Expression of bcl-2 oncogene in gastric precancerous lesions and its correlation with syndromes in traditional Chinese medicine

AIM: To observe the protein and mRNA expression of bcl-2 oncogene in gastric precancerous lesions (GPL) and to analyze its correlation with syndromes in traditional Chinese medicine (TCM). METHODS: Sixty-seven patients with GPL confirmed by gastroscopy and pathology were studied,including 39 cases of moderate gastric mucosal dysplasia,19 cases of severe gastric mucosa dysplasia, 9 cases of incomplete colon metaplasia. In syndrome differentiation of TCM,17 cases belonged to the syndrome of qi and yin deficiency of the spleen and stomach complicated by qi stagnation, 21 cases belonged to the syndrome of qi and yin deficiency of the spleen and stomach complicated by stomach heat, 29 cases belonged to the syndrome of qi and yin deficiency of the spleen and stomach complicated by blood stasis. Protein and mRNA expression of bcl-2 oncogene were detected by labeled streptavidin biotin (LSAB) immunohist-ochemistry and in situ hybridization respectively. RESULTS: Abnormal expression of protein and mRNA on bcl-2 oncogene was found in GPL,which increased gradually with the course of lesions. In moderate and severe gastric mucosal dysplasia and incomplete colon metaplasia,there was no difference in the expression of bcl-2 oncogene (P>0.05).In different accompanying syndromes, the expression of protein and mRNA on bcl-2 oncogene increased gradually in the following order: deficiency of both qi and yin of the spleen and stomach accompanying qi stagnation→stomach heat→blood stasis. In GPL, compared with accompanying blood stasis, there was an obvious difference in the expression of bcl-2 oncogene between the syndrome of qi and yin deficiency of the spleen and stomach and accompanying stomach heat, so did accompanying qi stagnation (the level of protein: X2=8.45, P<0.05;the level of mRNA: X2=7.35, P<0.05). CONCLUSION: Apoptosis-associated bcl-2 oncogene is abnormally expressed in GPL,which correlates with different accompanying syndromes in TCM.

The Expression of Apoptosis-Related Genes Bcl-2 and Bax Protein and Apoptosis Positivity in Cervical Carcinoma during Irradiation

To evaluate the apoptosis positivity, the expression of Bcl-2, bax proteinsin 30 patients with squamous cell cervix carcinoma before and after radiotherapy. Methods: By usingimmuno-histochemical and TDT-dUTP nick end labelling techniques, 30 cases of squamous cell cervicalcarcinoma were analyzed. Results: The apoptosis positivity before and after irradiation was 76.7%and 100% respectively, with the difference being significant (P 【 0.05); The positive rates of Bcl-2protein before and after irradiation were 73.3% and 46.7% respectively, with the difference beingsignificant (P 【 0.05); The positive rates of bax protein before and after irradiation were 86% and100% respectively, with the difference being significant (P 【 0.05). Conclusion: bax and Bcl-2protein play an important role in apoptosis induced by fractionated radiation therapy. Apoptosisinduced by irradiation is contributed to upregulation of bax protein or downregulation of Bcl-2protein.

Signal transduction mediated by Bid,a pro-death Bcl-2 family proteins, connects the death receptor and mitochondria apoptosis pathways

Two major apoptosis pathways have been defined in mammalian cells, the Fas/TNF-R1 death receptor pathway and the mitochondria pathway. The Bcl-2 family proteins consist of both anti-apoptosis and pro- apoptosis members that regulate apoptosis, mainly by controlling the release of cytochrome c and other mitochondrial apoptotic events. However, death signals mediated by Fas/TNF-R1 receptors can usually activate caspases directly, bypassing the need for mitochondria and escaping the regulation by Bcl-2 family proteins. Bid is a novel pro-apoptosis Bcl-2 family protein that is activated by caspase 8 in response to Fas/TNF-R1 death receptor signals. Activated Bid is translocated to mitochondria and induces cytochrome c release, which in turn activates downstream caspases. Such a connection between the two apoptosis pathways could be important for induction of apoptosis in certain types of cells and responsible for the pathogenesis of a number of human diseases.

