热休克蛋白70在缺糖损伤的HeLa细胞中对Bax和Bcl-2以及Bax构象改变的影响

目的 观察热休克蛋白70(Hsp70)对缺糖引起的HeLa细胞凋亡的影响,探讨其与凋亡相关的Bcl-2家族成员的相互作用关系. 方法 用人正义Hsp70重组质粒稳定转染HeLa细胞获得Hsp70过表达细胞.采用Hsp70过表达和正常HeLa细胞无糖培养建立两组细胞损伤模型,并均取3个平行样本.四甲基偶氮唑盐(MTT)法测细胞活率;Hoechst染色法和Giemsa染色法检测细胞凋亡率;RT-PCR法检测Bax和Bcl-2的表达变化,并计算其灰度比值;细胞免疫化学和荧光免疫法检测Bax构象改变情况. 结果 缺糖48h内,Hsp70明显抑制了HeLa细胞凋亡并增强其活力,同时也抑制了凋亡细胞中 Bax/Bcl-2的增高以及Bax的构象改变. 结论 缺糖诱导下,热休克蛋白70在HeLa细胞中能够通过与Bcl-2家族成员作用而抑制凋亡的发生.     

凋亡相关蛋白Bcl-2及Bax在糖尿病大鼠下颌下腺内的表达

目的:观察糖尿病大鼠下颌下腺内凋亡相关蛋白Bcl-2和Pax表达变化.方法:SD雄性大鼠用链脲佐菌素复制糖尿病动物模型,H-E染色观察下颌下腺形态学变化,免疫组织化学SABC技术检测Bcl-2及Bax蛋白表达变化.结果:糖尿病组大鼠下颌下腺组织萎缩,间质纤维增生.与对照组比较,糖尿病组大鼠下颌下腺导管上皮细胞Bcl-2表达下降,Bax表达显著增加.结论:Bcl-2及Bax表达在糖尿病病理变化过程中出现了一定的变化规律.     

镉影响大鼠胎盘发育及Bcl-2和Bax的表达

目的通过观察镉暴露后胎盘组织形态结构和凋亡相关蛋白表达量的改变，探讨镉对胎盘组织中细胞增殖与凋亡的影响。方法将孕6天（E6）的20只孕鼠随机分成染镉组和对照组，染镉组一次性腹腔注射氯化镉，剂量为2mgCd／kg体重。两组的孕鼠分别于E14和E18断椎处死，每只孕鼠随机取出6个胎盘，制备石蜡切片。行HE染色观察染镉后胎盘的形态改变，免疫组织化学技术显示镉对Bcl-2和Bax表达的影响。结果染镉组胎盘海绵带滋养层细胞、巨细胞和空泡化细胞增多，且迷路带及海绵带滋养细胞呈退行性改变。染镉组胎盘组织细胞中的Bcl-2蛋白表达量比相应的对照组表达量明显降低（E14：t=7．067，P〈0．01；E18：t=6．988，P〈0．01）；Bax蛋白表达量比相应的对照组表达量明显增多（E14：t=4．008，P〈0．01；E18：t=4．732，P〈0．01）；Bcl-2／Bax比值与相应对照组之间的差异有统计学意义（E14：t=9．517，P〈0．05；E18：t=23．380，P〈0．01）。结论镉可以通过影响Bcl-2和Bax的表达，改变Bcl-2／Bax比值，使胎盘组织细胞的增殖和凋亡平衡紊乱，导致胎盘发育异常。     

