白细胞介素6和维甲酸对肝癌细胞细胞周期动力学的影响

为探讨重组白细胞介素６（ＩＬ－６）和全反式维甲酸（ＲＡ）诱导肝癌细胞凋亡的作用用流式细胞仪测定ＩＬ－６和ＲＡ对ＨｅｐＧ２肝癌细胞的细胞周期动力学和调亡诱导率的影响。结果表明ＩＬ－６和ＲＡ作用于细胞凋亡周欺遥Ｓ期，抑制肝癌细胞的ＤＮＡ合成。ＩＬ－６诱发细胞凋亡率显著高于ＲＡ的作用，此效应与其作用时间和剂量有关。提示ＩＬ－６可促进体外培养的肝癌细胞凋亡，抑制其ＤＮＡ合成。但需进一步探讨ＩＬ－６治疗肝癌     

苦参碱对乙型肝炎肝纤维化患者血清IL-6、IL-8含量的影响

探讨氧化苦参碱对乙型肝炎肝纤维化的临床疗效。经肝穿活组织病理检查筛选 6 4例乙型肝炎肝纤维化患者 ,随机分为治疗组和对照组各 32例。两组治疗前后均采用放射免疫技术检测血清IL - 6、IL - 8及HA、LN、PC -Ⅲ含量。结果显示氧化苦参碱治疗前后血清IL - 6、IL - 8及HA、LN、PC -Ⅲ含量比较差异有显著性 (P <0 0 1) ,治疗后上述含量均明显下降 ,与对照组相比差异有显著性 (P <0 0 1)。证明氧化苦参碱具有抗肝纤维化效用     

血浆置换联合血液滤过对乙型肝炎相关慢加急性肝衰竭患者血清IL-17和IL-6的影响

目的探讨血浆置换联合血液滤过对乙型肝炎相关肝衰竭血清白细胞介素(IL)-17、IL-6的影响。方法 30例乙型肝炎慢加急性肝衰竭患者在内科治疗的基础上采用血浆置换联合血液滤过单次治疗。用ELISA检测各组血清IL-17、IL-6浓度,同时记录血清ALT、TBil等值并进行统计分析。结果肝衰竭组患者血清IL-17、IL-6水平分别为(123.5±23.0)pg/ml、(110.0±18.5)pg/ml,高于慢性乙型肝炎患者(48.5±6.3)pg/ml、(27.8±5.9)pg/ml和正常对照组(34.7±3.3)pg/ml、(12.1±5.1)pg/ml,P均<0.001;治疗后血清IL-17、IL-6水平分别为(84.7±21.4)pg/ml、(75.8±16.6)pg/ml,较治疗前下降(t=35.1,P<0.001;t=33.4,P<0.001);与好转组相比,人工肝对恶化组血清IL-17、IL-6清除效率降低(t=3.8,P<0.05;t=3.9,P<0.05);人工肝对血清IL-17、IL-6清除效率均与MELD评分呈负相关(r=-0.53、P=0.003;r=-0.43,P=0.015)。结论血浆置换联合血液滤过能有效降低肝衰竭患者血清IL-17、IL-6水平,其对IL-17、IL-6的清除效率可能与患者预后有关。     