Effects of Ethyl Pyruvate on Myocardial Apoptosis and Expression of Bcl-2 and Bax Proteins after Ischemia-reperfusion in Rats

In order to study the effects of ethyl pyruvate on cardiomyocyte apoptosis following ischemia/reperfusion （I/R） in vitro and the expression of Bcl-2 and Bax proteins, isolated rat hearts were perfused in a Langendorff model. Twenty-four rats were randomly divided into 3 groups （n=8 in each group）： control group was perfused for 120 min. In the I/R group, after 30 min stabilization the injury was induced by 30 min global ischemia followed by 60 min reperfusion. Ethyl pyruvate （EP） group was set up with the same protocol as I/R group except that it was supplied with 2 mmol/L EP 15 rain before ischemia and throughout reperfusion. Myocardial malonaldehyde （MDA） content was measured. Myocardial apoptotic index （AI） was tested by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling （TUNEL） method. The expression of anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bax in cardiac myocytes was detected by immunohistochemistry. As compared with control group, the content of MDA, myocardial AI and the expression of Bcl-2, Bax proteins were increased significantly in I/R group, but the content of MDA, myocardial AI and the expression of Bax protein were decreased obviously and the expression of Bcl-2 protein was up-regulated in EP group （P〈0.05）. These results demonstrate that EP could inhibit apoptosis of cardiac myocytes possibly via alleviating oxidative stress, up-regulating Bcl-2 and down-regulating Bax proteins.

Dioscin-induced Apoptosis of Human LNCaP Prostate Carcinoma Cells through Activation of Caspase-3 and Modulation of Bcl-2 Protein Family

Dioscin is a natural steroid saponin derived from several plants, showing potent anti-cancer effect against a variety of tumor cell lines. In the present study, we investigated the anti-cancer activity of dioscin against human LNCaP cells, and evaluated the possible mechanism involved in its antineoplastic action. It was found that dioscin（1, 2 and 4 μmol/L） could significantly inhibit the viability of LNCaP cells in a time- and concentration-dependent manner. Flow cytometry revealed that the apoptosis rate was increased after treatment of LNCaP cells with dioscin for 24 h, indicating that apoptosis was an important mechanism by which dioscin inhibited cancer. Western blotting was employed to detect the expression of caspase-3, Bcl-2 and Bax in LNCaP cells. The expression of cleaved caspase-3 was significantly increased, and meanwhile procaspase-3 was markedly decreased. The expression of anti-apoptotic protein Bcl-2 was down-regulated, whereas the pro-apoptotic protein Bax was up-regulated. Moreover, the Bcl-2/Bax ratio was drastically decreased. These results suggested that dioscin possessed potential anti-tumor activity in human LNCaP cells through the apoptosis pathway, which might be associated with caspase-3 and Bcl-2 protein family.

Influence of Tanshinone lla on heat shock protein 70,Bcl-2 and Bax expression in rats with spinal ischemia/reperfusion injury

Tanshinone lla is an effective monomer component of Danshen, which is a traditional Chinese medicine for activating blood circulation to dissipate blood stasis. Tanshinone Ila can effectively improve brain tissue ischemia/hypoxia injury. The present study established a rat model of spinal cord ischemia/reperfusion injury and intraperitoneally injected Tanshinone lla, 0.5 hour prior to model establishment. Results showed that Tanshinone Ila promoted heat shock protein 70 and Bcl-2 protein expression, but inhibited Bax protein expression in the injured spinal cord after ischemia/reperfusion injury. Furthermore, Nissl staining indicated a reduction in nerve cell apoptosis and fewer pathological lesions in the presence of Tanshinone Ila, compared with positive control Danshen injection.

Pretreatment with low-frequency repetitive transcranial magnetic stimulation may influence neuronal Bcl-2 and Fas protein expression in the CA1 region of the hippocampus: A possible anti-epilepsy mechanism in a lithium-pilocarpine-induced epileptic rat mod

