呼吸道合胞病毒感染对细胞凋亡及FasL、Fas、Bcl-2、Bax基因表达的研究

目的：研究呼吸道合胞病毒(RSV)感染与细胞凋亡的关系及对凋亡相关基因FasL、Fas、bcl-2和bax表达的影响。 方法： 采用A549细胞，在RSV感染后不同时点收集细胞，流式细胞仪和透射电镜检测细胞凋亡，免疫组织化学法检测凋亡相关基因FasL、Fas、Bcl-2和Bax表达情况。 结果： 流式细胞仪检测结果RSV感染后72 h（6.61%）、120 h（10.94%）的细胞凋亡指数明显高于对照组（4.32%、5.31%）；免疫组化法检测结果对照组FasL、Bax基因呈现无表达或局部弱表达；随着RSV感染时间的延长，bax、 Fas、 FasL基因的表达均高于对照细胞，bcl-2基因呈现弱表达或无表达。 结论： RSV在感染后期能诱导宿主细胞发生凋亡，促凋亡基因FasL、Fas 、Bax和抗凋亡基因Bcl-2表达水平的差异是RSV诱导凋亡的机制之一。     

IL-2对活化与未活化淋巴细胞凋亡的影响

目的：研究IL-2对活化与未活化淋巴细胞凋亡的影响。方法：RT-PCR法检测两种单向混合淋巴细胞反应体系中Fas/FasL的表达情况,选取一个合适的反应体系作为活化淋巴细胞的模型;加入外源的IL-2,利用FITC-Annexin-V/PI双染色法检测活化与未活化淋巴细胞的凋亡情况;用CFSE区分供体和受体细胞,再用流式细胞术检测细胞表面Fas的变化。结果：未活化的脾脏淋巴细胞,加入IL-2后,细胞凋亡率降低,Fas^＋细胞比例降低;经混合淋巴细胞反应活化的脾脏淋巴细胞,加入IL-2后,细胞凋亡率升高,Fas^＋细胞比例升高,并且这种作用对于供体细胞和受体细胞都是相同的。结论：IL-2可以抑制未活化的淋巴细胞凋亡,促进活化的淋巴细胞凋亡,这种作用与Fas分子表达量的变化有关。     

白介素12诱导T细胞凋亡时Fas/FasL表达和信号转导的研究

目的:为了解和探讨白介素12(IL-12)作用于T细胞,活化T细胞表面的IL-12受体β1/β2复合物,调节Th1/Th2平衡,诱导T细胞凋亡时对Fas/FasL表达和信号传导的作用。方法:用AnnexinV的方法流式细胞仪检测细胞凋亡;用半定量PCR的方法测定在不同抑制剂作用下对Fas/FasL信号传导的影响。结果:IL-12诱导人TIB-152、HTB-176和正常T细胞的凋亡;IL-12可上调T细胞的FasLmRNA表达。在IL-12作用6h后FasL的表达明显升高,表达的高峰值在24h。HA100抑制剂能促进T细胞的凋亡,PKC抑制剂是IL-12诱导T细胞凋亡信号传导的负性调节因子;AG490抑制剂不抑制IL-12上调的FasLmRNA表达作用,说明其阻断的Jak2通路不参与IL-12对FasL表达的信号传导过程;HA1004不影响T细胞表达FasLmRNA。结论:IL-12能诱导TIB-152、HTB-176和正常人T细胞的凋亡。FasL作为介导分子参与此过程,IL-12对T细胞FasLmRNA表达信号传递与PKC通路有关。而Jak2及PKA通路不参与此过程.     

白细胞介素12诱导T细胞凋亡对Bcl-2表达和信号分子的影响

目的:了解和探讨白细胞介素12(IL-12)作用于T细胞,活化T细胞表面的IL-12受体β,诱导T细胞凋亡对Bcl-2表达和信号转导的作用。方法:用AnnexinV流式细胞仪检测细胞凋亡率和半定量PCR的方法测定在不同抑制剂作用下对Bcl-2信号转导表达的影响。结果:IL-12在高浓度下诱导人的白血病T细胞株TIB-152和人的淋巴瘤T细胞株HTB-176及正常人T细胞的凋亡。在IL-12处理6h后Bcl-2的表达明显升高,表达的高峰值在24h,Bcl-2的升高不能抑制和阻碍T细胞的凋亡;IL-12诱导上调T细胞Bcl-2mRNA表达。HA100能促进T细胞的凋亡,PKC是IL-12诱导T细胞凋亡信号转导的负性调节因子;AG490不抑制IL-12上调的Bcl-2mRNA表达作用,AG490阻断的Jak2通路不参与IL-12诱导T细胞mRNA表达的信号转导及其调节;HA1004不影响T细胞表达mRNA,PKA通路不影响IL-12诱导T细胞表达Bcl-2mRNA的信号传递。结论:Bcl-2是凋亡介导分子之一,但是Bcl-2不能阻断Fas-FasL介导的T细胞凋亡。     

