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| 1 | 顺铂诱导宫颈癌Hela细胞凋亡及其作用机制的研究显示文摘目的:研究顺铂在体外诱导宫颈癌Hela细胞凋亡及其作用机制。方法:采用MTT法测定顺铂对Hela细胞增殖的影响;流式细胞仪和Hochest33258检测药物作用前后的细胞凋亡情况;RT-PCR检测HPVE6的mRNA水平表达;WesternBlot测定HPVE6、p53、p21、Bax、Bcl-2蛋白水平的表达。结果:顺铂抑制Hela细胞生长呈时效和量效关系;经10μg/ml顺铂分别在12、24、36、48小时作用Hela细胞,亚G1峰与对照组有显著性差异;RT-PCR提示顺铂作用Hela细胞后HPVE6的mRNA水平表达逐渐降低;WesternBlot提示顺铂作用Hela细胞后HPVE6的蛋白水平表达逐渐降低,p53、p21和Bax蛋白水平表达逐步升高,Bcl-2的表达无变化。结论:顺铂通过抑制HPVE6的表达,恢复p53的功能,引起细胞凋亡,起到杀伤肿瘤的作用。 | 柳友清 邢辉 韩晓兵 石小艳 梁缝奇 陈刚 马丁 | 2006 | 中国肿瘤临床2006，33，1： | 26 |
| 2 | Hydrogen sulfide induces apoptosis of pulmonary artery smooth muscle cell in rats with pulmonary hypertension induced by high pulmonary blood flow显示文摘肺的动脉的背景反常 apoptosis 光滑的肌肉房间(PASMC ) 是在肺的动脉的一个重要 pathophysiological 过程结构的改变和肺的高血压。我们在 39 只男 Sprague-Dawley 老鼠随机被分到4星期的控制的高肺的血 flow.Methods 导致的肺的高血压的开发期间在 PASMC 的 apoptosis 上调查了内长的氢硫化物( H_2S )的可能的效果,4星期的分流,4星期的 shunt+propargylglycine ( PPG ),11星期的控制,11星期的分流和11星期的 shunt+sodium hydrosulfide ( NaHS )组织。在 4 星期的分流, 4 星期的 shunt+PPG, 11 星期的分流和 11 星期的 shunt+NaHS 组的老鼠经历了腹的主动脉晚辈静脉 cava 分流。在 4 星期的 shunt+PPG 组的老鼠 intraperitoneally 与 PPG 被注射,内长的 H_2S 生产的一个禁止者,为 4 个星期。在 11 星期的 shunt+NaHS 组的老鼠 intraperitoneally 与 NaHS 被注射,一个 H_2S 施主,为 11 个星期。肺织物 H_2S 被硫化物敏感的电极评估。PASMC 的 Apoptosis 被终端 deoxynucleotidyl transferase 检测标记的调停的 dUTP 刻痕结束(TUNEL ) 。在 PASMC 的船边交货, bcl-2 和 caspase-3 的表情四个星期在推延的操作以后与免疫化学的 staining.Results 被分析, PASMC 的 apoptosis 和船边交货和 caspase-3 的表示显著地被减少(P < 0.01 ) ,但是 bcl-2 的表示显著地增加了(P < 0.01 ) 。PPG 管理进一步禁止了 PASMC 的 apoptosis, downregulated 船边交货和 caspase-3 的表示(P < 0.01 ) ,但是增加了 bcl-2 的表示(P < 0.01 ) 。在 11 星期推延以后操作, PASMC 的 apoptosis 和船边交货和 caspase-3 的表示显著地被减少(P < 0.01 ) ,但是 bcl-2 的表示显然增加了(P < 0.01 ) 。NaHS 管理显著地增加了 PASMC 的 apoptosis, upregulated 船边交货和 caspase-3 的表示,但是禁止了 bcl-2.Conclusions H_2S 的表示在高肺的血的发展导致 PASMC 的 apoptosis 由激活船边交货小径并且禁止 bcl-2 小径的导致流动的肺的高血压。 | LI Wei JIN Hong-fang LIU Die SUN Jing-hui JIAN Pei-jun LI Xiao-hui TANG Chao-shu DU Jun-bao | 2009 | Chinese Medical Journal2009，，24： | 26 |
| 3 | bcl-2在氧化低密度脂蛋白诱导人血管内皮细胞凋亡中的作用显示文摘目的观察氧化低密度脂蛋白(oxidized low density lipoprotein,oxLDL)对人血管内皮细胞株EA.hy926凋亡的影响,并探讨bcl-2在其中的作用。方法MTT法检测不同浓度的oxLDL(50、100、150、200μg/ml)对细胞增殖能力的影响;流式细胞仪和激光共聚焦显微镜检测不同浓度的oxLDL对细胞凋亡的影响;RT-PCR、Western blot和免疫荧光细胞化学法分别检测不同浓度的oxLDL对bcl-2 mRNA、蛋白表达及在细胞内表达的影响。结果oxLDL对EA.hy926细胞形态有明显影响,并能明显抑制EA.hy926细胞增殖能力,抑制作用随处理浓度增加而增大,半数抑制浓度(IC50)约为100μg/ml;不同浓度的oxLDL处理细胞24 h后,与对照组比较,早期凋亡、晚期凋亡和总凋亡细胞百分比均显著增加(P<0.05);oxLDL能够明显抑制细胞内bcl-2 mRNA、蛋白表达及在细胞内的表达水平。结论bcl-2基因在oxLDL诱导的血管内皮细胞凋亡中发挥重要作用,oxLDL可能通过下调bcl-2的表达促进血管内皮细胞凋亡。 | 陈春烨 张乾勇 易龙 金鑫 陈卡 吕静 糜漫天 | 2009 | 第三军医大学学报2009，31，8： | 18 |