BAOKGROUND： Bcl-2 and Fas proteins are well known as anti-apoptotic and pro-apoptotic factors respectively. However, whether the anti-epileptic mechanism of low-frequency repetitive transcranial magnetic stimulation （rTMS） involves an anti-apoptotic effect via regulating Bcl-2 and Fas protein expression remains to be determined. OBJECTIVE： To verify the correlation between the anti-epileptic mechanism following pretreatment of low-frequency rTMS and anti-hippocampal apoptosis. DESIGN, TIME AND SETTING： A randomized controlled animal experiment was performed at Institute of Neurological Disorders, Affiliated Hospital of North Sichuan Medical College between September 2007 and March 2008. MATERIALS： Pilocarpine （053K13011） was provided by Sigma, USA; lithium was provided by Shanghai Biotechnology Co., Ltd., China; Dantec Maglite-r25 rTMS instrument was provided by Dundee, Denmark. METHODS： A total of 21 adult male Wistar rats were randomly divided into control （n = 6）, rTMS pretreatment （n = 9）, and sham-stimulation （n = 6） groups. The rTMS pretreatment group was pretreated with low-frequency rTMS （0.5 Hz, 75% threshold intensity, 20 times/bundle, and 5 bundles/day）, while the sham-stimulation group was sham-stimulated with a similar sound for 7 successive days to establish lithium-pilocarpine-induced epileptic state models. MAIN OUTCOME MEASURES： Epileptic stroke latency; neuronal morphology was observed using hematoxylin and eosin staining; mean positive-reactive cell number and mean absorbance of Bcl-2 and Fas protein in the hippocampal CA1 region was observed using immunohistochemistry. RESULTS： Epileptic latency in the rTMS pretreatment group was significantly enhanced （P 〈 0.01）, and a number of degenerated neurons were observed to be apoptotic. Bcl-2 protein expression increased at each time point, but Fas protein expression decreased （P 〈 0.01）. CONCLUSION： Low-frequency rTMS has an anti-epileptic effect, which may be via regulation of Bcl-2 and Fas protein expression in the hippocampal region.

THE EXPERIMENTAL STUDY ON THE CELL APOPTOSIS AND EXPRESSION OF BCL-2 PROTEIN IN INTRACEREBRAL HEMORRHAGE IN MODEL OF RATS

Objective To study whether there is the apoptosis of neural cells and the expression of Bcl-2 protein in intracerebral hemorrhage (ICH) in model of rats, for the further understanding the mechanism of the delayed damage of the neural cells around the hematoma after ICH. Methods Fifty SD rats were randomly divided into 5 groups, ten in each. With the Group A as the control, the rest 40 were used to set up intracerebral hemorrhage model. The brains were taken out at 12 th , 24 th , 48 th and 72 th hours, respectively. Apoptosis cells were detected with terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL), and the expression of Bcl-2 protein was detected with immunochemical stainging methed (SP). Results In the control group, no apoptosis cells and Bc1-2 protein were detected. In rest groups, the apoptosis cells and Bc1-2 protein were expressed in different degree. Apoptosis rates verified and corresponded with the time after ICH, with the peak at 48 th -72 th hour after hemorrhage. The peak rate of apoptosis cells was (24.50±2.69)% and Bcl-2 protein expression was (20.76±1.97)% . There was significant difference between the experimental groups and control (P<0.05), and no linear relationship between the apoptosis rate and the expression of Bcl-2 protein. Conclusion Apoptosis may be an important factor in the secondary trauma of ICH. There is a time leg after hemorrhage. All this is instructive to clinical treatment in time. Bcl-2 protein keeps increasing in a certain time after hemorrhage, but not synchronize with the cell apoptosis. This indicates that bcl-2 has the effect to reduce the apoptosis of neural cells.