土槿乙酸诱导人黑色素瘤细胞凋亡

目的 研究土槿乙酸诱导人黑色素瘤（SK-28）细胞凋亡。方法 采用Hoechst33342/PI核荧光双染色法、DNA片段化分析检测细胞凋亡;用ELISA kit和RT-PCR检测p53、Fas、caspase-3、Bax和Bcl-2的蛋白和mRNA的表达。结果 土槿乙酸明显诱导SK-28细胞凋亡（p<0.05）;作用12h后,p53的蛋白表达水平显著增加,作用24h后,增加了Fas/APO-1蛋白表达和Bax mRNA表达,降低了Bcl-2 mRNA表达,提高了caspase-3活性。结论 土槿乙酸可通过激活p53 引发Bcl-2介导的线粒体途径和Fas/APO-1介导的死亡受体途径,诱导人黑色素瘤SK-28细胞凋亡。     

诱骗受体DcR3对佐剂型关节炎大鼠模型的作用分析

目的 研究诱骗受体DcR3 对佐剂型关节炎(AA)大鼠模型的作用及其机理.方法 注射弗式完全佐剂建立大鼠佐剂型关节炎(AA)模型,尾静脉注射DcR3蛋白,观察大鼠关节肿胀度、间接 ELISA 检测血清和滑膜液中细胞因子IL-1 β、TNF-α、IFN-γ的变化.RT-PCR检测滑膜和淋巴细胞中DcR3、Fas、FasL mRNA的表达以及脾脏中TGF-β、IFN-γ、TNF-α、IL-4、IL-10 mRNA的表达.Western blot分析滑膜细胞中Caspase-8、Caspase-3、Caspase-9、Bcl-2蛋白的表达.结果 DcR3 治疗AA大鼠后,足肿胀度降低;血液和滑膜液的IL-1β、TNF-α、IFN-γ水平下降;脾脏中TGF-β、IFN-γ、TNF-α mRNA 表达下调,IL-4、IL-10 mRNA表达上调;滑膜细胞中Caspase-8、Caspase-3蛋白表达上调,Bcl-2蛋白表达下调. 结论 DcR3 可以用于实验性大鼠AA的治疗,其治疗机制与调节滑膜细胞FasL、Fas mRNA的表达和血液淋巴细胞中 Fas mRNA的表达,促进滑膜细胞和自身反应性淋巴细胞的凋亡;调节脾脏细胞Th1/Th2细胞因子平衡相关.本研究为进一步阐明RA的发病机理奠定了重要基础,为有效治疗RA提供了新思路.     

高三尖杉酯碱对HL60细胞凋亡的影响及机制的研究

目的:研究高三尖杉酯碱对HL60细胞凋亡的影响及其机制。方法:运用高三尖杉酯碱作用HL60细胞后撤药实验筛选其诱导HL60细胞凋亡启动时相,流式细胞和免疫组化技术检测高三尖杉酯碱诱导HL60细胞凋亡启动时相凋亡信号分子Bcl-2、Bax、Fas/FasL、caspase-3、ERK2和p38的表达状况。结果:在高三尖杉酯碱诱导HL60细胞凋亡启动时相,Bcl-2表达降低,Bax表达增高,Bcl-2/Bax比值降低,ERK2表达减低,p38表达增加,caspase-3表达增加,Fas/FasL分子的表达无显著变化。结论:Bcl-2、Bax、MAPK途径和caspase-3参与高三尖杉酯碱启动HL60细胞凋亡的信号转导。     