| 4 | Enhancement of germ cell apoptosis induced by ethanol in transgenic mice overexpressing Fas Ligand显示文摘It was suggested that chronic ethanol exposure could result in testicular germ cell apoptosis, but the mechanism is still unclear. In the present study, we use a model of transgenic mice ubiquitously overexpressing human FasL to investigate whether Fas ligand plays a role in ethanol-induced testicular germ cell apoptosis. Both wild-type (WT)mice and transgenic (TG) mice were treated with acute ethanol (20% v/v) by introperitoneal injection for five times.After ethanol injection, WT mice displayed up-regulation of Fas ligand in the testes, which was shown by FITCconjugated flow cytometry and western blotting. Moreover, TG mice exhibited significantly more apoptotic germ cells than WT mice did after ethanol injection, which was demonstrated by DNA fragmentation, PI staining flow cytometry and TUNEL staining. In addition, histopathological examination revealed that degenerative changes of epithelial component of the tubules occurred in FasL overexpressing transgenic mice while testicular morphology was normal in wild-type mice after acute ethanol exposure, suggesting FasL expression determines the sensitivity of testes to ethanol in mice. In summary, we provide the direct evidences that Fas ligand mediates the apoptosis of testicular germ cells induced by acute ethanol using FasL transgenic mice. | JIAHUAHU JIEJIANG YINGHUAMA NAYANG MAOHUZHANG MINWU JIANFEI LIHEGUO | 2003 | Cell Research2003，13，5： | 16 |
| 5 | Induction of mitochondrion-mediated apoptosis of CHO cells by tripchloro lide显示文摘Tripchlorolide (TC) is a potent antitumor reagent purified from a Chinese herb Tripterygium Wilfordii Hook. f.. However, its cellular effects and mechanism of action are unknown. We showed here that TC induced apoptosis of Chinese Hamster Ovary (CHO) cells in time- and dose-dependent manners. TC resulted in the degradation of Bcl-2, the translocation of Bax from the cytosol to mitochondria, and the release of cytochrome c from mitochondria. Stable overexpression of human Bcl-2 could reduce the apoptosis of TCtreated cells by blocking the translocation of Bax and the release of cytochrome c. These results indicate that TC induces apoptosis of CHO cell by activating the mitochondrion-mediated apoptotic pathway involving the proteins of Bcl-2 family and cytochrome c. | YANREN LEIXIONG JIARUIWU | 2003 | Cell Research2003，13，4： | 11 |
