平不同,褪黑素水平对鸡、鸭外周血白细胞数和γ-IFN含量有显著影响。

毛细支气管炎患儿外周血IL-4,γ-IFN和IgE水平测定及分析

目的 检测毛细支气管 (简称毛支 )炎患儿外周血部分细胞因子含量的改变 ,分析其意义及与哮喘患儿的相似之处。方法 采用ELISA法测定 36例毛支患儿急性期外周血单核细胞诱生白细胞介素 - 4 (IL - 4 )、γ-干扰素 (γ -IFN)水平和IgE含量 ,同期测定 30例健康同龄婴儿作为对照。结果 毛支组γ -IFN水平下降 ,IL -4及IgE水平升高。结论 毛细支气管炎患儿急性期γ -IFN及IL - 4失衡 ,IgE产生增加 ,说明毛支的发病与T淋巴细胞分泌的细胞因子失衡有关 ,这和哮喘患儿的免疫改变相似 ,提示可能与以后的哮喘发病有一定的关系。

鼻息肉中核因子κB亚单位P50活性与IL-4、γ-IFN因子表达的关系

目的测定鼻息肉中核因子κB亚单位P50的活性及其与IL-4、γ-IFN表达的关系,探讨P50对TH1/TH2细胞因子表达调节的可能机制。方法采用SP免疫组化染色法检测40例鼻息肉患者与20例正常钩突黏膜中IL-4、γ-IFN、P50的表达,以核染阳性率来评估P50活性。对P50活性与IL-4,γ-IFN因子行直线相关分析。结果①鼻息肉中P50胞浆、胞核均有阳性表达,主要位于上皮细胞、炎症细胞及腺上皮细胞胞浆,P50活性显著增强(P<0.001),IL-4表达亦明显增强(P<0.001),γ-IFN表达无明显改变(P>0.05);②Pearson相关性分析提示,P50活性与IL-4表达呈直线正相关关系(r=0.70,P<0.001),而与γ-IFN表达无相关性(r=0.14,P=0.40)。结论鼻息肉中P50的活性明显增强,P50的激活上调IL-4的表达可能是鼻息肉中Th1/Th2因子失衡的重要环节之一。

γ-IFN对于兔盆腔常规分割照射后输尿管放射性损伤及纤维化的影响

目的:探讨γ-IFN对兔盆腔常规分割照射后输尿管放射性损伤及纤维化的影响。方法:建立兔放射性输尿管损伤的动物模型,52只新西兰兔随机分为常规照射组、γ-IFN组及正常对照组,除正常对照组外其余兔盆腔均接受6MV-X线照射。γ-IFN组从照射后第5天给予γ-IFN250,000U·kg-1,肌注每周1次,共5次。常规照射组给予5ml·kg-1的生理盐水。照射后4周,8周,12周,16周处死实验兔,取其照射范围内的输尿管组织。用HE染色,原位杂交染色及免疫组化方法分析γ-IFN对于放射性输尿管损伤及纤维化影响。结果:HE染色观察放射线导致输尿管损伤的组织结构变化,γ-IFN组与单纯照射组比较,照射后4,8,12周其损伤程度均有显著性差异(P<0.05),16周则无显著性差异(P>0.05);TGF-β1 mRNA原位杂交实验,γ-IFN组输尿管黏膜的TGF-β1 mRNA表达在照射后4,8,12,16周低于常规照射组,有显著性差异(P<0.05),与正常对照组比较也有显著性差异(P<0.05);Ⅲ型胶原免疫组化结果显示γ-IFN组与单纯照射组均存在显著性差异(P<0.05),较正常对照组差异有显著性(P<0.05)。结论:γ-IFN能够减轻实验兔放射性输尿管损伤,抑制放射后输尿管黏膜TGF-β1 mRNA的升高,降低Ⅲ型胶原的表达,减轻放射性输尿管损伤及纤维化的形成。