ALA-PDT对尖锐湿疣凋亡及细胞因子的影响

目的：检测5-氨基酮戊酸-光动力疗法(ALA-PDT)治疗前后尖锐湿疣皮损凋亡相关因子(Fas、caspase3、Bcl-2)及促炎症细胞因子(CCL-20、TNF-α、IL-1)的表达,探讨ALA-PDT治疗尖锐湿疣的可能机理。方法：收集10例尖锐湿疣患者ALA-PDT治疗前后皮损(同时以正常健康者皮肤组织对照),采用荧光定量PCR检测其Fas、caspase3、Bcl-2、CCL-20、TNF-α、IL-1 mRNA表达;Western blot检测其Fas、caspase3、Bcl-2、CCL-20、TNF-α、IL-1蛋白表达。结果：尖锐湿疣皮损组织内Fas、caspase3、Bcl-2、CCL-20、TNF-α、IL-1 mRNA和蛋白表达均高于正常皮肤组织(P<0.05);与治疗前比较,治疗后Bcl-2、CCL-20、TNF-α、IL-1 mRNA和蛋白表达水平明显降低(P<0.01),Fas、caspase3 mRNA和蛋白表达水平明显升高(P<0.01)。结论：ALA-PDT是一种能有效治疗尖锐湿疣的方法,它可诱导细胞表面凋亡蛋白Fas、caspase3的表达、减少凋亡抑制因子Bcl-2的表达,从而可能依靠内源性途径(线粒体介导的凋亡)和外源性途径(死亡受体介导的凋亡)促进尖锐湿疣角质形成细胞凋亡;并可能通过抑制促炎细胞因子CCL-20、TNF-α、IL-1而发挥局部免疫调节作用。     

催乳素对葡萄球菌肠毒素A诱导的人外周血T细胞凋亡的影响

目的探讨催乳素（PRL）在T细胞的活化诱导凋亡（activation induced cell death，AICD）中的作用。方法用葡萄球菌肠毒素（SEA）体外刺激人外周血T细胞作为T细胞AICD的模型，在第2次向模型中加入SEA诱导T细胞凋亡的同时，分别加入3种不同浓度的hPRL（20、300和1000ng/ml）进行干预，同时设不含hPRL的对照组。0～24h内，以MTT法检测T细胞的增殖情况。PI染色后用流式技术检测细胞凋亡情况，并通过琼脂糖凝胶电泳检测T细胞凋亡DNA。流式检测T细胞的Fas和FasL的表达水平变化。Westem blot法检测T细胞内凋亡相关蛋白Bcl-2和Bax。结果在T细胞的AICD模型中高浓度PRL组（300、1000ng／ml）其T细胞增殖得到显著维持（P〈0．05），各PRL处理组T细胞凋亡率比对照组降低了32．9％～78．2％（P〈0．05）。PRL组（300、1000ng/ml）Bax／Bcl-2比值比对照组下降了44．4％～46．0％（P〈0．05）。PRL可明显抑制细胞表面Fas和FasL的表达，其中各PRL处理组Fas的细胞阳性率比对照组下降了51．1％～75．0％（P〈0．01），FasL的细胞阳性率比对照组下降了28．2％～39．1％（P〈0．01）。结论在SEA诱导T细胞的AICD过程中，PRL可通过抑制Fas、FasL和Bax的表达，并提高Bcl-2的表达，来抑制T细胞凋亡，维持T细胞的增殖。     

HDV/HBV感染树鼠句肝组织中的肝细胞凋亡

目的探讨HDV/HBV感染树鼠句肝组织中Fas/FasL、Bcl2/Bax和ICE表达与HDV感染之间的关系,以及Fas/FasL、Bcl2/Bax和ICE在丁型肝炎肝细胞凋亡中的作用.方法采用免疫组化技术对HDV/HBV感染树鼠句肝组织中Fas/FasL、Bcl2/Bax和ICE的表达进行检测;应用原位末端标记技术对肝细胞凋亡进行检测.结果HDAg表达与Fas/FasL、Bcl2/Bax和ICE表达之间关系密切(P＜0.05),HDAg表达越强,Fas、FasL、Bax和ICE表达也越强,而Bcl2表达则越弱.Fas/FasL、Bcl2/Bax和ICE表达与肝细胞凋亡之间关系密切(P＜0.05),Fas、FasL、Bax和ICE表达越强,凋亡细胞越多;相反,Bcl2表达越强,凋亡细胞越少.结论肝细胞内HDAg表达可诱导Fas、FasL、Bax和ICE表达,但对Bcl2表达无明显诱导作用;Fas/FasL、Bcl2/Bax和ICE在肝细胞凋亡中起重要作用.     