同一创面不同病程糖尿病足创面组织细胞凋亡率、Bcl-2、Bax及肿瘤坏死因子α的相关性

文题释义：“4C”法：通过颜色(Colour)、毛细血管出血(Capillarybleeding)、收缩力(Contractility)和紧张度(Consistency)判断是否坏死的方法。一般认为组织呈现暗紫/黄/白色、质地软、切割不出血和刺激无收缩状态,为坏死指征,在临床清创时应被清除。细胞凋亡：是指机体为维持内环境稳定,由基因控制的细胞自主、有序性的死亡形式。主要分为生理和病理两大类,生理性凋亡是指机体内某些细胞生来就注定在一段时间后死去,在尽完自己的职责之后正常死亡;而病理性凋亡则是指细胞在没有完成自己的使命时受到不可抗外力刺激而不正常死亡,从而引发各种疾病。背景：研究发现,难愈性溃疡创面不易愈合与细胞凋亡失衡和炎症失调有关,以往的研究均在不同个体的某一类型组织取样研究,研究结果数据间可能存在个体差异的影响,且无同一糖尿病足创面不同病程组织的细胞凋亡率、Bcl-2、Bax、肿瘤坏死因子α表达水平之间相关性研究报道。目的：分析糖尿病足不同病程创面组织细胞凋亡率、Bcl-2、Bax和肿瘤坏死因子α表达水平间的关系及作用机制。方法：重庆医科大学附属第二医院急诊科收治的15例Wagner 2,3级糖尿病足患者,选择典型的糖尿病足创面,采用“4C”法将局部感染控制后的创面组织区分为坏死、过渡和正常组织后分别采集标本,测定细胞凋亡率、Bcl-2、Bax、Bax/Bcl-2和肿瘤坏死因子α,并对结果进行统计分析。研究经重庆医科大学附属第二医院伦理委员会批准,编号：(2019)329号,所有患者均签署了知情同意书。结果与结论：①糖尿病足创面正常、过渡、坏死组织的细胞凋亡率分别为(16.67±2.48)%、(43.68±2.22)%和(72.12±4.53)%,差异有显著性意义(P < 0.01);②坏死、过渡和正常组织间Bcl-2、Bax、肿瘤坏死因子α表达水平和Bax/Bcl-2差异有显著性意义(P < 0.01),Bcl-2表达：坏死组织<过渡组织<正常组织,Bax、肿瘤坏死因子α表达及Bax/Bcl-2：坏死组织>过渡组织>正常组织;③Bcl-2、Bax、Bax/Bcl-2、肿瘤坏死因子α和细胞凋亡率间呈曲线关系,曲线回归分析结果显示,糖尿病足创面内肿瘤坏死因子α与Bax、Bax/Bcl-2、细胞凋亡率呈高度正相关,与Bcl-2呈高度负相关;④从结果可得出,细胞凋亡机制与炎症反应参与了糖尿病足创面病理过程,其作用机制可能与下调Bcl-2表达,上调Bax和肿瘤坏死因子α表达,提高Bax/Bcl-2水平,引起组织细胞凋亡率增大有关。ORCID: 0000-0002-9760-8666(郑敏)中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

依达拉奉对脑缺血再灌注损伤大鼠Bcl-2和Bax表达的作用研究

为了研究依达拉奉抗细胞凋亡的脑保护作用机制,本实验采用依达拉奉对脑缺血再灌注损伤大鼠进行治疗干预,观察大鼠脑组织Bcl-2和Bax的表达。将36只SD大鼠随机分为假手术组、再灌注组、依达拉奉治疗组,再灌注术后24h断头取脑,免疫组织化学和RT-PCR法观察脑组织Bcl-2和Bax表达水平的变化。结果表明,大鼠脑缺血再灌注损伤后,Bcl-2和Bax含量显著增多;与再灌注组相比,依达拉奉治疗组Bcl-2的表达显著上调,Bax表达显著下调,Bcl-2/Bax比值显著升高。上述结果提示,依达拉奉的脑缺血保护作用可能与上调Bcl-2表达及下调Bax的表达有关。     

