Increased expression of tumor necrosis factor-a is associated with advanced colorectal cancer stages

AIM:To detect the expression of tumor necrosis factor-a(TNF-a)in colorectal cancer(CRC)cells among Saudi patients,and correlate its expression with clinical stages of cancer.METHODS:Archival tissue specimens were collected from 30 patients with CRC who had undergone surgical intervention at King Khalid University Hospital.Patient demographic information,including age and gender,tumor sites,and histological type of CRC,was recorded.To measure TNF-a m RNA expression in CRC,total RNA was extracted from tumor formalin-fixed,paraffinembedded,and adjacent normal tissues.Reverse transcription and reverse transcription polymerase chain reaction were performed.Colorectal tissue microarrays were constructed to investigate the protein expression of TNF-a by immunohistochemistry.RESULTS:The relative expression of TNF-a m RNA in colorectal cancer was significantly higher than that seen in adjacent normal colorectal tissue.High TNF-a gene expression was associated with StageⅢandⅣneoplasms when compared with earlier tumor stages(P=0.004).Eighty-three percent of patients(25/30)showed strong TNF-a positive staining,while only 10%(n=3/30)of patients showed weak staining,and 7%(n=2/30)were negative.We showed the presence of elevated TNF-a gene expression in cancer cells,which strongly correlated with advanced stages of tumor.CONCLUSION:High levels of TNF-a expression could be an independent diagnostic indicator of colorectal cancer,and targeting TNF-a might be a promising prognostic tool by assessment of the clinical stages of CRC.

Effects of erythropoietin on the expression of tumor necrosis factor-alpha and Bax after facial nerve axotomy in rats

This study sought to evaluate the effect of high-dose erythropoietin （EPO; 5 000 IU/kg） on the expression of tumor necrosis factor-alpha （TNF-α） and Bax in the facial nucleus after facial nerve transection in rats. A total of 42 Wistar rats of both genders were used in this study, and 40 rats were randomly divided into 2 groups： EPO group and model group. The EPO group was treated with EPO once a day for 5 days at a dose of 5 000 IU/kg body weight. The model group was treated with saline of the same amount. At day 3 after EPO （or saline） treatment, the right facial nerves of the 40 rats were transected at the level of the stylomastoid foramen, with the left sides untreated. The remaining 2 rats that did not undergo axotomy served as the control group. The surviving motor neurons in operated rats were counted in coronal paraffin sections of the facial nucleus. The expression of TNF-a and Bax in the facial nucleus was detected by immunohistochemical staining at days 3, 7, 14, 21, and 28 after axotomy. At days 14, 21, and 28 after facial nerve axotomy, a significantly greater proportion of facial motor neurons survived in the EPO group than in the model group. After axotomy, the expression of TNF-a and Bax increased in motor neurons in both the EPO and the model groups. TNF-o expression reached its peak level at day 14 after axotomy, while Bax expression reached its peak level at day 21. TNF-α expression was much lower in the EPO group than in the model group at all time points. No significant difference in Bax expression was found between the EPO and the model groups. These results indicate that high-dose EPO treatment attenuates the increase in TNF-α expression in the facial nucleus and reduces the loss of motor neurons after facial nerve transection in rats. However, high-dose EPO treatment has little effect on Bax expression.

Up-regulation of tumor necrosis factor-a pathway survival genes and of the receptor TNFR2 in gastric cancer