| 6 | Effects of vitamin E succinate on the expression of Fas and PCNA proteins in human gastric carcinoma cells and its clinical significance显示文摘AIM: To investigate the effects of vitamin E succinate (VES) on the expression of Fas and PCNA proteins as well as its clinical significance in human gastric carcinoma, and to explore the mechanism of VES-induced inhibition of gastric carcinoma cell growth. METHODS: Immunohistochemical methods were used to detect Fas and PCNA expression both in human gastric cancer SGC-7901 cells treated with VES at different doses and in human gastric carcinoma tissues. RESULTS: After the SGC-7901 cells were treated with VES at 5, 10, 20 mg/L for 48 h, the positive rates of Fas expression were 16%, 27% and 48%, respectively, significantly increased compared to that of control group (P<0.05); while the positive rates of PCNA expression in groups treated with different doses of VES were 20%, 18% and 7%, respectively, which were significantly decreased compared to that of the control group (P<0.05). In human gastric carcinoma tissues, the Fas positive expression rate was 42.4%(25/59), which declined with the decrease in the degree of tumor differentiation (P<0.05) and with the existence of lymph node metastasis (P<0.001). While the PCNA positive expression rate was 91.5%(54/59), no relationship was observed between PCNA expression and clinicopathologic parameters. CONCLUSION: VES inhibited the growth of gastric cancer cells by indudng Fas expression and inhibiting PCNA expression. It is, therefore, considered that the expression of Fas and PCNA genes, through tumor cell apoptosis and proliferation, respectively, may be useful as a clinical predictive index in the application of VES to gastric carcinoma therapy, where as Pas may be of more value than PCNA. | KunWu LanZhao YaoLi Yu-JuanShan Li-JieWu | 2004 | World Journal of Gastroenterology2004，10，7： | 8 |
| 7 | Regulation of swelling-activated chloride channels in embryonic chick heart cells显示文摘Swelling-activated Cl- currents, I(Cl,swell), were measured during hyposmotic shock in white Leghornembryonic chick heart cells using the whole-cell recording of patch-clamp technique. Genistein, an inhibitorof protein tyrosine kinase (PTK), suppressed I(Cl,swell). Under isosmotic condition phorbol 12-myristate 13-acetate (PMA), an activator of PKC, elicited the Cl- current similar to that in hyposmotic solution, whereashyposmotic shock did not elicit I(Cl,swell) in chelerythrine chloride(an inhibitor of PKC)-treated cells. Con-focal microscopy experiments using FITC-phalloidin as a fluorescent label of F-actin showed that the actinnetwork was moved from cortical region of the cell to the center after hyposmotic shock as compared withthe image under isosmotic condition. When the cells were treated with cytochalasin B (CB) or cytochalasinD (CD) under isosmotic