乙肝患者血清γ-IFN和IL-4检测及临床意义

目的 :了解各种临床类型乙型肝炎患者血清中γ IFN和IL - 4水平 ,以研究Th1和Th2应答在乙肝发病中的作用。方法 :ELISA定量检测乙肝病人和正常对照血清中γ IFN和IL - 4水平 ,然后进行统计学分析。结果 :急性乙肝组的血清IL - 4、IL - 4/γ IFN比值和γ IFN水平无显著性差异 ;慢性肝炎组血清IL - 4、IL - 4/γ IFN比值较高 ,但γ IFN水平较低 ;重症肝炎组血清IL - 4、IL - 4/γ IFN比值较低 ,γ IFN水平较高 ;血清ALT水平高 ,其IL - 4及IL - 4/γ IFN比值就高 ,其γ IFN则低 ;而ALT正常的乙肝患者 ,其血清IL - 4水平与对照组似 ,但γ IFN水平较低 ,IL- 4/γ IFN比值则较高。结论 :Th1/Th2不同的应答模式 ,和乙肝病人肝细胞损伤、乙肝慢性化密切相关。正常的Th1/Th2平衡应答模式 ,常表现为急性肝炎 ;Th1优势应答 ,则肝细胞损害较重 ,但可能与清除染毒肝细胞有关 ;Th2优势应答 。

γ-IFN、蟾蜍灵单用与联用抑制HL-60细胞的作用

目的 :观察γ干扰素 (γ- IFN)、蟾蜍灵单用与联用抑制人白血病 HL - 6 0细胞的作用。方法 :MTT比色法观察上述两种物质对细胞的抑制作用 ,以流式细胞仪检测细胞周期。结果 :(1 )γ- IFN可抑制 HL - 6 0细胞的增殖 ,但抑制作用不随其剂量增加而增加 ;(2 )蟾蜍灵可抑制 HL - 6 0细胞的增殖 ,其半数抑制浓度约为 0 .0 3μmol/ L ,随蟾蜍灵浓度增加 ,抑制程度增加 ;(3)γ- IFN与蟾蜍灵联用后 ,抑制作用增强。结论 :蟾蜍灵可抑制 HL - 6 0细胞的增殖 ,在γ-

1020例慢性乙型肝炎接受LAM或联用α-IFN治疗终点后的研究

目的 评价拉米夫定或联用α 干扰素治疗慢性乙型肝炎终点后的效果。 方法 对 10 2 0例接受拉米夫定或联用α 干扰素治疗病人终点后 6个月进行随访 ,并作统计分析。 结果 (1)拉米夫定治疗组完全应答率为44 94% ,拉米夫定加α 干扰素治疗组为 5 0 78% ,P <0 0 1;(2 )拉米夫定治疗HBVDNA高含量效果明显 ,拉米夫定加α 干扰素治疗HBVDNA低含量效果好 ;(3 )短病程治疗效果优于长病程 ;(4 )治疗后加重病例多为长病程、HBVDNA高含量及单用拉米夫定的男性病人 ,发生严重急性恶化病例 5例 ,仅占总病例 0 49%。 结论 (1)抗病毒药物拉米夫定与α 干扰素联合应用较单一拉米夫定治疗效果好 ,发生治疗后加重反应和较少 ,但需个体化 ;(2 )为避免发生严重急性恶化病例 ,停用拉米夫定后应严密随访ALT及HBVDNA ,特别是停药后 2个月内。一旦发生严重急性恶化 ,除积极护肝治疗外 。

γ-IFN治疗慢性乙型肝炎疗效观察

血清抗-HBe和HBV-DNA同时阳性的慢性乙型肝炎患者常被认为体内感染有HBV pre C/C基因突变株,其γ-IFN疗效尚无一致意见。我们应用γ-IFN(安福隆)治疗此类病人30例,现将结果报告如下。 资料和方法 1 病例选择 60例慢性乙型肝炎均为我科住院及门诊患者,其中男31例,女29例;年龄8～54岁,平均34.5岁。60例随机分成A、B两组各30例两组性别、年龄、病史和ALT均具可比性(P】0.05)。全部病例均符合1995年5月北京第5次全国传染病寄生虫病会议修订的病毒性肝炎分型诊断标准,A组2例行肝活检病理诊断。