人参皂甙Rg1对大鼠肢体缺血再灌注后脑组织Bax和Bcl-2表达的影响

目的:探讨肢体缺血再灌注(LIR)后脑组织Bax和Bcl-2基因表达的变化及人参皂甙Rg1对其影响.方法: 复制大鼠LIR模型,用人参皂甙Rg1进行干预,测定脑组织丙二醛(MDA)含量,采用尼氏染色观察脑组织病理学改变,TUNEL法检测细胞凋亡情况,免疫组织化学方法检测Bax、Bcl-2表达,免疫印迹法检测Bax、Bcl-2表达变化.结果: 大鼠LIR后,脑组织海马区、中脑红核区神经元细胞受损,脑组织出现水肿裂隙,Bax的表达明显上调,与细胞凋亡数量的增加相一致,Bcl-2表达也相应增加.人参皂甙Rg1干预组与LIR组相比,MDA含量、凋亡细胞数、Bax表达降低.Bcl-2表达降低不明显.结论: LIR后有细胞凋亡机制参与脑损伤的发生,人参皂甙Rg1可能通过抑制Bax表达,降低Bax/Bcl-2比值,从而减轻脑损伤.     

Changes in and effects of Kupffer cells on residual tumor after cryoablation in rabbit hepatic VX2 tumor

Objective: Cryoablation can directly kill tumor cells through sudden changes in temperature. It can also enhance lymphocyte function and cause distant tumor regression far from the ablation treatment area. In order to further explore the changes of immune function after cryoablation, the changes of Kupffer cells (KCs), the main immune cells in the liver, and their effects on untreated tumors in vivo were studied. Methods: Rabbit VX2 liver cancer models were constructed. The growth of liver tumors was confirmed by ultrasound after transplantation for 3 weeks. Fifteen Japanese white rabbits were divided into a tumor control group and cryoablation group. Cryoablation group was treated with cryoablation of a single or partial tumor. Histologic and immunohistochemical changes of the treatment area and untreated tumor area before and after cryoablation were observed, and the phagocytic function changes of KCs around the untreated area and treatment area were observed by electron microscopy. Results: Cryoablation areas showed necrosis, infiltration of inflammatory cells (including KCs), and fibrosis of tissue. The number of inflammatory cells in the unfrozen tumor area was increased in the same treated rabbit. There was a significant difference in the maximum diameter of unfrozen tumors between the frozen group and control group at 15th days after cryoablation (P<0.05), while the difference was not obvious at the 3rd and 7th day (P>0.05). Electron microscopy showed that the number of debris fragments engulfed by KCs around the tumor after cryoablation was significantly higher than that of the control group. In the same rabbit, we compared the amount of debris between tissue surrounding the unfrozen area and around the cryoablation area. There was a significant difference on the 3rd day after cryoablation, P=0.043, while there was no significant difference on the 7th day, P=0.348. Conclusion: After cryoablation, inflammatory cells aggregated around the cryoablated area. The activity of KCs had been increased and the function of phagocytosis enhanced. KCs had a certain inhibitory effect on the untreated tumor in the same animal at the early stage (within 15 days), but it was not enough to restrain the growth of the untreated tumors.     

半夏提取物调节Bax、Bcl-2、Caspase-3蛋白表达诱导白血病细胞凋亡

背景:温热中药半夏拥有可人工广泛种植、易提纯等优势,其提取物可抑制慢性髓系白血病、急性髓系白血病、急性T淋巴白血病细胞增殖,但是作用机制尚不明确。目的:探讨中药半夏提取物对3种白血病细胞凋亡的作用机制。方法:慢性髓系白血病细胞株(K562)、急性髓系白血病M3细胞株(HL-60)、急性T淋巴白血病细胞株(C8166)在半夏提取物5种浓度梯度中分别作用24,48,72 h,采用CCK-8法评估3种白血病细胞增殖情况并从中筛选出有明显抑制作用的中(300 mg/L)、高(500 mg/L)质量浓度。然后进一步采用流式细胞术检测3种白血病细胞早期凋亡发生率,采用RT-PCR与Western blot检测Bax、Bcl-2、Caspase-3 mRNA及蛋白水平。结果与结论:①5种质量浓度的半夏提取物作用3种白血病细胞具有细胞增殖抑制作用,中(300 mg/L)、高(500 mg/L)质量浓度半夏提取物增殖抑制率较高,与低质量浓度组(100 mg/L)、对照组比较差异有显著性意义(P<0.01);②中、高质量浓度半夏提取物可诱导3种白血病细胞早期凋亡;③中、高质量浓度半夏提取物可以下调3种白血病细胞的Bcl-2 mRNA表达,上调Bax及Caspase-3 mRNA表达(P<0.05;P<0.01);④中、高质量浓度半夏提取物作用72 h后,K562、C8166细胞的Bcl-2蛋白条带明显减弱,而HL-60细胞无减弱变化;Bax及Caspase-3蛋白条带明显增强;⑤结果表明,半夏提取物能有效抑制髓系白血病、T淋巴细胞白血病细胞的增殖,促进其凋亡,其作用机制可能与其调节Bax/Bcl-2、Caspase-3蛋白表达有关。     