condition the disruption of the F-actin integrity was observed, and I(Cl,swell) wasnot elicited. With combination treatment of CB with PMA, hyposmotic solution could not elicited I(Cl,swell).The results suggested that the role of PTK, probably receptor tyrosine kinase, for regulation of I(Cl,swell)appeared to be at upstream site related to the role of F-actin. Then PKC signal pathway was activatedsomehow and finally change in the polymerization state of cytoskeleton led to activate the swelling-activatedCl- channels. These results demonstrate clearly that PTK, PKC and F-actin are important factors for reg-ulation of I(Cl,swell), in embryonic chick heart cells as compared with often controversial results reported indifferent cell types. | HUAWEI YANAIMEI 等 | 2003 | Cell Research2003，13，1： | 6 |
| 8 | 益气养阴、活血化瘀方对实验性病毒性扩张型心肌病小鼠心肌细胞凋亡的影响显示文摘目的观察益气养阴、活血化瘀方对实验性病毒性扩张型心肌病小鼠心肌细胞凋亡的影响,探讨其防治病毒性扩张型心肌病的作用机制。方法采用多次腹腔注射柯萨奇B3m病毒的方式,建立重复感染的早期病毒性扩张型心肌病动物模型。将BALB/c小鼠210只随机分为4组,空白组30只,模型组、中药高剂量组、中药低剂量组各60只。中药高剂量组、中药低剂量组用益气养阴、活血化瘀方治疗4周后,采用原位末端标记法(TUNEL),观察益气养阴、活血化瘀方对实验性病毒性扩张型心肌病小鼠心肌细胞凋亡的影响。结果中药高、低剂量组与模型组相比,可改善小鼠心肌组织病理形态学及超微结构的变化,抑制心肌细胞凋亡。结论益气养阴、活血化瘀方能够减轻病毒性扩张型心肌病小鼠的病理损伤,抑制心肌细胞肥大,抑制心肌细胞凋亡,从而对病毒性扩张型心肌病起到一定的防治作用。 | 周亚滨 张丽丽 高运吉 张占军 | 2008 | 中西医结合心脑血管病杂志2008，6，5： | 5 |
| 9 | 褪黑素对小鼠肝癌细胞凋亡及自然杀伤细胞活性的影响显示文摘目的 探讨褪黑素 (MLT)在体内对H2 2肝癌细胞凋亡及免疫调节作用的影响及其机制。方法 应用免疫组织化学染色方法及原位末端脱氧核苷酸转移酶标记法 (TUNEL)对Bcl 2、Bax的表达及凋亡细胞进行检测 ,MTT比色法检测脾细胞NK杀伤活性。结果 实验发现MLT治疗组、预防组及 5 Fu组Bcl 2和Bax的表达及凋亡细胞数明显高于生理盐水组 (P <0 0 1)。Bax/Bcl 2比例在MLT预防组最大。NK杀伤活性在MLT治疗组、预防组较其它组明显增高 (P <0 0 5 )。结论 MLT在体内有促进肿瘤细胞凋亡的作用 ,且可使NK杀伤活性增高 ,推测Bcl 2。 | 宫丽华 任大宏 熊密 鲁志强 王西明 | 2003 | 华中科技大学学报(医学版)2003，32，3： | 4 |
| 10 | 病毒性心肌炎心肌细胞凋亡机制研究显示文摘在病毒性心肌炎的发病机制及病理生理过程中,关于心肌细胞是否发生凋亡,以及凋亡的诱导原因和重要程度,一直众说纷纭,没有确切定论。本文参考近年来一些文章的实验结果,介绍了病毒性心肌炎发生凋亡的情况,以及诱导凋亡出现的机制,主要概括为:在病毒的刺激下,炎症细胞分泌细胞因子,进而通过胞外受体,信号转导进入心肌细胞激活凋亡通路;此外,病毒直接侵入心肌细胞,诱导细胞凋亡发生。 | 王仑 宋晓东 | 2003 | 中国分子心脏病学杂志2003，3，5： | 4 |
| 11 | Coxsackievirus B3-induced apoptosis and Caspase-3显示文摘Cell death can be classified into two categories: apoptosis and necrosis. Apoptotic pathway can beeither caspase-dependent or caspase-independent. Caspase-independent cytopathic effect (CPE) has beendescribed. In order to evaluate the pattern of HeLa cell death induced by Coxsackievirus B3 (CVB3)and whether apoptosis involves caspase activation, we co-cultivated HeLa cells with CVB3 and detectedthe cytopathic changes, the alteration of mRNA and protein expression of caspase-3 gene plus caspase-3activity, as well as analyzing DNA fragmentation before and after caspase-3 activity inhibition. Accordingto the results, we propose that CVB3 may induce apoptosis and necrosis