IL-2和γ-IFN对晚期肝癌患者淋巴细胞粘附肿瘤细胞能力的影响

目的 研究重组 ＩＬ－ ２（ｒＩＬ－２）和 γ－ＩＦＮ对晚期肝癌患者淋巴细胞粘附肿瘤细胞能力的影响。方法 晚期肝癌患者２４例，用 ｒＩＬ－２和 γ－ＩＦＮ预培养患者外周血淋巴细胞 ４ｈ，采用肿瘤淋巴细胞花环试验测定淋巴细胞粘附肿瘤细胞直接接触效应与活性．结果 ｒＩＬ－２对正常人和肝癌患者的淋巴细胞免疫粘附肿瘤能力都有明显的的提升效应，但单独使用 ｒＩＬ－２对肝癌患者淋巴细胞免疫粘附肿瘤细胞的提升效应较差，ｒＩＬ－２与γ－ＩＦＮ联合使用可显著增强淋巴细胞对肿瘤细胞的免疫粘附功能．结论 肝癌患者淋巴细胞免疫粘附肿瘤细胞能力明显低下，ｒＩＬ－２与γ－ＩＦＮ联合使用具有协同刺激肝癌患者淋巴细胞活性之作用．

TLR2在红色毛癣菌感染中对角质形成细胞分泌γ-IFN和IL-8的影响

目的观察红色毛癣菌刺激人角质形成细胞后γ-IFN及IL-8浓度的变化,以及TLR2对γ-IFN和IL-8分泌的影响。方法用红色毛癣菌悬液分别刺激TLR2抗体处理前后的角质形成细胞,采用ELISA方法检测不同时间点细胞上清液中γ-IFN及IL-8的浓度,并设置阴性对照;比较TLR2抗体处理前后γ-IFN及IL-8浓度的变化。结果红色毛癣菌刺激角质形成细胞后,γ-IFN及IL-8浓度明显升高(P<0.05),4 h即开始,至16 h达高峰;用TLR2抗体中和TLR2后,上清液中IL-8的浓度在2 h、4 h、8 h、16 h各时间点较中和前低,差异有统计学意义(P<0.05);γ-IFN的浓度2 h、4 h、8 h时间点较中和前低,差异有统计学意义(P<0.05),而在16 h时间点,上清液中γ-IFN的浓度与中和前比较略低,但差异没有统计学意义(P>0.05)。结论红色毛癣菌刺激角质形成细胞后,可促进角质形成细胞分泌γ-IFN和IL-8;TLR2在角质形成细胞分泌γ-IFN和IL-8的过程中发挥重要的调节作用。