重组人生长激素对烟雾吸入性损伤大鼠肺泡Ⅱ型细胞的增殖及Bcl-2和Bax蛋白表达的影响

目的 研究重组人生长激素(recombinant human growth hormone,rhGH)对烟雾吸人性损伤大鼠肺泡Ⅱ型细胞(ATⅡ)增殖及Bcl-2和Bax蛋白表达的影响.方法　清洁级雄性SD大鼠70只,体重160～180 g,采用随机数字表法随机分为3组:正常对照组(C组)、单纯吸人性损伤组(Ⅰ组)和吸人性损伤+rhGH治疗(R组),后2组各再分为6、10、14日亚组.烟雾造成吸人性肺损伤模型,rhGH经腹部皮下注入(1.33 U/kg),连续应用7 d.各时相点剖胸取肺,行常规病理切片进行病理形态学观察并用免疫组化方法观察肺泡Ⅱ型细胞(ATⅡ)增殖以及Bcl-2和Bax蛋白表达的变化.结果 rhGH能显著增加新增殖ATⅡ数量;正常大鼠肺组织Bcl-2和Bax mRNA无表达,皮下注射rhGH后6、10、14日R组Bcl-2蛋白表达阳性细胞分别为(31.01±2.70)、(52.34±3.44)、(50.15±4.00)个/HP,明显高于I组的(24.76±2.82)、(37.92±4.28)、(35.58±3.64)个/HP(P<0.05);R组Bax蛋白表达阳性细胞为(21.16±2.79)、(31.22±5.62)、(26.27±5.41)个/HP,明显低于Ⅰ组[(26.51±2.61)、(41.50±4.14)、(34.55±2.94)个/HP,P<0.05].结论 经皮下注入外源性rhGH能有效刺激ATⅡ的增殖,上调Bcl-2蛋白表达及下调Bax蛋白表达,改变Bcl-2/Bax的比值从而抑制细胞凋亡.     

Bax、Bcl-2在培养新生鼠皮层神经元中的表达及L-NAME的干预作用

目的　探讨Bax与Bcl-2在体外培养的皮层神经元的表达及非选择性一氧化氮合酶抑制剂NG-硝基-L-精氨酸甲酯（L-NAME）的干预作用。 方法　原代培养SD新生大鼠皮层神经元,并采用neuron specific enolase (NSE)免疫荧光方法进行细胞纯度鉴定。神经元随机分为正常组、N-甲基-D-天门冬氨酸（NMDA）组、NG-Nitro-L-arginine Methyl Ester（L-NAME）组,分别采用ELISA检测各组细胞中一氧化氮合酶（nitric oxide synthase, NOS）的表达,采用RT-PCR、Western blot分别检测各组细胞中Bax、Bcl-2 mRNA及蛋白的表达。 结果　NSE免疫荧光大多数细胞为NSE阳性细胞,神经元纯度高达90%;L-NAME组中NOS及Bax的表达均高于正常组而低于NMDA组, Bcl-2的表达低于正常组而高于NMDA组。 结论　L-NAME对NMDA诱导的神经细胞凋亡起明显的保护作用,其可能是通过上调Bcl-2的表达、下调Bax的表达发挥作用。     

Bax,Bcl-2, fas and Fas-L antigen expression in human seminoma: correlation with the apoptotic index