阿奇霉素对MPP患儿的疗效及对血清sIL-2R、IL-6、IL-17及IL-23的影响

目的探讨阿奇霉素治疗肺炎支原体肺炎(mycoplasma pneumoniae pneumonia, MPP)患儿的临床效果及对患儿血清可溶性白细胞介素-2 受体(soluble interleukin-2 receptor, sIL-2R)、IL-6、IL-17、IL-23 水平的影响。方法选取我院 2018 年 1—8 月收治的 142 例 MPP 患儿作为研究对象,采用随机数字表法分为阿奇霉素组和红霉素组各 71 例,2 组基础治疗保持一致;对比 2 组患儿的临床效果,sIL-2R、IL-6、IL-17 及 IL-23 水平,各项临床症状缓解时间及不良反应。结果阿奇霉素组的咳嗽消失时间、肺部啰音消失时间、退热时间均短于红霉素组(P 均< 0.05);治疗前,2 组患儿的sIL-2R、IL-6、IL-17 及 IL-23 水平差异无统计学意义(P 均> 0.05);治疗 7 d 后,阿奇霉素组患儿的 sIL-2R、IL-6、IL-17及 IL-23 水平均低于红霉素组(P 均< 0.05);治疗 10 d 后,阿奇霉素组的临床效果优于红霉素组(P < 0.05);阿奇霉素组的不良反应发生率为 5.63%低于红霉素组的 16.90%(P < 0.05)。结论阿奇霉素治疗 MPP 患儿效果优于红霉素,能有效缓解患儿的临床症状并降低 sIL-2R、IL-6、IL-17 及 IL-23 水平。     

抗肝昏肠液对实验性肝性脑病大鼠模型IL—6的影响

目的：探讨抗肝昏肠液对肝性脑病大鼠白细胞介素6（IL－6）的影响。方法：采用药物诱导加结扎、切除2／3肝脏的方法建立大鼠肝性脑病模型,用抗肝昏肠液大、小剂量治疗的患者为治疗组,以乳果糖治疗的患者为对照组,观察药物对肝性脑病大鼠IL－6、脑电图、血氨、肝功能及肝组织病理学等的影响。结果：抗肝昏肠液大、小剂量对IL－6及其他指标都有不同程度的改善,大剂量组疗效优于乳果糖组。结论：抗肝昏肠液能显著降低IL－6含量。其影响可能与以下作用有关：（1）阻断肠道对氨、内毒素等有毒物质的吸收、促进其排除;（2）抑制单核巨噬细胞系统介导的细胞毒作用;（3）促进肝功能恢复,行使对内毒素等的清除功能。从而抑制IL－6对肝脏进一步的免疫损伤,促进肝性脑病的复苏。     

WBC、IL-6对急性心肌梗死患者近期预后的影响

目的 观察急性心肌梗死（AMI）患者人院外周血白细胞（WBC）总数、血浆白细胞介素-6（IL-6）对近期预后的影响。方法 首发AMI患者103例，通过检测WBC、IL-6，以发病后30天内是否发生心血管不良事件（包括心源性死亡、心力衰竭、心源性休克、恶性心律失常）为观察终点。结果 36例发生心血管事件组外周血WBC总数和IL-6显著高于67例无心血管事件组。AMI时外周血WBC总数和IL-6水平为发生心血管事件的预测因素。结论 WBC、IL-6与AMI患者近期预后相关。     

抑制促肝再生磷酸酶-3对大肠癌细胞迁移能力的影响

目的:观察促肝再生磷酸酶-3(phosphatase ofregeneration liver-3,PRL-3)抑制剂原钒酸钠(sodium orthovanadate,SoV)对大肠癌细胞株Colo-320迁移能力的影响.方法:应用Western blot方法检测PRL-3在7株大肠癌细胞中的表达,筛选表达最强的1株做下一步抑制实验.选择PRL-3拮抗剂SoV,通过细胞划痕实验观察其在0.5 μmol/L浓度下对癌细胞运动能力的影响,高倍倒置显微镜下计算细胞迁移距离.细胞爬片原位杂交观察SoV对PRL-3 mRNA的表达.结果:PRL-3表达最强的结肠癌细胞株为Colo-320.细胞划痕实验显示,SoV作用48 h细胞仅迁移相当于4-7个细胞的距离,400×倍镜下精确测量20个细胞在0-48 h迁移距离,计算对照组细胞迁移速度为39.12±10.11μm/h,SoV为12.84±6.78 μm/h,差异非常显著(P<0.00001).SoV作用细胞48 h后原位杂交结果未见PRL-3 mRNA阳性表达.结论:SoV能显著抑制Colo-320细胞迁移能力,其机制可能与抑制PRL-3酶活性以及基因转录有关.     