EHD2、miR-let-7c和lncRNA FOXD2-AS1在人喉鳞状细胞癌组织中的表达及其关联性分析

目的:探讨Eps15同源结构域蛋白2 (EHD2)、微小RNA let-7c (miR-let-7c)和长链非编码RNA (lncRNA)FOXD2-AS1在喉鳞状细胞癌(LSCC)组织中的表达水平,阐明EHD2/miRlet-7c/FOXD2-AS1信号轴与LSCC发生的关联性。方法:收集40例LSCC患者的癌组织标本,按照病理类型分为低级别组(中或高分化,32例)和高级别组(低分化,8例),按照肿瘤淋巴结转移(TNM)临床分期分为TNM早期组(Ⅰ-Ⅱ期,13例)和TNM晚期组(Ⅲ-Ⅳ期,27例),按照有无淋巴结转移分为转移组(21例)和无转移组(19例)。另取40例对应癌旁正常组织标本作为对照组。采用免疫组织化学法检测各组标本中EHD2表达情况,分析其与LSCC患者临床病理参数之间的关系,采用生物信息学方法筛选出miR-let-7c作为候选微小RNA (miRNA),与其启动子区域存在结合位点的FOXD2-AS1作为候选lncRNA。取10对新鲜的LSCC组织标本和癌旁正常组织标本,采用实时荧光定量PCR (RT-qPCR)法检测2组样本中EHD2 mRNA、miRNA-let-7c和FOXD2-AS1表达水平,并验证其关联性。结果:与癌旁正常组织比较,LSCC组织中EHD2表达水平明显降低(P<0.01),且TNM早期组患者LSCC组织中EHD2阳性表达率明显高于TNM晚期组(P<0.05),病理类别和有无淋巴结转移与EHD2表达无明显关联(P>0.05)。与癌旁正常组织比较,LSCC组织中miR-let-7c表达水平明显降低(P<0.01),FOXD2-AS1表达水平明显升高(P<0.05)。LSCC组织中FOXD2-AS1与miR-let-7c表达水平呈负相关关系(r=-0.67,P<0.05),miR-let-7c与EHD2 mRNA表达水平呈负相关关系(r=-0.83,P<0.01)。结论:EHD2和miR-let-7c在LSCC组织中呈低表达,可能是新的抑癌基因;FOXD2-AS1在LSCC组织中高表达,可能是新的原癌基因;FOXD2-AS1/miR-let-7c/EHD2信号轴可能参与了LSCC的发生发展。

Regulatory Effect of Bcl-2 Family Proteins in CPB-induced Cardiomyocyte Apoptosis in Dog Hearts

Summary: Whether conventional hypothermic CPB induces myocyte apoptosis in dog hearts and modulation of bcl-2, bcl-xl, bax, bad, and caspase-3 pathways in this setting was investigated. Ten healthy adult dogs were randomized into sham-operated and CPB groups. Samples of left ventricle were obtained before, during and 3 h after CPB. In situ TUNEL was used to detect apoptotic myocytes. Immunohistochemistry and flow cytometry were employed for detection of expressions of bcl-2, bcl-xl, bax and bad proteins. Z-DEVD-AMC substrate cleavage and TBARS methods were used to measure the activity of caspase-3 and the content of lipid peroxide in LV myocardium, respectively. After CPB, the number of apoptotic myocytes in CPB group was significantly increased. The results of immunohistichemistry demonstrated that bcl-2, bcl-xl, bax and bad proteins were constitutionally present on the sarcolemma of the LV myocytes. FACS results showed that, after CPB, expressions of bax and bad in CPB group were significantly upregulated, while the expressions of bcl-2 and bcl-xl were not significantly changed in both groups. The activity of caspase-3 and the content of lipid peroxide in LV myocardium in CPB group were also significantly increased after CPB. The present study shows that there exists myocardiocyte apoptosis in dog hearts undergoing conventional hypothermic CPB and the myocyte apoptosis is initiated by ischemia and performed during reperfusion. Moreover, the CPB-induced myocyte apoptosis was associated with upregulation of expressions of bax and bad proteins, activation of caspase-3 and increase of oxidative stress.

THE QUANTITATIVE MEASUREMENT OF BCL-2, P53 PROTEIN AND PCNA EXPRESSION IN BREAST CARCINOMA AND THEIR CORRELATION WITH PROGNOSIS

To study quantitative index of bci-2, P53, Nroliferating cell nuclear antigen (PCNA),ER and PR in breast carcinoma and their correiation and their relatiousbip with prognosis, the ex expression of bcl-2, P53 and PCNA were studied by immunohistochemical technique. The measurementof ER and PR used enzyme linked affinuity histochemical methods. The quantitative index was analyzed by image technique. All analyses were hased on 60 breast carcinomas. The results were as follows:the more bcl-2 protein, the lower histological graded the longer survival term and the highersurvival rate (P< 0. 05). The quautitative measurement of bcl-2, P53 and PCNA expression were ofvalue in evaluating the degree of differentiation and prognosis in breast carcinoma. The quantitativeand qualitative measurement or p53 protein expression showed a Ⅰwerful evidence in evaluatingprognosis of bcl-2 were more significant in evaluating poor prognosis of breast carcinoma. A relationship between bcl-2 and ER, PR showed a better value for response to endocrine therapy in breastcarcinoma patients.