in HeLa cells, the latter appearingmuch earlier. Caspase-3 is activated at the levels of both transcription and translation, and procaspase-3 isproteolytically cleaved, thus leading to the continuous increasing of both caspase-3 precursor protein and itssubunit. However, besides CPE, apoptosis induced by CVB3 is not a direct consequence of the activationof caspase-3, or caspase-3 is not the only effector molecule in apoptotic cell death, for caspase-3 inhibitorcan not decrease DNA fragmentation. Some other biochemical mechanisms may participate in the process,whose role weakens the effect of inhibiting caspase-3 activity. | JIAN PING YUAN,WEI ZHAO,HONG TAO WANG,KAI Yu WU,TAO LI,XIAO KUI GUO,SHAN QING TONGDepartment of Microbiology and Parasitology,Shanghai Second Medical University,Shanghai 200025,China | 2003 | Cell Research2003，13，3： | 4 |
| 12 | 黄芪三萜皂苷对CVB3病毒所致细胞凋亡的保护作用显示文摘目的应用分子生物学技术探讨黄芪三萜皂苷(total extract of astragalus,TEA)对柯萨奇B组3型病毒(CVB3)致细胞凋亡的保护作用。方法利用CVB3感染Vero细胞建立细胞凋亡模型并使用TEA对模型进行治疗,检测DNA Ladder以了解凋亡细胞DNA断裂情况;通过TUNNEL标记法、Annexin-V/PI染色、Hoechst33258染色观察细胞凋亡程度,比较各组间细胞凋亡的差异。结果 CVB3感染后,Vero细胞DNA的紫外成像呈现阶梯状条带,TEA组可观察到DNA断裂程度降低;TUNNEL检测可看到凋亡存在,病毒组显色较深,细胞凋亡程度较TEA组严重;Annexin-V/PI染色可见病毒组Vero细胞膜呈绿色荧光,细胞核显红色,核凝聚及裂解,并有凋亡小体存在,TEA组细胞状态改善;Hoechst33258染色结果表明,病毒组Vero细胞核显蓝色荧光,可看到凋亡中期核染色质凝聚、边缘化及晚期凋亡小体的典型变化。TEA组细胞状态改善,凋亡细胞数目减少。正常细胞对照组的细胞贴壁状态良好。流式细胞仪检测结果表明,黄芪三萜皂苷能够显著的降低试验组Vero细胞的凋亡率。结论 TEA对CVB3病毒感染的Vero细胞具有一定的保护作用,抑制细胞凋亡,其作用机制尚需做进一步探讨。 | 魏青 刘小玲 郑兰兵 刘小雷 刘天龙 孙建军 | 2012 | 中南药学2012，10，10： | 2 |
| 13 | 动脉粥样硬化性高血压损伤动脉并加速血管细胞的凋亡与钙化显示文摘动脉粥样硬化和高血压是关系密切的慢性动脉疾病。在多种情况下,它们共存且相互作用,产生威胁生命的并发症,如心肌梗死和脑梗死。在动脉粥样硬化和高血压的多种病理变化中,动脉壁血管细胞凋亡增加、发生表型转变独具特色。有些分子通路在动脉粥样硬化病变的细胞组分变化中起作用。维持正常的血管结构和形态需要保持凋亡和增殖的平衡。在动脉粥样硬化和高血压的发病过程中,多种潜在的有害因素可能导致血管细胞功能异常或损伤。暴露于促动脉粥样硬化和高血压因素中的血管会由收缩型向合成型转变。降低血管细胞存活率和促进钙化是两个主要的病理变化,这些过程受影响不同表观因子表达的表观过程调节。阐明这些通路可能有助于发现动脉粥样硬化性高血压及其并发症,包括急性冠状动脉综合征的治疗新策略。 | GAO Shan-shan GENG Yong-Jian 练桂丽(编译) | 2016 | 中华高血压杂志2016，24，8： | 2 |
| 14 | 病毒性心肌炎和扩张型心肌病心肌Fas蛋白表达显示文摘目的探讨病毒性心肌炎(viral myocarditis,VMC)和扩张型心肌病(dilated cardiomyopathy,DCM)的发病机制及相互关系。方法应用改良的免疫组织化学技术观察VMC、DCM和对照组(各20例)心肌Fas蛋白的表达,并对其阳性反应结果进行Ridit检验。结果与对照组相比,VMC和DCM组Fas蛋白阳性表达明显升高,经Ridit检验,3组阳性结果差异有统计学意义(P<0.005);进一步采用两两比较Ridit检验,对照组和其他两组之间差异有统计学意义(P<0.05),而VMC和DCM组间差异无统计学意义(P>0.05)。结论VMC和DCM心肌组织中Fas蛋白表达明显高于对照组,提示VMC和DCM的发病都有细胞凋亡的参与;凋亡可能是VMC引起心肌损伤及演变为心肌病的一个发病机制。 | 吴小侨 李永宏 朱献 吴茂旺 胡升明 | 2008 | 法医学杂志2008，24，6： | 2 |
| 15 | 血管平滑肌细胞体外摄取寡核苷酸探针的研究显示文摘目的:以99mTc标记针对c-myc和bcl-2 mRNA的寡核苷酸并检测其在血管平滑肌细胞(VSMC)中的摄取情况,初步探讨其在粥样硬化病变中的诊断价值。方法99mTc标记寡核苷酸后分别加入体外培养对数生长期及平台期猪冠状动脉VSMC,37℃条件下温育,检测不同时段摄取百分数。结果:增殖期或平台期VSMC对bcl-2探针的摄取均低于对c-myc探针的摄取。在c-myc探针组,增殖期细胞较平台期摄取高反义探针较正义探针摄取高。结论:增殖期VSMC对c-myc反义探针的摄取增高和(或)对bcl-2反义探针的摄取减少,有望成为粥样病变的早期诊断指标。 | 秦光明 张永学 曹卫 安锐 高再荣 曹国祥 | 2005 | 微循环学杂志2005，15，2： | 1 |