白细胞介素2和6对肝癌细胞表达血管内皮生长因子D的调节

目的探讨白细胞介素(IL)-2和IL-6对肝癌细胞表达血管内皮生长因子(VEGF)-D的调节。方法采用由IL-2或IL-6分别对肝癌细胞株SMMC-7721和BEL-7402进行刺激,采取逆转录-聚合酶链式反应技术(RT-PCR)观察其VEGF-D基因表达。结果 IL-2使细胞株SMMC-7721和BEL-7402产生VEGF-D mRNA减少;IL-6对肝癌细胞株BEL-7402 VEGF-D mRNA表达存在促进效果,但是无法从作用时间上来显著判断。IL-6对肝癌细胞株SMML-7721 VEGF-D mRNA表达存在促进效果,当浓度条件满足情况下,促进作用和作用时间存在正相关。结论抑制肝癌细胞VEGF-D mRNA的表达方面,IL-2作用比较明显,对肝癌淋巴转移能够形成一定作用;肝癌细胞BEL-7402和SMML-7721 VEGF-D mRNA的表达方面,IL-6带来的促进效果明显,但是对肝癌作用需更多研究。     

慢性乙型肝炎病毒携带者血清IL-1、IL-6和CRP水平与肝组织学相关研究

目的探讨慢性HBV携带者血清IL-1I、L-6和CRP水平与肝组织学变化的相关性。方法采用双抗体夹心ELISA法检测血清IL-1I、L-6;免疫比浊法检测血清CRP。采用在B超引导下快速肝穿刺活检术,肝组织炎症活动度分为轻度(G1-2/S0-2),中度(G3/S1-3),重度(G4/S2-4)。结果中、重度肝组织炎症活动者血清IL-1I、L-6和CRP水平显著高于轻度或无炎症改变者(P<0.05),轻度和无炎症改变者与正常对照组间比较无显著差异(P>0.05)。结论慢性HBV携带者血清IL-1I、L-6和CRP水平可以做为反应肝组织炎症活动程度的指标。     

IL-6联合sIL-6R对人甲状腺细胞增殖及相关基因表达的影响

目的 探讨白细胞介素-6(IL-6)联合可溶性IL-6受体(sIL-6R)对人甲状腺细胞增殖及相关基因表达的影响.方法 通过手术标本获得甲状腺组织,采用甲状腺细胞培养技术,提取并培养甲状腺细胞.以不同浓度(0、1、5、10、20 μg/L)的IL-6分别联合sIL-6R 100μg/L干预细胞24、48 h,予以IL-6单克隆抗体进行阻断.以MTT法检测IL-6干预后的细胞活力,并在显微镜下观察细胞形态学变化;以RT-PCR测定IL-6、IL-6受体及糖蛋白130的表达,实时定量PCR检测IL-6干预后甲状腺细胞的钠-碘转运体(NIS)、甲状腺过氧化物酶(TPO)、甲状腺球蛋白(TG)、促甲状腺激素受体(TSHR)基因的表达.结果 甲状腺细胞表达IL-6、糖蛋白130,但几乎不表达IL-6受体.IL-6联合sIL-6R培养24、48 h后,甲状腺细胞活力显著增加(F=65.28、78.47;P均＜0.05),而使用IL-6单克隆抗体进行阻断,发现随着IL-6单克隆抗体浓度的增加,甲状腺细胞活性亦显著下降(F=60.15,P＜0.05);随着IL-6浓度的增加,甲状腺细胞数量越多,体积越大.IL-6能够抑制NIS、TPO、TG基因的表达(t=6.92～12.12,P均＜0.05),而对TSHR基因无明显影响.结论 IL-6联合sIL-6R能够促进甲状腺细胞增殖,同时也能够抑制甲状腺相关基因的表达.     