CyclinD1、C-erbB2及bcl-2基因在卵巢上皮性肿瘤中的表达及其临床意义

目的 :检测癌基因CyclinD1、C erbB2及bcl 2在卵巢上皮肿瘤中的表达 ,探讨它们在卵巢肿瘤发生、发展中的作用及临床、病理意义。方法 :应用免疫组化SP法检测72例恶性卵巢肿瘤、12例交界性卵巢肿瘤、2 1例良性肿瘤及 10例正常卵巢组织中Cy clinD1、C erbB2及bcl 2基因的表达情况。结果 :1.卵巢恶性、交界性及良性肿瘤中Cy clinD1阳性率依次为 2 7.78%、33.3%、9.5 2 %。恶性及交界性肿瘤阳性率明显高于良性肿瘤 ,其阳性率与组织学分级呈负相关 ,而与患者年龄、临床分期、组织学类型无关 ;2 .卵巢恶性、交界性及良性肿瘤中C erbB2的阳性率依次为 5 6 .9%、4 1.6 7%、14.2 8%。恶性及交界性肿瘤阳性率明显高于良性肿瘤 ,差异有显著性。C erbB2阳性表达在组织分化差及期别晚的肿瘤中较分化好、期别早者高 ;3.卵巢恶性、交界性、良性肿瘤中bcl 2的阳性表达率依次为 6 3.89%、5 0 %、2 8.5 %。恶性及交界性肿瘤与良性肿瘤之间的表达差异有显著性。组织分化差、期别早的肿瘤中bcl 2的阳性率较分化好、期别晚者高 ;4 .两种及两种以上基因同时表达率 (5 1.4 % )显著高于单基因表达 (2 7.79% )。CyclinD1与C erbB2基因表达呈负相关。结论 :CyclinD1、C erbB2及bcl 2基因在卵巢癌发生、发展中起重要作用 ,表明细胞?

二氮嗪预处理上调Bcl-2/Bax蛋白比值减少缺氧复氧所致体外培养的海马神经元凋亡(英文)

线粒体内膜ATP敏感钾通道(mitochondrial ATP-sensitive potassium channel,mitoK_(ATP)通道)的激活在药物预处理增强神经元对各种损伤的耐受力过程中发挥着重要作用。神经元内含有丰富的mitoK_(ATP)通道,二氮嗪(diazoxide,DZ)为选择性的mitoK_(ATP)通道开放剂,本实验探讨了DZ预处理能否减少缺氧复氧所致的海马神经元凋亡,以及DZ如何调控Bc1-2蛋白和Bax蛋白的表达。原代培养9～10 d的Sprague-Dawley大鼠海马神经元随机分为5组：对照组、DZ Oμmol/L、DZ 30μmol/L、DZ 100μmol/L和DZ 100μmol/L+5-羟癸酸(5-hydroxydecanoate,5-HD)100μmol/L。除对照组外,其他四组神经元自缺氧前3 d开始,每天DZ预处理1 h,连续3 d。体外缺氧4 h,于复氧后24 h,四唑蓝比色法测定海马神经元存活率,annexin V- FITC流式细胞术测定凋亡率,Western blot法检测Bcl-2和Bax蛋白的表达量。结果显示：与对照组比较,缺氧复氧损伤显著降低海马神经元的存活率,升高凋亡率。与其他浓度比较,100μmol/L DZ预处理使神经元存活率升高约15%,而凋亡率降低约12%：Bcl-2蛋白表达增强约60%,Bax蛋白表达下降近30%。5-HD消除DZ对神经元的保护作用。因此,100μmol/L DZ可通过上调Bcl-2蛋白表达,降低Bax蛋白表达,减少缺氧复氧后海马神经元的凋亡。