泪腺炎患者血清性激素变化及其与γ-IFN、IL-4的相关性

目的观察泪腺炎患者血清中雌二醇(estradiol,E2)、睾酮(testosterone,T)、泌乳素(prolactin,PRL)水平的变化,并探讨这种变化与血清中γ-干扰素(γ-interferon,γ-IFN)、白细胞介素-4(interleukin-4,IL-4)变化的关系。方法收集42例2013年11月至2014年10月我院确诊为泪腺炎的患者炎症期(炎症期组)与炎症缓解期(缓解期组)的血清,40例同年龄段于我院体检的正常人血清作为正常对照组,采用电化学发光法检测血清中E2、T、PRL的水平,酶联免疫吸附法测定血清中γ-IFN、IL-4水平。结果泪腺炎患者炎症期组血清E2、PRL水平分别为(64.12±35.92)ng·L-1和(17.63±8.59)μg·L-1,显著高于缓解期组的(43.16±26.57)ng·L-1和(10.30±5.59)μg·L-1及正常对照组的(41.92±21.68)ng·L-1和(9.08±2.61)μg·L-1,差异均有统计学意义(均为P<0.05);炎症期组与缓解期组血清T分别为(0.80±1.36)μg·L-1和(0.79±1.42)μg·L-1,与正常对照组的(1.76±2.49)μg·L-1相比差异均有统计学意义(均为P<0.05)。炎症期组血清γ-IFN、IL-4水平分别为(353.12±108.36)ng·L-1和(1200.43±314.69)ng·L-1,显著高于缓解期组的(192.68±43.16)ng·L-1和(919.38±227.16)ng·L-1及正常对照组的(190.93±36.40)ng·L-1和(853.37±172.31)ng·L-1,差异均有统计学意义(均为P<0.05)。E2与γ-IFN、IL-4水平呈正相关(均为P<0.05);T与γ-IFN、IL-4水平呈负相关(均为P<0.05);PRL与γ-IFN、IL-4水平呈正相关(均为P<0.05)。女性患者炎症期组血清γ-IFN水平为(344.46±112.06)ng·L-1,高于男性的(292.98±71.27)ng·L-1(P<0.05),E2/T比值为665.36,明显高于男性的13.91(P<0.05)。结论泪腺炎患者血清中性激素E2、PRL的升高、T的降低及E2/T比例失调可能介导Th1、Th2细胞免疫通路的平衡紊乱从而致病。女性体内高水平的雌激素可能是导致女性易患自身免疫性疾病的主要原因。

Influence of HLA-DRB1 alleles and HBV genotypes on interferon-α therapy for chronic hepatitis B

AIM. To investigate the influence of HLA-DRB1 alleles and HBV genotypes on inberferon-α therapy for chronic hepatitis B. METHODS： HLA-DRBI＊03, ＊07, ＊09,＊12, ＊15 alleles were determined using polymerase chain reaction/sequence specific primer （PCR/SSP） technique in 126 patients with chronic hepatitis B and 76 normal control subjects in Shandong Province, and HBV genotypes were determined by nested-PCR analysis using type-specific primers in 126 patients. RESULTS： The positivity of HLA-DRB1＊07 allele in chronic hepatitis B group was significantly higher than that in normal control group （X^2 = 6.33, P〈0.025, RR = 2.37）. Among the 126 patients, genotype B was found in 38 （30.2%）, genotype C in 69 （54.8%）, and mixed genotype （B＋C） in 19 （15.0%）, genotypes D-F were not found. Among the 46 DRB1＊07（＋） patients, 7 were responders and 39 were non-responders among them （X^2 = 6.71, P〈0.05）. The positivity of HLADRB1＊07 and prevalence of HBV genotype C were significantly higher in non-responders than in responders. CONCLUSION： High positivities of HLA-DRB1 ＊07 allele and HBV genotype C are closely associated with the lower response to interferon-α therapy for chronic hepatitis B.

Adeno-associated virus mediated interferon-gamma inhibits the progression of hepatic fibrosis in vitro and in vivo

AIM:To investigate the effects of adeno-associated virus (AAV) mediated expression of human interferon-γ for gene therapy in experimental hepatic fibrosis in vitro and in vivo. METHODS: We constructed the recombinant AAV encoding human INF-γ (rAAV- INF-γ) and took the primary rat hepatic stellate cells and carbon tetrachloride induced rats as the experimental hepatic fibrosis model in vitro and in vivo. Immunocytochemistry analysis was used to reveal the expression of α-SMA, the marker protein expressed in hepatic stellate cells. The mRNA expression of TGF-β, TIMP-1, and MMP-13 were analyzed by RT-PCR method. In vivo study, the hydroxyproline content in liver and serum AST, ALT were also detected. RESULTS: In vitro study, AAV vector could mediated efficient expression of human INF-γ, which inhibit the activation of hepatic stellate cells, decrease the expression of α-SMA and mRNA of TIMP-1, TGF-β, with the MMP-13 unchanged. In vivo study, the histological examination revealed that rAAV- INF-γ could inhibit the progression of the hepatic fibrosis. In the rAAV-INF-γ induced group, the hydroxyproline content and serum AST, ALT level were decreased to 177±28 μg/g wet liver, 668.5±140.0, 458.4±123.5 U/L, compare with the fibrosis control group 236±31 μg/g wet liver, 1 019.1±276.3, 770.5±154.3 U/L, respectively (P<0.01). mRNA expression of TIMP-1 in the rAAV-INF-γ induced rat liver was decreased while no significant change was observed in TGF-β and MMP-13. CONCLUSION: All these results indicated that rAAV-INF-γ has potential effects for gene therapy of hepatic fibrosis, which could inhibit the progression of hepatic fibrosis.