体外培养的肝癌细胞株与正常肝细胞株蛋白质的差异表达

目的:运用SELDI蛋白质芯片技术分析体外培养的肝癌细胞株(HepG2)与正常肝细胞株(L02)蛋白质表达差异．方法:在体外培养HepG2和L02细胞株,收获细胞,将细胞用细胞裂解液裂解后,采用SELDI蛋白质芯片技术用IMAC3 及WCX2芯片检测HepG2、L02的蛋白质谱．结果:体外培养的肝癌细胞株与正常肝细胞株的蛋白质存在差异表达,IMAC3芯片共捕获61个蛋白,发现差异峰7个,与 L02细胞相比,其中3个差异蛋白在肝癌细胞中高表达,4个差异蛋白在肝癌细胞中低表达．WCX2芯片共捕获91个蛋白, 发现差异峰14个,其中3个差异蛋白在肝癌细胞中高表达,11 个差异蛋白在肝癌细胞中低表达．结论:SELDI蛋白芯片技术检测肝癌细胞株与正常肝细胞株蛋白质的差异表达方法简便,敏感性高,重复性好．     

Circulating levels of interleukin-6, its soluble receptor and interleukin-6/interleukin-6 receptor complexes in patients with type 2 diabetes mellitus

We evaluated the relationship between plasma fibrinogen concentration and the serum levels of interleukin-6 (IL-6), its soluble receptor, and their complex in patients with type 2 diabetes mellitus. The study comprised 57 patients with type 2 diabetes and 15 normal healthy controls. Serum levels of IL-6, soluble IL-6 receptor (IL-6R), and circulating IL-6/IL-6R complex were determined by enzyme-linked immunosorbent assays. Correlations between the different study parameters and serum IL-6, IL-6R, or IL-6/IL-6R complex levels were determined by multiple linear regression analysis. Any association between the different study parameters and the serum levels of IL-6, IL-6R, or IL-6/IL-6R complex were determined by stepwise linear regression analysis. The serum IL-6 level in diabetic subjects was significantly higher than in normal healthy controls (3.48 ± 3.29 pg/ml vs 0.784 ± 0.90 pg/ml, mean ± SD, respectively, P = 0.0001). The specific optical density of the serum IL-6/IL-6R complex in diabetic patients was also significantly higher than in normal healthy controls, although there was no significant difference in the serum IL-6R level between diabetic patients and controls. The serum IL-6 concentration was correlated significantly with the HbA_1C level (β = 0.58, P = 0.04) by multiple regression analysis. Stepwise regression analysis revealed that the levels of serum IL-6 (F = 8.251), HbA_1C (F = 1.08), and serum urea nitrogen (F = 5.603) were associated with the plasma fibrino gen concentration. These results suggest that hyperglycaemia and increased levels of serum IL-6 can increase the plasma fibrinogen concentration, one of the known risk factors for atherosclerosis in patients with type 2 diabetes mellitus. Received: 24 August 1998 / Accepted in revised form: 2 February 1999     

Prognostic significance of plasma interleukin-6/-8 in pancreatic cancer patients receiving chemoimmunotherapy

AIM: To investigate the association of plasma levels of interleukin(IL)-6 and-8 with Wilms' tumor 1(WT1)-specific immune responses and clinical outcomes in patients with pancreatic ductal adenocarcinoma(PDA) treated with dendritic cells(DCs) pulsed with three types of major histocompatibility complex classⅠand Ⅱ-restricted WT1 peptides combined with chemotherapy.METHODS: During the entire treatment period, plasma levels of IL-6 and-8 were analyzed by ELISA. The induction of WT1-specific immune responses was assessed using the WT1 peptide-specific delayed-type hypersensitivity(DTH) test.RESULTS: Three of 7 patients displayed strong WT1-DTH reactions throughout long-term vaccination with significantly decreased levels of IL-6/-8 after vaccinations compared with the levels prior to treatment. Moreover, overall survival(OS) was significantly longer in PDA patients with low plasma IL-6 levels( 2 pg/m L) after 5 vaccinations than in patients with high plasma IL-6 levels(≥ 2 pg/m L)(P = 0.025). After disease progression, WT1-DTH reactions decreased severely and were ultimately negative at the terminal stage of cancer. The decreased levels of IL-6/-8 observed throughout long-term vaccination were associated with WT1-specific DTH reactions and long-term OS.CONCLUSION: Prolonged low levels of plasma IL-6/-8 in PDA patients may be a prognostic marker for the clinical outcomes of chemoimmunotherapy.     