Regulation of T-cell apoptosis: a mixed lymphocyte reaction model

Despite the capacity for antigen-specific activation and rapid clonal expansion, homeostatic mechanisms ensure that the mature immune system contains a relatively stable number of T cells. In recent years, it has become apparent that this stability is a consequence of apoptotic death of most of the specific T cells generated during an immune response. Clearly this process must be tightly regulated in order to retain sufficient T-cell progeny to mediate an effective response, whilst allowing the rapid deletion of these cells at the end of the response to prevent lymphadenopathy and cross-reactive autoimmunity. In this study, the factors that regulate the sensitivity of T cells to apoptosis were investigated in vitro after the induction of primary T-cell activation within a mixed lymphocyte reaction (MLR). It was found that activated T cells rapidly acquire the expression of both Fas and Fas ligand (FasL) on their surface and contain high levels of the precursor form of the pro-apoptotic enzyme, caspase 8 (FLICE). However, these T cells were resistant for up to 5 days to apoptosis following the stimulation of Fas; a maximal apoptotic response was observed after 7 days. This time point coincided with a marked reduction in expression of the FLICE inhibitory protein (FLIP) and maximal activity of caspase 8. At time points beyond day 7, the number of viable cells in the MLR decreased further despite a reduction in the expression of FasL. However, the expression of interleukin-2 (IL-2) at these late time points was low, resulting in a decrease in expression of the anti-apoptotic protein Bcl-2. This can produce apoptosis by allowing leakage of cytochrome-c from mitochondria resulting in direct activation of the caspase cascade. In this study, it is shown that T cells are resistant to apoptosis for the first 5 days after activation as a consequence of insensitivity of the Fas pathway and the presence of intracellular Bcl-2. After between 5 and 7 days, the cells become sensitive to Fas-mediated apoptosis while retaining Bcl-2 expression. At later time points, Fas ligation is reduced but the cells respond to a decreased availability of IL-2 by reducing Bcl-2 expression; this encourages further apoptosis by allowing the direct activation of caspase enzymes.     

Caspase抑制剂对大鼠心肌缺血／再灌注损伤Fas／FasL表达的影响

目的探讨大鼠心肌缺血／再灌注时caspase抑制剂对心肌细胞凋亡及Fas／FasL基因mRNA表达的影响及其机制。方法以穿线结扎或松扎左冠状动脉制备大鼠心肌缺血／再灌注模型。42只大鼠随机分为假手术组、Z-VAD-fmk治疗组和缺血／再灌注对照组,并分设缺血4-5min后再灌注3,6,12h3个时相点。以缺口末端标记法检测心肌细胞凋亡的变化,逆转录聚合酶链反应法检测Fas／FasL基因mRNA的表达改变,并分析心肌组织病理学损伤程度。结果心肌缺血／再灌注后心肌细胞凋亡指数及Fas/FasL基因mRNA表达均增高,caspase抑制剂预处理下调Fas／FasL表达水平,减少心肌细胞凋亡。结论心肌细胞凋亡与Fas／FasL系统参与了心肌缺血／再灌注损伤过程,caspase抑制剂Z-VAD-fmk通过抑制凋亡和下调Fas／FasL表达,减低再灌注损伤。     

自然流产模型小鼠蜕膜细胞凋亡及相关基因的表达

目的 通过比较正常妊娠模型小鼠及自然流产模型小鼠蜕膜细胞凋亡及Bcl-2、Bax、Fas、FasL蛋白的表达,从细胞及分子水平探讨自然流产的发病机制.方法建立正常妊娠模型CBAXBALB/c和自然流产模型CBAXDBA/2.用免疫组化SABC法测定两组模型孕13 d蜕膜细胞Bcl-2、Bax、Fas、FasL蛋白的表达,并通过MIAS-2000医用彩色病理图像免疫组化测量系统对其表达进行半定量分析,其结果用平均灰度值表示;同时应用DNA缺口原位末端标记技术(TUNEL)测定两组模型孕13天蜕膜细胞凋亡情况.结果与正常妊娠模型相比,自然流产模型蜕膜细胞Bcl-2蛋白的表达降低(P＜0.01);Bax蛋白的表达明显升高(P＜0.01);FasL的表达明显升高(P＜0.01);Fas的表达两组比较无明显差异(P＞0.05).蜕膜细胞凋亡指数(AI),自然流产模型明显高于正常妊娠模型(P＜0.01).结论 早孕期蜕膜组织细胞凋亡异常是自然流产的机制之一,Bcl-2/Bax,Fas/FasL途径可能是诱导早孕期蜕膜细胞凋亡的重要因素.     