Apoptosis plays a crucial role in the regulation of spermatogenesis in male germ cells and is, at least in part, modulated by Bcl-2, Bax, and the Fas pathway. Seminomas have a favourable outcome and respond to radio-/chemotherapy with an increased rate of apoptosis. The expression of Bax, Bcl-2, Fas and Fas-ligand (Fas-L) in human seminoma was evaluated and correlated with the apoptotic index. Twenty-nine classical seminomas were examined by immunohistochemistry and Western blotting using antibodies against Bax, Bcl-2, Fas and Fas-L. Apoptosis was detected by in-situ end-labeling of fragmented DNA and the apoptotic index (AI) was determined. Expression of Fas was found in 26 (89.7%) of Fas-L in 24 seminomas (82.2%); none of the tumours expressed Bcl-2. No correlation between the AI and Fas, Fas-L or Bcl-2 expression was found. Bax was demonstrated in 20/29 tumours (69%). Bax-positive tumours showed an increased AI of 4.75 +/- 2.38% in contrast to 2.60 +/- 1.23% of the Bax-negative tumours (P = 0.002). The number of Bax-positive tumour cells and apoptotic cells revealed a significant correlation using chi2-test (P = 0.04) and linear regression (r = 0.54, P = 0.001). Therefore, Bax seems to play a determinant role in the modulation of apoptosis in human seminoma that may be linked to a favourable outcome.     

高脂血症对大鼠主动脉内皮细胞Bax、Bcl-2蛋白表达的影响

目的:探讨高脂血症SD大鼠主动脉内皮细胞凋亡蛋白Bax、Bcl-2表达的变化及其诱导内皮细胞凋亡的可能机制。方法:清洁级大鼠17只,随机分为高脂血症模型组(8只)和对照组(9只),分别以高脂饲料和普通饲料喂养16周后,检测血脂水平,采用免疫组织化学方法检测两组大鼠主动脉内皮细胞Bax、Bcl-2的表达,同时用HE染色和电镜观察主动脉组织形态学改变。结果:与对照组相比,模型组大鼠血清甘油三酯(TG)、总胆固醇(TC)水平升高(P<0.01),主动脉内皮细胞Bax蛋白表达明显增加(P<0.01),Bcl-2蛋白表达明显减少(P<0.01),Bcl-2/Bax比值明显降低(P<0.01);模型组主动脉内膜增厚和平滑肌细胞增殖,内皮组织部分脱落,内皮细胞胞膜破裂,胞质脱失,核膜不完整。结论:高脂血症可引起大鼠血管内皮细胞凋亡蛋白Bax、Bcl-2水平及比值改变,加重血管内皮损伤,促进细胞凋亡,加速动脉粥样硬化进程。     

敲低膜联蛋白A7对人肝癌HepG2细胞Bcl-2和Bax表达的影响

目的 探讨敲低膜联蛋白A7表达对人肝癌细胞系HepG2细胞凋亡及凋亡相关蛋白Bcl-2和Bax表达的影响。方法 将HepG2细胞接种于6孔板,分为3组：siRNA干扰组、阴性对照组和空白对照组,其中干扰组只转染靶向膜联蛋白A7的siRNA,阴性对照组只转染阴性对照siRNA,空白对照组只加转染试剂。通过Western blotting鉴定膜联蛋白A7在转染后48h可被最大程度的抑制,于是在转染后48h采用流式细胞术检测各组细胞凋亡率,通过免疫组织化学、Western blotting和RT PCR检测Bcl-2和Bax蛋白及mRNA的表达。 结果 与阴性对照组和空白对照组相比,siRNA干扰组细胞凋亡率显著增高（P<0.05）,Bcl-2蛋白和mRNA的表达均显著降低（P<0.05）,而Bax蛋白和mRNA均未发生显著变化（P>0.05）。结论 敲低膜联蛋白A7可促进HepG2细胞的凋亡,降低Bcl-2和Bax的比值。     