BACKGROUND Gastric carcinogenesis can be induced by chronic inflammation triggered by Helicobacter pylori(H. pylori) infection. Tumor necrosis factor(TNF)-α and its receptors(TNFR1 and TNFR2) regulate important cellular processes, such as apoptosis and cell survival, and the disruption of which can lead to cancer. This signaling pathway is also modulated by microRNAs(miRNAs), altering gene expression.AIM To evaluate the mRNA and miRNAs expression involved in the TNF-α signaling pathway in gastric cancer(GC) tissues and its relationship.METHODS Quantitative polymerase chain reaction(qPCR) by TaqMan? assay was used to quantify the RNA transcript levels of TNF-α signaling pathway(TNF, TNFR1,TNFR2, TRADD, TRAF2, CFLIP, NFKB1, NFKB2, CASP8, CASP3) and miRNAs that targets genes from this pathway(miR-19 a, miR-34 a, miR-103 a, miR-130 a,miR-181 c) in 30 GC fresh tissue samples. Molecular diagnosis of H. pylori was performed by nested PCR for gene HSP60. A miRNA:mRNA interaction network was construct using Cytoscape v3.1.1 from the in silico analysis performed using public databases.RESULTS Up-regulation of cellular survival genes as TNF, TNFR2, TRADD, TRAF2, CFLIP,and NFKB2, besides CASP8 and miR-34 a was observed in GC tissues, whereas mediators of apoptosis such as TNFR1 and CASP3 were down-regulated. When the samples were stratified by histological type, the expression of miR-103 a and miR-130 a was significantly increased in the diffuse-type of GC compared to the intestinal-type. However, no influence of H. pylori infection was observed on the expression levels of mRNA and miRNAs analyzed. Moreover, the miRNA:mRNA interaction network showed several interrelations between the miRNAs and their target genes, highlighting miR-19 a and miR-103 a, which has as predicted or validated target a large number of genes in the TNF-α pathway,including TNF, TNFR1, TNFR2, CFLIP, TRADD, CASP3 and CASP8.CONCLUSION Our findings show that cell survival genes mediated by TNF/TNFR2 binding is up-regulated in GC favoring its pro-tumoral effect, while pro-apoptotic genes as CASP3 and TNFR1 are down-regulated, indicating disbalance between apoptosis and cell proliferation processes in this neoplasm. This process can also be influenced by an intricate regulatory network of miRNA:mRNA.

Intragingival injection of Porphyromonas gingivalis-derived lipopolysaccharide induces a transient increase in gingival tumour necrosis factor-a, but not interleukin-6,in anaesthetised rats

This study used in vivo microdialysis to examine the effects of intragingival application of lipopolysaccharide（LPS） derived from Porphyromonas gingivalis（Pg-LPS） on gingival tumour necrosis factor（TNF）-a and interleukin（IL）-6 levels in rats. A microdialysis probe with an injection needle attached to the surface of the dialysis membrane was implanted into the gingiva of the upper incisor. For comparison, the effects of LPS derived from Escherichia coli（Ec-LPS） on IL-6 and TNF-a levels were also analysed. Pg-LPS（1 mg/1 m L） or Ec-LPS（1 or 6 mg/1 m L） was applied by microsyringe, with gingival dialysates collected every hour. Enzyme-linked immunosorbent assay（ELISA） revealed that gingival dialysates contained approximately 389 pg？m L21 of IL-6 basally; basal TNF-a levels were lower than the detection limit of the ELISA. Pg-LPS failed to alter IL-6 levels but markedly increased TNF-a levels, which remained elevated for 2 h after treatment. Neither IL-6 nor TNF-a were affected by Ec-LPS. Reverse transcriptase-polymerase chain reaction（RT-PCR） analysis revealed that the gingiva expresses Toll-like receptor（TLR） 2 and TLR4 m RNA. Immunohistochemical examination showed that TLR2 and TLR4 are expressed by gingival epithelial cells. The present study provides in vivo evidence that locally applied Pg-LPS, but not Ec-LPS, into the gingiva transiently increases gingival TNF-a without affecting IL-6. The present results suggest that TLR2 but not TLR4 expressed on gingival epithelial cells may mediate the Pg-LPS-induced increase in gingival TNF-a in rats.

Relationship of Tumor Necrosis Factor-α and Nitrogen Oxide with Treatment of Frequent Relapse Nephrotic Syndrome by Shenkangling(肾康灵)Granule in Children

Objective: To observe the relationship of tumor necrosis factor-o (TNF-a) and nitrogen oxide (NO) with the treatment of frequent relapse nephrotic syndrome (FRNS) and to explore the patho-genesis of FRNS and the therapeutic mechanism of Shenkangling (肾康灵,SKL) Granule in children. Methods: Sixty children suffering from FRNS were randomly divided into the treated group and control group, 30 in each, and the other 30 healthy children were taken as healthy group. The patients were treated with prednisone for a long-term course, and those with no effect or partial effect shown were treated with additional Tripterygium or Cytoxan in the control group, while in the treated group patients were treated with prednisone and additional SKL. The two groups were compared as to their changes of TNF-a, NO before and after treatment, and the relapses after treatment. Results: The levels of TNF-a and NO in the sick children before treatment were markedly higher than those after treatment and normal group (P< 0. 01). The positive correlation between TNF-o of FRNS cases and relapse risk displayed more significance than that between the relapse of FRNS and NO. The difference between treated group and control group was significant (P<0. 01). Conclusion: TNF-a can be regarded as the monitoring parameter of the active phase in FRNS, and the higher the level, the more possible the relapse would occur. SKL could markedly reduce the relapse rate of FRNS in children.