Induction of salivary gland epithelial cell injury in Sjogren's syndrome: in vitro assessment of T cell-derived cytokines and Fas protein expression

Sjogren's syndrome (SS) is an exocrinopathy characterized by T cell infiltrates, salivary gland epithelial cell (SGEC) apoptosis and high Fas and FasL expression. To address the participation of T cell-derived cytokines and of Fas apoptotic pathway in SS glandular lesions, we utilized non-neoplastic SGEC lines established from SS patients and controls. Possibly attesting to their intrinsic activation, cell lines derived from SS patients displayed significantly higher constitutive Fas and FasL than controls. Surface co-expression of Fas and FasL was not associated with spontaneous fratricide apoptosis. SGEC were resistant to anti-Fas-mediated apoptosis (possibly owing to the constitutive expression of anti-apoptotic proteins cFLIP and Bcl-2), but became sensitive after protein or RNA synthesis inhibition. IFN-gamma and TNF-alpha were able to upregulate surface Fas and FasL, whereas IL-1beta downregulated surface FasL. IFN-gamma (but not several other cytokines) reduced the survival of SGEC in a dose- and time-dependent manner and induced Fas/FasL-mediated apoptosis, directly and via anoikia. Dexamethasone inhibited the upregulation of Fas and FasL by IFN-gamma and the induction of SGEC apoptosis and detachment by anti-Fas mAb or IFN-gamma. Our findings indicate the injurious role of IFN-gamma for the salivary epithelia of SS patients through the induction of Fas-mediated apoptosis and anoikia.     

Characterization of the expanded T cell population in infectious mononucleosis: apoptosis, expression of apoptosis-related genes, and Epstein-Barr virus (EBV) status

Infectious mononucleosis (IM), a manifestation of primary infection with EBV, is characterized by a massive expansion of the T cell population. In this study we examined this expanded T cell population regarding its EBV status, its proliferative and apoptotic activity, and its expression of apoptosis-related genes. Whereas previous studies were performed on ex vivo cultures or on peripheral blood, our investigations included in vivo analysis of IM tonsillectomy specimens (14 cases) by in situ hybridization for viral RNA (EBERs) combined with immunohistochemistry (IHC; CD3, CD45RO, CD20, CD79a, Ki-67, Bcl-2, Bax, Fas, FasL) and the TUNEL method. Of the EBER+ cells 50-70% showed expression of the B cell markers CD20/CD79a. The remainder of the EBER+ cells expressed neither B nor T cell antigens. No co-expression of EBERs and T cell antigens was detected in any of the specimens. In accordance with a high rate of apoptosis (up to 2.37%) within the expanded T cell population, Bcl-2 expression was drastically reduced and FasL expression remarkably increased. The levels of Bax and Fas expression showed no or moderate up-regulation. In conclusion, the massive expansion of IM T cells is not caused by EBV infection of these cells but merely represents an intense immune reaction. Through altered expression of Bcl-2/Bax and Fas/FasL, the activated T cells are subject to enhanced apoptosis while residing within the lymphoid tissue, which eventually allows the efficient silencing of this potentially damaging T cell response.     

Increased serum IL-10 in lupus patients promotes apoptosis of T cell subsets via the caspase 8 pathway initiated by Fas signaling

We sought to investigate the expression of Fas and FasL on T cell surface and caspase 8 involvement in T cell apoptosis promoted by serum IL-10 in systemic lupus erythematosus(SLE) patients.Cells and sera were obtained from 35 SLE patients.Apoptosis of T cells in patients with SLE was increased and associated with the SLE disease activity index(SLEDAI).Elevated expression of Fas and FasL on T cell surface contributed to increased apoptosis of T cells.Increased IL-10 in the sera of SLE patients was capable of inducing Fas and FasL expression on CD4~+T cell surface,promoting apoptosis of this cell subset.Decreased IL-10 serum levels and low expression of Fas were found in 5 patients of the first follow-up group after 2-month treatment.In another group with one-year treatment,the SLEDAI declined to inactive scores.Serum IL-10 was decreased significantly,and expression of Fas and FasL on T cells was also reduced.Declined apoptosis was predominant only in CD4~+T cell subset.When sera with high level of IL-10 were used to culture PBMCs from healthy controls,activated caspase 8 was elevated in CD3~+T,CD4~+T and CD8~+T cells.The study showed that serum IL-10 induced apoptosis of T cell subsets via the caspase8 pathway initiated by Fas signaling.Increased apoptosis of T cells contributes to autoantigen burden,which is pathogenic in the development of SLE.     