Ⅰ型糖尿病脑病模型大鼠空间学习记忆以及海马齿状回细胞凋亡和Bax与Bcl-2蛋白表达的变化

目的探讨1型糖尿病脑病海马齿状回细胞凋亡、Bax与Bcl-2蛋白表达、空间学习记忆之间的相互关系。方法通过腹腔注射链脲佐菌素(溶于柠檬酸缓冲液)建立1型糖尿病脑病模型大鼠,通过腹腔注射柠檬酸缓冲液建立载体模型大鼠。应用Morris水迷宫、TUNEL技术、Bax与Bcl-2免疫组化方法,观察各组大鼠海马齿状回颗粒下区(SGZ)、颗粒细胞层(GCL)的Bax、Bcl-2、TUNEL阳性细胞和空间学习记忆的变化。结果糖尿病脑病组大鼠的SGZ、GCL的Bax阳性细胞数、TUNEL阳性细胞数、水迷宫的逃避潜伏期和游泳距离均明显高于载体模型组或正常对照组大鼠的对应指标(P<0.01);而糖尿病脑病组大鼠的Bcl-2阳性细胞数则明显低于载体模型组或正常对照组大鼠(P<0.01),但以上各组3类阳性细胞的形态和分布却均无明显差异。结论体内长期缺乏胰岛素可打破凋亡基因Bax与抗凋亡基因Bcl-2的蛋白表达水平之间原有的正常动态平衡状态,致使海马齿状回的细胞倾向于多发生细胞凋亡事件,这可能是引发1型糖尿病脑病神经发生障碍及空间学习记忆异常的一个因素。     

DCC基因在大肠癌中的表达及与Bcl-2, Bax关系

目的：探讨DCC(deleted in colorectal carcinoma)基因在大肠癌组织中的表达情况及与Bcl-2，Bax蛋白之间的关系。 方法：采用免疫组织化学法结合图像分析技术观察74例大肠癌组织中DCC，Bcl-2，Bax蛋白的表达情况。 结果：大肠癌组织中，DCC蛋白失表达率为 54.1% (40/74)，其表达在不同的肿瘤分化程度 (P＝0.002)及Dukes分期中有差异 (P＝0.042)； Bcl-2蛋白表达阳性率为60.8% (45/74)，其表达与不同的大肠癌临床Dukes分期 (P＝0.032)及是否有淋巴结转移 (P<0.001)中有差异；Bax蛋白表达阳性率为48.6% (36/74)，在不同的大肠癌组织学类型、分化程度、Dukes分期及淋巴结是否转移中均无差异 (P>0.05)。大肠癌中DCC蛋白表达与Bcl-2表达水平呈负相关（r＝－0.201, P＝0.043），与Bax表达水平呈正相关（r＝0.296, P＝0.005）。 结论：大肠癌中DCC表达缺失频率较高，且可能通过上调Bcl-2蛋白表达和下调Bax蛋白表达阻止细胞凋亡，从而促进大肠癌发生。     

Bcl-2, Bax, and Bcl-x expression in the CA1 area of the hippocampus following transient forebrain ischemia in the adult gerbil

Delayed neuronal death was produced in the CA1 area of the hippocampus following 5 min of forebrain ischemia in adult gerbils. Immunohistochemistry and Western blotting to Bcl-2, Bax, and Bcl-x was examined in control (age-matched, non-operated and sham-operated) and ischemic gerbils. Bcl-2 immunoreactivity was low in CA1 neurons, but Bax was highly expressed in CA1 neurons of control gerbils. Moderate Bcl-x immunoreactivity was observed in control CA1 neurons. Strong Bcl-2 and Bcl-x immunoreactivity was found in CA1 neurons following ischemia. Bcl-2, Bax, and Bcl-x were localized in dying cells, thus suggesting that expression of Bcl-2 was not sufficient to prevent nerve cells from dying. Although the Bcl-x antibody does not discriminate between Bcl-xL and Bcl-xS content in tissue sections, Western blots disclosed a marked increase in the intensity of the band corresponding to Bcl-xS, but not of the band corresponding to Bcl-xL in ischemic hippocampi, thus indicating that the increase in Bcl-xS is associated with delayed cell death following transient forebrain ischemia in the adult gerbil. Received: 24 June 1997 / Accepted: 29 January 1998     