| 16 | 溶血磷脂酸抑制顺铂诱导的卵巢癌细胞凋亡显示文摘目的:探讨溶血磷脂酸(lysophosphatidic acid,LPA)对顺铂诱导的卵巢癌细胞凋亡的抑制作用及其作用机制。方法:体外培养卵巢癌细胞株SKOV3,采用MTT法检测LPA对顺铂(cisplatin,DDP)作用后卵巢癌细胞株SKOV3增殖活性的影响,Hoechst33258荧光染色观察凋亡细胞,用FCM法分析细胞周期变化和细胞凋亡率,DNA片段凝胶电泳观察凋亡细胞的DNA'梯状'条带,免疫细胞化学法及RT-PCR法分别检测细胞凋亡相关蛋白及其mRNA的表达。结果:LPA能降低DDP对SKOV3细胞生长的抑制作用,同时增加G0/G1期细胞比例,降低S期细胞比例和凋亡率。Hoechst33258染色检测示LPA作用后凋亡小体明显减少。DNA片段凝胶电泳示LPA作用后不产生明显的凋亡片段。10μmol/L的LPA作用SKOV3细胞48h后,bcl-2基因及其蛋白表达水平升高,而bax基因及其蛋白表达水平降低(P<0.01)。结论:LPA可通过上调bcl-2基因及蛋白表达,下调bax基因及蛋白表达,抑制DDP诱导的卵巢癌细胞凋亡。因此,针对LPA的治疗有望提高DDP疗效,改善卵巢癌患者的预后。 | 刘红 房朝晖 吴小华 | 2008 | 肿瘤2008，28，7： | 1 |
| 17 | 柯萨奇病毒对细胞凋亡影响的研究进展显示文摘柯萨奇病毒引起的多种疾病与其对宿主细胞凋亡的影响有关,其作用机制主要包括ERK途径、caspase途径、PKB激酶途径、JNK激酶途径、线粒体与凋亡信号的调控及Ca2+依赖途径等。本文就最新的柯萨奇病毒分子参与细胞凋亡调控的研究进展加以综述,以飨读者。 | 黎帆 付颖媛 | 2006 | 实用临床医学(江西)2006，7，6： | 0 |
| 18 | Apoptosis of HeLa Cells Induced by Cisplatin and Its Mechanism显示文摘To study the apoptosis induced by cisplatin in cervical cancer cell line HeLa and its mechanism,cell growth inhibition of cisplatin on HeLa cells was analyzed by MTT assay.Cell apop-tosis was examined by cytometry and Hoechst33258 staining after treatment with cisplatin.The ef-fects of cisplatin on transcription of E6 were analyzed by RT-PCR.The protein expressions of E6,p53,p21,Bax and Bcl-2 were studied by Western blotting.Cisplatin inhibited proliferation in a time-and dose-dependant manner.Cytometically,sub-G1 peak showed higher apoptosis rates in the ex-perimental group than those in the control.Hoechst33258staining exhibited apoptosis induced by cis-platin.RT-PCR revealed that cisplatin decreased transcription of E6.Western blotting showed that cisplatin decreased protein expression of E6 and increased protein expression of p53,p21and Bax.It had no effect on protein expression of Bcl-2.It is concluded that cisplatin can induce apoptosis in HeLa cells by suppressing HPV E6 and thereby restoring the function of p53. | 柳友清 邢辉 韩晓兵 石小燕 梁缝奇 陈刚 卢运萍 马丁 | 2008 | Journal of Huazhong University of Science and Technology(Medical Sciences)2008，28，2： | 0 |
| 19 | 联合检测PROG与CA125有鉴别恶性卵巢CA的意义显示文摘目的探讨孕酮在卵巢癌与非卵巢癌中的特异性研究。方法用雅培I2000针对检测中CA-125异常高值的标本同时检测血清中的PROG。结果对于CA-125显著增高的卵巢癌患者同时检测孕酮有鉴别意义,同时也可以作为卵巢癌与其它非卵巢癌的鉴别,同时可以作为卵巢癌治疗预后的一个评估。孕酮在非妊娠人群中的检测值低于妊娠和卵巢癌患者,同时对比对于非卵巢癌患者CA-125升高不明显的非卵巢癌患者,有助于早期诊断和作为预后评估。 | 肖建波 | 2014 | 科学咨询2014，0，38： | 0 |
| 20 | 缺锌——动脉粥样硬化形成的危险因素显示文摘锌是重要的抗氧化剂和膜稳定剂,锌缺乏主要通过以下四个信号传导过程而影响内皮细胞的功能,即p53基因的调节、核因子κB的激活、半胱天冬氨酸酶的激活以及NO的信号传导作用。本文就缺锌在动脉粥样硬化形成中的作用作一综述。 | 颜利求 朱学良 | 2005 | 国外医学(心血管疾病分册)2005，32，1： | 0 |
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