Preliminary results of Thymosin-a1 versus interferon-α treatment in patients with HBeAg negative and serum HBV DNA positive chronic hepatitis B

INTRODUCTIONIn China ,the incidence and mortality of gastric cancer rank the second among all cancers. Recent development of cancer [1-20].The aim of this study was investigat the insight of apoptosis and bcl-2, p53 and C-myc protein expression in the development of gastric cancer .

Inhibition of hepatitis B virus DNA replicative intermediate forms by recombinant interferon-γ

AIM: To evaluate the in vitro anti-HBV activity of recombinant human IFN-γ, alone and in combination with lamivudine. METHODS: A recombinant baculovirus-HBV/HepG2 culture system was developed which could support productive HBV infection in vitro. Expression of HBsAg and HBeAg in infected HepG2 culture medium was detected by commercial enzyme immunoassays. HBV DNA replication intermediates were detected in infected cells by Southern hybridization and viral DNA load was determined by dot hybridization. RESULTS: IFN-γat 0.1 to 5μg/L efficiently down regulated HBsAg expression in transduced HepG2 cells. At 5μg/L, IFN-γalso suppressed HBV DNA replication in these cells. While treatment with a combination of lamivudine and IFN-γshowed no additive effect, sequential treatment first with lamivudine and then IFN-γwas found to be promising. In this culture system the best HBV suppression was observed with a pulse of 2μmol/L lamivudine for two days, followed by 1μg/L IFN-γfor another four days. Compared to treatment with lamivudine alone, the sequential use of 0.2μmol/L lamivudine for two days, followed by 5μg/L IFN-γfor six days showed a 72% reduction in HBV cccDNA pool. CONCLUSION: This in vitro study warrants further evaluation of a combination of IFN-γand lamivudine, especially in IFN-αnon-responder chronic hepatitis B patients. A reduced duration of lamivudine treatment would also restrict the emergence of drug-resistant HBV mutants.

Anti-rods/rings autoantibody generation in hepatitis Cpatients during interferon-α/ribavirin therapy

Chronic inflammation associated with hepatitis C virus(HCV) infection can lead to disabling liver diseases with progression to liver cirrhosis and hepatocellular carcinoma. Despite the recent availability of more effective and less toxic therapeutic options, in most parts of the world the standard treatment consists of a weekly injection of pegylated interferon α(IFN-α) together with a daily dose of ribavirin. HCV patients frequently present circulating non-organ-specific autoantibodies demonstrating a variety of staining patterns in the indirect immunofluorescence assay for antinuclear antibodies(ANA). Between 20% to 40% of HCV patients treated with IFN-α and ribavirin develop autoantibodies showing a peculiar ANA pattern characterized as rods and rings(RR) structures. The aim of this article is to review the recent reports regarding RR structures and anti-rods/rings(antiRR) autoantibody production by HCV patients after IFN-α/ribavirin treatment. Anti-RR autoantibodies first appear around the sixth month of treatment and reach a plateau around the twelfth month. After treatment completion, anti-RR titers decrease/disappear in half the patients and remain steady in the other half. Some studies have observed a higher frequency of anti-RR antibodies in relapsers, i.e., patients in which circulating virus reappears after initially successful therapy. The main target of anti-RR autoantibodies in HCV patients is inosine-5'-monophosphate dehydrogenase 2(IMPDH2), the rate-limiting enzyme involved in the guanosine triphosphate biosynthesis pathway. Ribavirin is a direct IMPDH2 inhibitor and is able to induce the formation of RR structures in vitro and in vivo. In conclusion, these observations led to the hypothesis that anti-RR autoantibody production is a human model of immunologic tolerance breakdown that allows us to explore the humoral autoimmune response from the beginning of the putative triggering event: exposure to ribavirin and interferon.