枸杞多糖调控老年大鼠T细胞凋亡及相关基因表达的研究

目的 :探讨枸杞多糖对老年大鼠T细胞过度凋亡及相关基因表达的调节作用。方法 :利用TUNEL标记的流式细胞术和荧光实时定量PCR技术 ,研究了老年大鼠和年轻大鼠T细胞凋亡百分率及抗凋亡和促凋亡基因 (Fas,FasL ,TNFR1,Bax ,Bcl 2 ,TNFR2 )mRNA表达情况 ,并研究了枸杞多糖对老年大鼠T细胞凋亡百分率及促凋亡和抗凋亡基因mRNA表达的影响。结果 :枸杞多糖能够有效地降低老年大鼠T细胞的过度凋亡 ,而且可以下调促凋亡的TNFR1基因mRNA表达并上调抗凋亡的Bcl 2基因mRNA表达。结论 :枸杞多糖下调促凋亡基因表达的同时上调抗凋亡基因的表达 ,从而改善老年大鼠T细胞过度凋亡的状态     

Increased expression of apoptosis-associated proteins in puromycin aminonucleoside nephrosis

Increased apoptosis has been reported in acute puromycin aminonucleoside nephrosis (PAN). The aim of this study was to investigate if increased apoptosis is related to increased expression of apoptosis-associated proteins (AAP) in this model of nephrosis. Sprague-Dawley rats were made nephrotic by intraperitoneal injection of one dose of puromycin aminonucleoside. Renal tissues were obtained at 1, 2 and 7 weeks after injection and apoptosis was investigated by TUNEL and by electron microscopy. Fas, Fas ligand, p53, Bax and Bcl-2 expressions were analyzed by the respective monoclonal and polyclonal antibodies, using indirect immunofluorescence. In the glomerulus of nephrotic animals, increased apoptosis was accompanied with increased expression of p53, Fas and Bax. In the interstitium, high expression of apoptosis, Fas, Fas-L and Bax were observed and in tubules increased apoptosis was accompanied with increased expression of p53, Fas and Fas-L. Bcl-2 was increased in interstitium and tubules during PAN. The incidence of apoptosis during PAN was correlated with the expression of AAP in glomerulus (p53), interstitium (Fas, Fas-L and Bax) and tubules (Fas, Fas-L, p53 and Bcl-2). There was correlation between Fas and Fas-L expression in interstitium and tubules. About 4% of glomerular and 25% of tubular p53 positive cells were apoptotic cells. The data suggest that increased local expression of AAP could contribute to renal apoptosis in the glomerular, interstitial and tubular compartments during this experimental model of nephrosis.     

Taxol对宫颈癌U14细胞增殖、凋亡及α2,6-SA和ST6Gal mRNA表达的影响

目的:研究泰素(Taxol)对小鼠宫颈癌U14细胞株增殖、凋亡以及α2,6-唾液酸(SA)和α2,6-唾液酸转移酶(ST6Gal)mRNA表达的影响,为进一步探讨宫颈癌Taxol化疗机制提供新思路。方法:Taxol处理U14细胞后,MTT检测Taxol对U14细胞的IC_(50)值。流式细胞术检测细胞α2,6-SA、细胞凋亡相关因子(Bcl-2、Bax、caspase8和caspase 3)、凋亡率和细胞周期改变。qPCR检测ST6Gal1和ST6Gal2 mRNA的表达。结果:与对照组相比,Taxol对U14细胞有明显的抑制作用,减弱α2,6-SA荧光强度,上调Bax表达,下调Bcl-2表达,降低Bcl-2/Bax比值,并增强caspase 8和caspase 3活性;Taxol处理显著增加U14细胞凋亡率及S期细胞和G2/M期细胞比率,此外还下调ST6Gal1 mRNA表达。结论:α2,6-SA和ST6Gal可能参与了Taxol对U14细胞细胞周期和凋亡调控的多重作用。