多囊卵巢综合征中卵巢初级小卵泡bcl-2、bax的表达

目的 :探讨凋亡调节蛋白 bcl-2及 bax在多囊卵巢综合征 ( PCOS)患者的卵泡选择、发育的作用。方法 :1 8例 PCOS患者及 1 3名正常人 2 40个小卵泡按直径分为 4个组 ,采用免疫组织化学方法及 Konton Ibas灰度值的定量测定 ,用 SPSS软件统计 ,定量分析凋亡调节蛋白 bcl-2及 bax在 PCOS各级初级小卵泡中的表达。结果 :PCOS组各级窦前卵泡组间 bax蛋白表达有显著差异 ,随着卵泡直径的增加 bax表达明显增多 ,但直径 >1 2 0 μm的卵泡 bax表达减少 ,bcl-2 / bax灰度比值显著变小。 bcl-2蛋白表达相对稳定 :PCOS组直径在 60～ 1 2 0μm的卵泡 bcl-2表达显著高于正常对照组 ( P<0 .0 5 )。结论 :正常人及 PCOS卵巢组织各级窦前卵泡和窦卵泡均表达 bcl-2及 bax,随着卵泡的增大 ,bcl-2的表达增加 ,当卵泡直径 >1 2 0 μm时 ,细胞凋亡减弱 ,卵泡的增长加速。PCOS患者卵巢中各级窦前卵泡和窦卵泡凋亡蛋白 bcl-2及 bax的表达是正常的。

膀胱癌中p53、c-myc和bcl-2的表达及意义

目的 :研究癌基因和抗癌基因蛋白产物在膀胱移行细胞癌组织中异常表达与病理分级、临床分期间关系。方法 :应用免疫组化S P法检测 96例膀胱移行细胞癌中 p5 3、c myc和bcl 2的表达水平。 结果 :96例膀胱移行细胞癌中 p5 3、c myc和bcl 2的阳性表达率分别为 6 0 4%、6 8 8%和 81 3 %。结果表明p5 3、c myc和bcl 2异常表达与膀胱移行细胞癌的分级和分期间差异有统计学意义。结论 :p5 3、c myc和bcl 2表达在膀胱癌的发生发展中起重要作用。在膀胱癌变过程中 。

p53、bcl-2、caspase-3在非小细胞肺癌组织中的表达及相关性分析

目的探讨p53、bcl-2、caspase-3在老年晚期非小细胞肺癌(NSCLC)组织中的表达及相关性。方法收集经手术后病理学检查确诊的117例老年晚期NSCLC患者的临床资料和存档石蜡组织标本。免疫组织化学方法检测肿瘤组织中p53、bcl-2、caspase-3蛋白的表达情况,分析p53、bcl-2、caspase-3蛋白表达的相关性及其与患者临床病理学特征的关系。结果 117例老年晚期NSCLC组织标本中,p53、bcl-2、caspase-3的阳性表达率分别为42.74%(50/117)、38.46%(45/117)、36.75%(43/117)。p53阳性表达率在低分化、中央型、有淋巴结转移的鳞癌患者中较高;bcl-2阳性表达率在高分化、有淋巴结转移患者中较高;caspase-3阳性表达率在高分化、无淋巴结转移患者中较高。NSCLC组织中bcl-2与caspase-3表达呈正相关(r=0.262,P=0.003)。结论 p53、bcl-2、caspase-3可能在老年晚期NSCLC的发生和发展过程中起重要调控作用,为临床病理诊断提供理论依据。

槲皮素联合顺铂对肺腺癌小鼠移植瘤Bcl-2和Bax表达的调控及意义

目的:观察槲皮素联合顺铂对肺腺癌LA795细胞的T739小鼠移植瘤的抑制作用,检测移植瘤中Bcl-2和Bax的表达水平及肿瘤细胞凋亡指数,探讨其作用机制。方法:将32只接种了LA795肺腺癌细胞的T739小鼠随机分成对照组(A组)、顺铂组(B组)、槲皮素组(C组)、槲皮素+顺铂组(D组)。用药16 d后,观察肿瘤生长情况,接种后24 d活杀各组小鼠,移植瘤标本称瘤体质量和测量体积,免疫组织化学和图像分析系统定量检测肿瘤组织的Bcl-2和Bax表达,原位凋亡TUNEL法检测肿瘤细胞凋亡指数。结果:B、C、D各用药组肿瘤的生长受到明显抑制,瘤体质量明显低于A组,其抑瘤率分别为38.57%、26.03%和51.58%,联合用药组抗瘤作用进一步增强。Bcl-2表达在A组高于B、C、D组,Bax表达在A组明显低于B、C、D组,各用药组与对照组相比差异均有统计学意义(P<0.05或P<0.01);肿瘤细胞的凋亡指数在各用药组都比对照组明显提高,差异有统计学意义(P<0.01)。结论:槲皮素联合顺铂可明显抑制肺腺癌细胞在小鼠体内的生长,其作用机制可能是通过调控肿瘤中Bcl-2和Bax的表达,从而抑制细胞增殖和促进细胞凋亡。