Tumor necrosis factor-a and its role as a mediator in myocardial infarction:A brief review

Tumor necrosis factor-a (TNF-a) contributes to myocardial infarction (MI) injury. Polymorphism of TNF-a gene promoter region and secretion and release of TNF-a and its transformation by a series of signaling pathways are all changed at different points of pathophysiological process in MI. Researches also investigated TNF-a antagonists and their potential therapeutic role in the setting of MI and heart failure at both molecular and clinical level. This article briefly reviews TNF-a and its mechanism as a mediator in MI. Copyright ? 2015, Chinese Medical Association Production. Production and hosting by Elsevier B.V. on behalf of KeAi Communications Co., Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Sustained Contraction of Isolated Rabbit Thoracic Aortic Rings in Endothelial-dependent Manner Induced by βγ-CAT

In vertebrates, non-lens βγ-crystallins are widely expressed in various tissues and their functions are not well known. The molecular mechanisms of trefoil factors （TFFs）, which involved in mucosal healing and tumorigenesis, have remained elusive. βγ-CAT is a novel multifunctional protein complex of non-lens βγ-crystallin and trefoil factor from frog skin secretions. Here we report that βγ-CAT could induce sustained contraction of isolated rabbit aortic rings in dosage （2-35nmol/L） and endothelium dependent manners （P〈0.01 ）. In addition, in situ immunofluorescence indicated that positive TNF-α signals were mainly detected at the endothelial cell layer of βγ-CAT （25nmol/L） treated rings. Furthermore, βγ-CAT induced primary cultured rabbit thoracic aortic endothelial cells （RAECs） rapidly to release TNF-α. After βγ-CAT （25nmol/L） treated for 10 and 30min, the levels of the endothelial cells released TNF-ct were 34.17±5.10 pg/mL and 98.01±4.67 pg/mL （P〈0.01）, respectively. In conclusion, βγ-CAT could induce sustained contraction of isolated aortic rings, and the contractile effect might be partially explained by the release of TNF-α. These findings will give new insight into understanding the functions and physiological roles of non-lens βγ-crystallins and trefoil factors.

迪银片治疗寻常性银屑病的临床及实验室观察

目的 观察迪银片治疗寻常性银屑病的临床及实验室检测结果。方法 80例寻常性银屑病患者在接受迪银片治疗前及第 12周分别根据皮损求得PASI值 ,并相应检测血清sIL 2R ,IL 2 ,TNF α。结果 ①迪银片治疗 12周后 ,治愈 6例 ,显效 3 8例 ,进步 2 8例 ,总有效率 5 5 %。②血清sIL 2R ,TNF α水平治疗前后差异有高度显著性 (t =3 .0 7、3 .2 0 ,P均 <0 .0 1) ,IL 2水平治疗前后差异有显著性 (t =2 .19,0 .0 1<P <0 .0 5 )。③血清sIL 2R、TNF水平与PASI有关(r =0 .5 14、0 .416,P均 <0 .0 1) ,IL 2水平与PASI无关 (r =0 .2 0 9,P <0 .0 5 )。结论 迪银片可以减轻银屑病的活动程度 ,sIL 2R ,TNF α水平与疾病严重程度相关。

骨质疏松模型骨组织中IL-6,IL-1β,TNF-α的表达特征

目的:通过测定切除卵巢骨质疏松模型小鼠骨组织中白介素6 (IL- 6)、白介素1β(IL- 1β)、肿瘤坏死因子α(TNF -α)相关细胞因子的表达特征,探讨其在骨质疏松发病过程中的生物学意义。方法:选用4月龄雌性BALB/C小鼠随机分假手术对照组和去卵巢骨质疏松模型组,术后第12周用ABC免疫组织化学方法测定骨组织中IL -6,IL- 1β,TNF -α的蛋白含量并进行细胞定位。结果:免疫组织化学染色结果显示, 3种蛋白在模型组和对照组均有阳性表达,主要位于骨小梁周边成骨细胞、破骨细胞及骨髓细胞胞浆中,模型组蛋白含量明显高于对照组且与骨密度呈负相关(P<0. 01或P<0. 05)。结论:小鼠骨质疏松模型骨组织相关破骨细胞分化因子IL- 6,IL -1β,TNF -α表达增高,导致破骨活动增强,骨吸收大于骨形成,最终导致骨质疏松。