High levels of serum interleukin-6 increase mortality of hepatitis B virus-associated acute-on-chronic liver failure

BACKGROUND Patients with hepatitis B virus-associated acute-on-chronic liver failure(HBVACLF) present a complex and poor prognosis.Systemic inflammation plays an important role in its pathogenesis,and interleukin-6(IL-6) as a pro-inflammatory cytokine is related with severe liver impairment and also plays a role in promoting liver regeneration.Whether serum IL-6 influences HBV-ACLF prognosis has not been studied.AIM To determine the impact of serum IL-6 on outcome of patients with HBV-ACLF.METHODS We performed a retrospective study of 412 HBV-ACLF patients.The findings were analyzed with regard to mortality and the serum IL-6 level at baseline,as well as dynamic changes of serum IL-6 within 4 wk.RESULTS The serum IL-6 level was associated with mortality.Within 4 wk,deceased patients had significantly higher levels of IL-6 at baseline than surviving patients [17.9(7.3-57.6) vs 10.4(4.7-22.3),P = 0.011].Patients with high IL-6 levels( 11.8 pg/m L) had a higher mortality within 4 wk than those with low IL-6 levels(≤ 11.8 pg/m L)(24.2% vs 13.2%,P = 0.004).The odds ratios calculated using univariate and multivariate logistic regression were 2.10(95% confidence interval [CI]:1.26-3.51,P = 0.005) and 2.11(95%CI:1.15-3.90,P = 0.017),respectively.The mortality between weeks 5 and 8 in patients with high IL-6 levels at 4 wk was 15.0%,which was significantly higher than the 6.6% mortality rate in patients with low IL-6 levels at 4 wk(hazard ratio = 2.39,95%CI:1.05-5.41,P = 0.037).The mortality was 5.0% in patients with high IL-6 levels at baseline and low IL-6 levels at 4 wk,7.5% in patients with low IL-6 levels both at baseline and at 4 wk,11.5% in patients with low IL-6 levels at baseline and high IL-6 levels at 4 wk,and 16.7% in patients with high IL-6 levels both at baseline and at 4 wk.The increasing trend of the mortality rate with the dynamic changes of IL-6 was significant(P for trend = 0.023).CONCLUSION A high level of serum IL-6 is an independent risk factor for mortality in patients with HBV-ACLF.Furthermore,a sustained high level or dynamic elevated level of serum IL-6 indicates a higher mortality.     

一氧化氮、白介素、肿瘤坏死因子与肝硬化患者预后的关系

目的:探讨血清一氧化氮(NO)、IL-6、IL-10、肿瘤坏死因子(TNF)水平与肝硬化患者预后之间的关系.方法:采用硝酸还原酶法、ELISA法、双抗体夹心酶联免疫分析法分别测定30例健康对照者和56例肝硬化患者治疗前后的血清NO,IL-6,IL-10及TNF水平.结果:肝硬化患者的NO,IL-6,TNF水平显著升高,IL-10水平明显降低.治疗后肝功能减退组的NO (129.21±27.32μmol/L vs 92.18±25.68μmol/L,P<0.05)、IL-6(198.5±23.2 mg/L vs 147.0±19.1 mg/L,P<0.05)、TNF(179.2±23.5 pg/dL vs 121.4±17.5 pg/ dL,P<0.05)水平较治疗前有显著升高,IL-10水平则明显下降(33.4±7.2 mg/L vs 51.6±18.5 mg/L,P<0.05),而治疗后肝功能恢复组NO(58.63±12.25μmol/L vs 94.36±23.45μmol/L,P<0.05)、IL-6(90.3±12.7 mg/ L vs 148.5±15.8 mg/L,P<0.05)、TNF(78.2±14.3 pg/dL vs 124.9±20.1 pg/dL,P<0.05)水平较治疗前降低(P<0.05),IL-10水平则明显升高(89.3±18.9 mg/L vs 48.8±9.5 mg/L,P<0.05).结论:NO,IL-6,IL-10,TNF与肝硬化患者预后有关.     