硫化砷诱导K562细胞凋亡中Bcl-2和Bax的表达

目的 研究 Bcl- 2和 Bax在硫化砷诱导的 K5 6 2细胞凋亡中的表达 ,探讨其在硫化砷诱导的细胞凋亡中的作用 .方法 K5 6 2细胞经一定剂量硫化砷作用特定时间后 ,MTT法检测细胞生长、增殖状态 ,光镜及透射电镜下观察细胞形态及凋亡情况 ,S- P免疫组化染色检测 Bcl- 2、Bax的表达并进行图像分析 .结果 硫化砷对 K5 6 2细胞生长增殖有时间剂量依赖性抑制作用 ;175～ 14 0 0μg· L- 1 硫化砷作用 18～ 14 4 h后 ,K5 6 2细胞出现凋亡细胞的形态学改变 ;免疫组化染色表明 K5 6 2细胞低表达 Bcl- 2蛋白 (A值为 0 .15 2± 0 .0 2 3,阴性对照 A值 0 .10 8± 0 .0 12 ) ,硫化砷处理后对其表达无明显影响 (A值为 0 .138± 0 .0 2 8,P>0 .0 5 ) .硫化砷作用后 ,Bax蛋白的表达量 A值由 0 .2 4 0± 0 .0 13增加到 0 .316± 0 .0 2 1(P<0 .0 1) .结论 硫化砷可抑制 K5 6 2细胞的生长和增殖并诱导其发生凋亡 ,其机制可能与 Bax蛋白上调有关 .

基于不同时间窗的延迟亚低温对颅脑创伤大鼠Bcl-2、Bax和Caspase-3表达的影响

目的探讨不同时间窗的延迟亚低温(MHT)治疗对颅脑创伤(TBI)大鼠脑组织Bcl-2、Bax和Caspase-3蛋白表达的影响。方法 36只清洁级成年雄性SD大鼠随机均分为常温治疗(NT)组、MHT 15 min组、MHT 2 h组及MHT 4 h组。采用电子可控性皮质损伤装置制备大鼠TBI模型,造模完成后NT组给予常温(37℃)维持6 h,3个亚低温组分别于TBI后15 min、2 h、4 h给予低温(33.0±1.0)℃维持6 h。3 d后对各组大鼠进行改良神经功能缺损评分(m NSS),HE染色观察海马CA1区组织病理学变化,免疫组化染色和Western blot检测Bcl-2、Bax和Caspase-3蛋白表达情况。结果各组大鼠表现为不同程度的神经行为缺陷,与NT组相比,3个亚低温组m NSS评分均降低(P<0.01)。HE染色结果显示3个亚低温组神经细胞结构较规则、排列相对整齐,神经元坏死数量减少,核碎裂、溶解现象减轻。与NT组相比,3个亚低温组均能上调Bcl-2表达,下调Bax和Caspase-3表达(P<0.05)。以上实验结果均显示MHT 15 min组疗效优于MHT 2 h组,而MHT 2 h组和MHT4 h组疗效相当。结论恰当地延迟亚低温治疗在一定程度上能够抑制神经细胞凋亡,缓解脑损伤进展。

补肾调冲含药血清对离体卵巢颗粒细胞Bcl-2、P53蛋白表达的影响

[目的]探讨补肾调冲方对大鼠离体卵巢颗粒细胞原癌基因蛋白表达的影响。[方法]采用血清药理学的方法,以不同含药量的大鼠血清与体外培养的卵巢颗粒细胞共同孵育24 h,用免疫组化法检测Bcl-2、P53蛋白的表达。[结果]补肾调冲含药血清可增强Bcl-2蛋白的阳性表达。[结论]原癌基因作为卵巢内局部调节因子,参与卵巢颗粒细胞凋亡过程。补肾调冲含药血清可通过促进卵巢颗粒细胞内抑癌基因的蛋白表达,抑制颗粒细胞的凋亡。