血必净对内毒素致急性肺损伤大鼠炎症反应的影响

目的探讨血必净在内毒素(LPS)诱导的大鼠急性肺损伤(ALI)发病中的影响。方法健康雄性Wistar大鼠40只随机分成4组。正常对照组(NC):经尾静脉注射4ml/kg的生理盐水(5min内);假手术组(SO):沿腹中线做一条长1.5cm的切口,取出盲肠,2min后将盲肠还纳腹腔,逐层缝合腹壁切口,并生理盐水4ml/kg尾静脉注射(5min内);盲肠结扎穿孔组(CLP):采用盲肠结扎手术复制脓毒症模型,并生理盐水4ml/kg尾静脉注射(5min内);CLP+血必净组:手术方法同CLP组,术后血必净4ml/kg尾静脉注射(5min内)。于制模后15h采集动脉血测量血气,然后分离血清,采用酶联免疫吸附试验(ELISA)检测血清中肿瘤坏死因子α(TNF-α)、白细胞介素(IL)-6和IL-8含量的变化,并与NC组进行比较。观察大鼠肺组织苏木素-伊红(HE)染色结果。结果CLP组大鼠血清中TNF-α、IL-6及IL-8的含量明显升高,CLP组大鼠动脉血氧分压(PaO2)的含量显著降低。肺组织HE染色观察CLP组大鼠肺泡间隔增宽,肺间质见多量炎性细胞浸润,肺泡腔变窄、出血、中性粒细胞渗出及炎症渗出物。CLP+血必净组中性粒细胞渗出及炎症渗出物明显减轻。结论血必净能减轻内毒素血症所致的肺脏炎症反应,对内毒素致ALI时肺脏具有保护作用。

肺气虚证患者血清IL-8、TNF的水平及临床意义

目的测定肺气虚证患者肺功能及细胞因子水平,为肺气虚证本质的研究提供一些依据。方法对58例老年肺气虚证患者及20例正常对照者进行肺功能、白细胞介素-8、肿瘤坏死因子测定。结果肺气虚证患者的肺功能明显低于对照组(P<0.01),而白细胞介素-8、肿瘤坏死因子均值明显高于对照组(P<0.01),不同程度肺气虚证候患者组间比较也有显著差异(P<0.01)。结论肺气虚证患者气道阻塞,肺功能下降,而白细胞介素-8、肿瘤坏死因子水平升高,两者成负相关关系,共同参与肺气虚证的慢性气道炎症反应。

癫痫患者外周血清中β淀粉样蛋白与IL-8、TNF-α水平的改变

目的观察癫痫患者外周血β淀粉样蛋白(Aβ1-28)、肿瘤坏死因子(TNF-α)和白细胞介素8(IL-8)水平变化,以探讨是否与癫痫的发病存在相关性。方法收集36例癫痫患者和40例正常人血清,应用放射免疫分析法分别检测31例癫痫患者血清Aβ1-28、24例患者血清IL-8和13例患者血清TNF-α的水平变化,应用SPSS及Origin统计软件进行数据分析。结果癫痫患者血清Aβ1-28和IL-8水平明显增高(P=0.05),癫痫组患者血清TNF-α水平较正常对照组水平增高,但差异无显著性(P>0.05)。癫痫组部分患者血清IL-8水平同TNF-α水平进行相关性分析,结果二者呈正相关。结论血清Aβ1-28、IL-8水平与癫痫发病可能存在相关性,而血清TNF-α水平与癫痫发病的相关性则不明显,在癫痫患者外周血中IL-8和TNF-α可能存在协同作用。

快针结合运动疗法治疗老年腰椎间盘突出症的疗效观察

目的:观察快针结合运动疗法治疗老年腰椎间盘突出症的疗效。方法:将80例老年腰椎间盘突出症患者随机分为治疗组和对照组,各40例,治疗组采用快针结合运动疗法,对照组采用传统针灸疗法。比较两组疗效及血清TNF-α、IL-6的变化。结果:治疗组总有效率(92.5%)高于对照组(82.5%),血清TNF-α、IL-6水平均低于对照组,差异均有统计学意义(P<0.05)。结论:快针结合运动疗法治疗老年腰椎间盘突出症患者的疗效优于传统针灸,并能降低患者血清TNF-α、IL-6炎性因子水平。