白细胞介素-6与胃癌易感性的相关研究

目的评价IL-6 174G/C和IL-6 572G/C基因多态性与胃癌风险的相关关系,以及IL-6基因多态性与幽门螺杆菌(H.pylori)感染和吸烟的交互作用。方法采用病例对照研究方法,纳入咸宁市中心医院消化内科2008年1月-2011年5月新发胃癌246例,非肿瘤患者274例作为对照组。采用PCR-RFLP方法测定IL-6 174G/C和IL-6 572G/C的基因分型。结果研究发现携带IL-6 174CC基因型和C等位基因型胃癌发病风险显著增高,调整后的OR(95%CI)分别为1.88(1.07~3.48)和1.56(1.14~2.52)。携带IL-6 174GC和CC基因型在H.pylori阳性感染者中和吸烟者中均能增加患胃癌的风险,IL-6 174G/C基因多态性与H.pylori感染有交互作用(P0.05)。研究未发现IL-6 572G/C基因多态性与胃癌发病风险有相关关系。结论本研究结果表明IL-6基因多态性具有促进胃癌发生和发展的作用,IL-6可以作为胃癌遗传学的检测指标,用于检验胃癌易感个体的生物学指标。     

Genetic association of interleukin-6 polymorphism (-174 G/C) with chronic liver diseases and hepatocellular carcinoma

Interleukin-6 (IL-6) is a pleiotropic cytokine which is expressed in many inflammatory cells in response to different types of stimuli, regulating a number of biological processes. The IL-6 gene is polymorphic in both the 5’ and 3’ flanking regions and more than 150 single nucleotide polymorphisms have been identified so far. Genetic polymorphisms of IL-6 may affect the outcomes of several diseases, where the presence of high levels of circulating IL-6 have been correlated to the stage and/or the progression of the disease itself. The -174 G/C polymorphism is a frequent polymorphism, that is located in the upstream regulatory region of the IL-6 gene and affects IL-6 production. However, the data in the literature on the genetic association between the -174 G/C polymorphism and some specific liver diseases characterized by different etiologies are still controversial. In particular, most of the studies are quite unanimous in describing a correlation between the presence of the high-producer genotype and a worse evolution of the chronic liver disease. This is valid for patients with hepatitis C virus (HCV)-related chronic hepatitis and liver cirrhosis and hepatocellu-lar carcinoma (HCC) whatever the etiology. Studies in hepatitis B virus-related chronic liver diseases are not conclusive, while specific populations like non alcoholic fatty liver disease/non-alcoholic steatohepatitis, autoimmune and human immunodeficiency virus/HCV coinfected patients show a higher prevalence of the lowproducer genotype, probably due to the complexity of these clinical pictures. In this direction, a systematic revision of these data should shed more light on the role of this polymorphism in chronic liver diseases and HCC.     

Assessment for the minimal invasiveness of laparoscopic liver resection by interleukin-6 and thrombospondin-1