Precise prediction model and simplified scoring system for sustained combined response to interferon-α

AIM:To establish a predictive algorithm which may serve for selecting optimal candidates for interferon-α(IFN-α) treatment.METHODS:A total of 474 IFN-α treated hepatitis B virus e antigen(HBeAg)-positive patients were enrolled in the present study.The patients' baseline characteristics,such as age,gender,blood tests,activity grading(G) of intrahepatic inflammation,score(S) of liver fibrosis,hepatitis B virus(HBV) DNA and genotype were evaluated;therapy duration and response of each patient at the 24th wk after cessation of IFN-α treatment were also recorded.A predictive algorithm and scoring system for a sustained combined response(CR) to IFN-α therapy were established.About 10% of the patients were randomly drawn as the test set.Responses to IFN-α therapy were divided into CR,partial response(PR) and non-response(NR).The mixed set of PR and NR was recorded as PR+NR.RESULTS:Stratified by therapy duration,the most significant baseline predictive factors were alanine aminotransferase(ALT),HBV DNA level,aspartate aminotransferase(AST),HBV genotype,S,G,age and gender.According to the established model,the accuracies for sustained CR and PR+NR,respectively,were 86.4% and 93.0% for the training set,81.5% and 91.0% for the test set.For the scoring system,the sensitivity and specificity were 78.8% and 80.6%,respectively.There were positive correlations between ALT and AST,and G and S,respectively.CONCLUSION:With these models,practitioners may be able to propose individualized decisions that have an integrated foundation on both evidence-based medicine and personal characteristics.

Inhibitory effect of interferon-α-2b on expression of cyclooxygenase-2 and vascular endothelial growth factor in human hepatocellular carcinoma inoculated in nude mice

AIM： To evaluate the effects of interferon-α-2b （IFN- α-2b） on expression of cyclooxygenase-2 （COX-2） and vascular endothelial growth factor （VEGF） in human hepatocellular carcinoma （HCC） inoculated in nude mice and to study the underlying mechanism of IFN-α- 2b against HCC growth. METHODS： Thirb/-two nude mice bearing human HCC were randomly divided into four groups （n = 8）. On the 10th day after implantation of HCC cells, the mice in test groups （groups A, B and C） received IFN-α- 2b at a serial dose （10000 IU for group A, 20000 IU for group B, 40000 IU for group C sc daily） for 35 d. The mice in control group received normal saline （NS）. The growth conditions of transplanted tumors were observed. Both genes and proteins of COX-2 and VEGF were detected by RT-PCR and Western blot. Apoptosis of tumor cells in nude mice was detected by TUNEL assay after treatment with IFN-α-2b. RESULTS： Tumors were significantly smaller and had a lower weight in the IFN-α-2b treatment groups than those in the control group （P 〈 0.01）, and the tumor growth inhibition rate in groups A, B and C was 27.78%, 65.22% and 49.64%, respectively. The expression levels of both genes and proteins of COX-2 and VEGF were much lower in the IFN-α-2b treatment groups than in the control group （P 〈 0.01）. The apoptosis index （AI） of tumor cells in the IFN-α-2b treatment groups was markedly higher than that in the control group （P 〈 0.01）. Group B had a higher inhibition rate of tumor growth, a lower expression level of COX-2 and VEGF and a higher AI than groups A and C （P 〈 0.05）, but there was no significant difference between groups A and C. CONCLUSION： The inhibitory effects of IFN-α-2b on implanted tumor growth and apoptosis may be associated with the down-regulation of COX-2 and VEGF expression. There is a dose-effect relationship. The medium dose of IFN-α-2b for inhibiting tumor growth is 20 000 IU/d.