CHF患者血红蛋白水平差异与血清BNP、TNF-α、sICAM-1的关系以及对MWS和LVMI的影响

目的研究慢性心力衰竭(CHF)患者血红蛋白水平与血浆B型钠尿肽(BNP)、血清肿瘤坏死因子-α(TNF-α)、可溶性细胞间黏附分子-1(sICAM-1)的关系及对左心室质量指数(LVMI)和平均室壁应力(MWS)、心功能的影响。方法对入选的121例CHF患者测定了血红蛋白浓度、血浆BNP、血清TNF-α和sICAM-1水平,超声心动图测量左室射血分数(LVEF),评价心功能;计算LVMI和MWS;按血红蛋白水平分为CHF贫血组和非贫血组,同时选择27例正常人作为对照组。结果CHF患者Hb水平和LVEF低于正常对照组,而血浆BNP、血清TNF-α和sICAM-1水平以及MWS和LVMI高于对照组(P<0.01);随着心功能恶化,Hb水平和LVEF则逐渐降低,而血浆BNP、血清TNF-α和sICAM-1水平以及MWS和LVMI逐渐升高;CHF贫血组患者血浆BNP、血清TNF-α和sICAM-1水平以及MWS和LVMI均升高,明显高于非贫血组患者P<0.01);随着贫血程度的加重,CHF患者血浆BNP、血清TNF-α和sICAM-1水平以及MWS和LVMI进一步升高(P<0.01);CHF患者MWS和LVMI与Hb水平、血浆BNP、TNF-α和sICAM-1水平均呈正相关(P<0.01)。结论CHF患者Hb水平的降低和TNF-α和sICAM-1水平的升高参与了心功能不全心室重构发生发展的病理生理过程,而CHF患者贫血的出现使心功能不全心室重构程度加重化。

单核细胞及中性粒细胞与内皮细胞粘附的区别

为探讨单核细胞及中性粒细胞与肿瘤坏死因子－ ２ 诱导的内皮细胞粘附的区别，采用髓过氧化酶法测定白细胞与内皮细胞的粘附和抗粘附分子单克隆抗体对其粘附的影响，用酶联免疫法测定内皮细胞粘附分子的表达。结果表明，肿瘤坏死因子－ α呈浓度依赖性地增加内皮细胞与中性粒细胞或单核细胞的粘附，并可诱导内皮细胞上粘附分子的表达增加。肿瘤坏死因子－ α激活内皮细胞后６ 小时，与中性粒细胞的粘附率最高，而激活后２４ 小时，与单核细胞的粘附率最高。抗细胞间粘附分子－ １ 及抗 Ｅ－ 选择素单克隆抗体可显著抑制中性粒细胞与肿瘤坏死因子－ α激活的内皮细胞的粘附，而抗细胞间粘附分子－ １ 及抗血管细胞粘附分子－ １ 单克隆抗体则可抑制单核细胞与肿瘤坏死因子－ α激活的内皮细胞的粘附。结果提示，两种类型的白细胞与肿瘤坏死因子－ α诱导的内皮细胞的粘附具有不同的特点。

肿瘤坏死因子对原发性高血压左室构型的影响

目的:探讨肿瘤坏死因子(TNF)在原发性高血压心肌肥厚过程中的病理生理作用。方法:原发性高血压病人64例,对照组30例,以超声心动图测定左心室质量指数(LVM I)和室壁相对厚度(RW T),根据LVM I与RW T把高血压组分成四种构型。用发光免疫法测定血清TNF含量。结果:1.高血压组TNF含量显著高于正常对照组,并且与血压升高程度呈正相关;2.正常构型组TNF含量显著高于正常对照组;3.向心性重构组及向心性肥厚组显著高于正常构型组,但两组之间的差别不显著;4.离心性肥厚组TNF显著高于其他构型组;5.TNF与LVM I、左室舒张期末容积(EDV)及收缩期末容积(ESV)正相关,与左心室射血分数(EF)负相关。结论:TNF促进了左室构型向离心性肥厚的发展。