BACKGROUNDLaparoscopic surgery has been introduced as a minimally invasive technique for the treatment of various field. However, there are few reports that have scientifically investigated the minimally invasive nature of laparoscopic liver resection (LLR).AIMTo investigate whether LLR is scientifically less invasive than open liver resection.METHODSDuring December 2011 to April 2015, blood samples were obtained from 30 patients who treated with laparoscopic (n = 10, 33%) or open (n = 20, 67%) partial liver resection for liver tumor. The levels of serum interleukin-6 (IL-6) and plasma thrombospondin-1 (TSP-1) were measured using ELISA kit at four time points including preoperative, immediate after operation, postoperative day 1 (POD1) and POD3. Then, we investigated the impact of the operative approaches during partial hepatectomy on the clinical time course including IL-6 and TSP-1.RESULTSSerum level of IL-6 on POD1 in laparoscopic hepatectomy was significantly lower than those in open hepatectomy (8.7 vs 30.3 pg/mL, respectively) (P = 0.003). Plasma level of TSP-1 on POD3 in laparoscopic hepatectomy was significantly higher than those in open hepatectomy (1704.0 vs 548.3 ng/mL, respectively) (P = 0.009), and have already recovered to preoperative level in laparoscopic approach. In patients with higher IL-6 Levels on POD1, plasma level of TSP-1 on POD3 was significantly lower than those in patients with lower IL-6 Levels on POD1. Multivariate analysis showed that open approach was the only independent factor related to higher level of IL-6 on POD1 [odds ratio (OR), 7.48; 95% confidence interval (CI): 1.28-63.3; P = 0.02]. Furthermore, the higher level of serum IL-6 on POD1 was significantly associated with lower level of plasm TSP-1 on POD3 (OR, 5.32; 95%CI: 1.08-32.2; P = 0.04) in multivariate analysis. CONCLUSIONIn partial hepatectomy, laparoscopic approach might be minimally invasive surgery with less IL-6 production compared to open approach.     

NF-κB在肝癌细胞株SMMC-7721中的表达及意义

目的　了解NF -kB和ⅠkB在肝癌细胞中的表达情况及意义。方法　通过RT -PCR和Westernblot方法研究NF -kB和ⅠkB在肝癌细胞和正常肝细胞中的mRNA和蛋白表达的变化情况。结果　在肝癌细胞株SMMC -772 1中P65、P5 0mRNA表达增强而ⅠkBmRNA表达下降 (P <0 0 1) ;Westernblot结果显示肝癌细胞株SMMC -772 1细胞的胞核中P5 0、P65蛋白高水平表达 ,而正常肝细胞仅检测出极低水平的P5 0、P65蛋白 ,但是在SMMC -772 1细胞的胞质中ⅠkB蛋白低水平表达 ,正常肝细胞高水平表达。结论　肝癌细胞株SMMC -772 1中NF -kB的P5 0、P65亚基表达升高、ⅠkB表达下降与肿瘤细胞的生长密切相关。     

小白菊内酯对多发性骨髓瘤细胞蛋白酶体活性及白细胞介素-6表达的影响

目的探讨小白菊内酯(parthenolide,PTL)对多发性骨髓瘤(multiple myeloma,MM)细胞蛋白酶体活性及白细胞介素-6(interleukin-6,IL-6)表达的影响,以期了解PTL抗MM的分子机制。方法2006年5月至2007年3月华中科技大学同济医学院附属协和医院血液病研究所,体外培养人MM细胞系PRMI8266,与不同浓度的PTL作用不同时间。以荧光底物法检测细胞蛋白酶体活性,逆转录聚合酶链反应(RT-PCR)检测IL-6基因表达,酶联免疫吸附试验(ELISA)法检测MM细胞培养上清中IL-6的质量浓度。结果2~10μmol/L的PTL作用16h对PRMI8266细胞蛋白酶体的糜蛋白酶活性具有明显抑制作用,其效应呈现浓度依赖性;10μmol/L可达到接近50%的活性抑制。RT-PCR检测结果表明,2,5,10μmol/L的PTL作用24h,MM细胞的IL-6基因 mRNA表达强度与对照相比均明显降低;2,5,10μmol/L的PTL作用MM细胞48h后,培养上清中IL-6质量浓度分别为(92.6±4.3)ng/L、(67.1±5.7)ng/L、(43.5±4.9)ng/L,与对照组(148.7±8.2)ng/L相比,差异有显著性意义(P<0.01)。结论PTL能明显抑制PRMI8266细胞的蛋白酶体活性,降低IL-6基因表达,减少MM细胞IL-6的自分泌。提示PTL抑制蛋白酶体活性及IL-6表达可能是其抗MM的机制之一。