Ziyuglycoside II-induced apoptosis in human gastric carcinoma BGC-823 cells by regulating Bax/Bcl-2 expression and activating caspase-3 pathway

Ziyuglycoside II is an active compound of Sanguisorba officinalis L. that has anti-inflammation, antioxidation, antibiosis, and homeostasis properties. We report here on the anticancer effect of ziyuglycoside II on human gastric carcinoma BGC-823 cells. We investigated the effects of ziyuglycoside II on cell growth, cell cycle, and cell apoptosis of this cell line. Our results revealed that ziyuglycoside II could inhibit the proliferation of BGC-823 cells by inducing apoptosis but not cell cycle arrest, which was associated with regulation of Bax/Bcl-2 expression, and activation of the caspase-3 pathway. Our study is the first to report the antitumor potential of ziyuglycoside II in BGC-823 gastric cancer cells. Ziyuglycoside II may become a potential therapeutic agent against gastric cancer in the future.     

海藻硫酸多糖对巨噬细胞所致肿瘤细胞凋亡的调节作用

目的 研究海藻硫酸多糖（sulfated polysaccharides from seaweed,SPS)对巨噬细胞（Mψ）所致HepG2细胞凋亡的调节作用。方法 用MTT比色法,检测Mψ产生的TNF，NO（尤其是NO）及SPS对HepG2细胞的细胞毒性作用。将Mψ与HepG2按一定比例共孵育后，检测培养上清中NO2^-/NO3^-及细胞中cGMP的含量；用透射电镜观察HepG2细胞凋亡的形态学改变。结果 SPS对HepG2细胞没有直接的细胞毒性，但可通过促进Mψ产生NO和TNF，增强Mψ对HepG2细胞的细胞毒性，增加共孵育细胞体系中cGMP的含量，并可明显促进HepG2细胞的凋亡。结论 SPS可间接增强Mψ对HepG2细胞的细胞毒性，并可明显促进HepG2细胞的凋亡。     

Significance of apoptosis related proteins on malignant transformation of ovarian tumors: A comparison between Bcl-2/Bax ratio and p53 immunoreactivity

In this study, we compared the immunoreactivities of Bcl-2, Bax and p53 proteins in ovarian tumors and related the immunohistochemical findings to the histological type of the tumors. Formalin-fixed, paraffin wax-embedded tissue sections from 40 patients who had serous-mucinous borderline tumors and serous-mucinous adenocarcinoma of the ovary (n = 10 each) were stained with hematoxylin–eosin (H&E). After histopathological examination, serial sections were stained immunohistochemically with primary antibodies to Bcl-2, Bax and p53 using an avidin–biotin-peroxidase method. A semi-quantitative grading system was used to compare the immunohistochemical staining intensities. The nuclear DNA fragmentation of apoptosis was determined using TUNEL method. As a result of immunohistochemical staining, increased immunoreactivity of Bcl-2 was observed in adenocarcinomas when compared to borderline tumors (P < 0.001). Strong immunoreactivity of Bcl-2 and mild immunoreactivities of Bax and p53 were detected in ovarian adenocarcinomas. There were no significant statistical differences in the immunoreactivity of Bax among the histological type of ovarian tumors. Whereas a balance was observed between the immunoreactivities of Bcl-2 and Bax in the borderline cases, and this balance was strongly changed toward the anti-apoptotic Bcl-2 protein in patients with adenocarcinoma. TUNEL staining of sections indicated apoptotic cells in the serous borderline tumors were about 8-fold higher than in the serous adenocarcinoma. The results of this study on apoptosis-related factors might help to develop novel protective and therapeutic approaches, such as isoflavonoids and isothiocyanates, which were associated with decreased Bcl-2/Bax ratio, against the malignant epithelial ovarian tumors.