肿瘤坏死因子体内抗瘤活性的研究

本文以S180瘤细胞株为靶细胞建立了动物肿瘤模型，分别以TNF单用、TNF－CTX合用和脂质体－TNF复合物三种给药方式，进行了肿瘤坏死因子（TNF）体内抗癌试验。结果表明，TNF——CTX合用，具有协同抗瘤作用，且能减轻副作用；脂质体——TNF复合物能明显减轻TNF的毒性反应，而不影响TNF的抗癌作用。

测定血清肿瘤坏死因子在急性危重病中的临床意义

测定了54例急性危重病患者和21例正常人血清肿瘤坏死因子水平。结果表明:血清肿瘤坏死因子在急性心肌梗塞组(26.40±19.74U/ml)、脑卒中组(18.25±4.94U/ml)和心衰组(38.57±48.18U/mkl)均较正常对照组(15.80±1.70U/ml)升高(P<0.05)。在54例危重患者中有7例血清肿瘤坏死因子明显升高。作者认为危重病患者血清肿瘤坏死因子升高与病变的严重程度、有无并发症和感染有关。

心力衰竭患者血红蛋白、血清BNP、TNF-α、NO和ICAM-1水平的变化及关系以及对心室重构、心功能的影响

目的:研究慢性心力衰竭(CHF)患者血红蛋白水平与血浆B型钠尿肽(BNP)、血清肿瘤坏死因子-α(TNF-α)、一氧化氮(NO)和细胞间黏附分子-1(ICAM-1)的关系及对心室重构、心功能的影响。方法:对入选的121例CHF患者测定了血红蛋白浓度、血浆BNP、血清TNF-α、NO和ICAM-1水平,超声心动图测量左室射血分数(LVEF),评价心功能;计算左心室质量指数(LVMI)和平均室壁应力(MWS);按血红蛋白水平分为CHF贫血组和非贫血组,同时选择27例正常人作为对照组。结果:CHF患者Hb水平和LVEF低于正常对照组,而血浆BNP、血清TNF-α、NO和ICAM-1水平以及MWS和LVMI高于对照组(P<0.01);随着心功能恶化,Hb水平和LVEF则逐渐降低,而血浆BNP、血清TNF-α、NO和ICAM-1水平以及MWS和LVMI逐渐升高;CHF贫血组患者血浆BNP、血清TNF-α、NO和ICAM-1水平以及MWS和LVMI均升高,明显高于非贫血组患者和健康对照组(P<0.01);随着贫血程度的加重,CHF患者血浆BNP、血清TNF-α、NO和ICAM-1水平以及MWS和LVMI进一步升高(P<0.01);CHF患者MWS和LVMI与Hb水平、血浆BNP、TNF-α、NO和ICAM-1水平均呈正相关(P<0.01)。结论:CHF患者Hb水平的降低和TNF-α、NO和ICAM-1水平的升高参与了心功能不全心室重构发生发展的病理生理过程,而CHF患者贫血的出现使心功能不全心室重构程度加重化。

干扰素对慢性乙型肝炎血清IL-1β、IL-6和TNF-α活性的临床研究

通过检测慢性乙型肝炎患者经干扰素治疗前后血清ＩＬ－ １β、ＩＬ－ ６ 和ＴＮＦ－ α活性的变化规律，探索干扰素抗病毒作用的机制。用ＥＬＩＳＡ 法检测ＨＢｓＡｇ、抗ＨＢｓ、抗ＨＢｃ、ＨＢｅＡｇ、抗ＨＢｅ，用聚合酶链反应（ＰＣＲ） 检测ＨＢＶ－ ＤＮＡ，用双抗体夹心法检测ＩＬ－ １β、ＩＬ－ ６ 、ＴＮＦ－ α。结果１ ．干扰素治疗组治疗后ＩＬ－ １β、ＩＬ－ ６ 和ＴＮＦ－ α均显著低于治疗前。而对照组则无明显差异。２ ．治疗组ＨＢｅＡｇ 和ＨＢＶ－ ＤＮＡ阴转的２０ 例中，治疗前ＩＬ－ １β、ＩＬ－ ６ 和ＴＮＦ－ α明显高于未转阴组（ Ｐ＜ ０－０１ ，Ｐ＜ ０－０５ 和Ｐ＜ ０－０５） 。慢性乙型肝炎患者血清ＩＬ－ １β、ＩＬ－ ６ 和ＴＮＦ－ α活性测定可以作为评估干扰素抗病毒作用的参考指标之一。