三萜皂苷Saxifragifolin D抑制人肝癌耐药细胞HepG2/ADM生长并诱导细胞凋亡作用研究

目的研究Saxifragifolin D(SD)对人肝癌耐药细胞HepG2/ADM的生长抑制及诱导凋亡作用。方法采用MTT法观察SD对HepG2/ADM细胞的增殖抑制作用,应用流式细胞仪分析SD对细胞周期的影响,AnnexinⅤ-FITC/PI双染检测凋亡细胞比率,JC-1染色观察SD对细胞内线粒体膜电位的影响,Western blot检测凋亡相关蛋白caspase-9,caspase-3和PARP的激活及c-Raf,MEK和ERK蛋白的表达和磷酸化水平。结果 SD可以明显抑制人肝癌耐药细胞HepG2/ADM的增殖。细胞周期检测发现SD诱导细胞产生亚二倍体凋亡峰,同时细胞凋亡率也由对照组的5.3%增加到34.8%和47.8%。线粒体膜电位检测结果显示SD导致细胞内线粒体膜电位的明显降低。Western blot检测结果表明caspase-9,caspase-3被激活,PARP被剪切活化,cytochrome C由线粒体释放至胞质,c-Raf、MEK和ERK蛋白的磷酸化水平降低。结论 SD可以抑制人肝癌耐药细胞HepG2/ADM增殖并诱导其凋亡,作用机制可能与线粒体功能障碍及抑制c-Raf/MEK/ERK通路的活化有关。     

口服甲苯磺酸索拉非尼患者的观察及护理

甲苯磺酸索拉非尼是多种激酶抑制剂,由拜耳和ONYX公司共同研制的一种多靶点的生物靶向新药。索拉非尼具有双重抗肿瘤效应,一方面,它可以通过抑制RAF/MEK/ERK信号传导通路,直接抑制肿瘤生长;另一方面,又可通过抑制血管内皮生长因子受体（VEGFR）和血小板源性生长因子受体（PDGFR）而阻断肿瘤新生血管的形成,间接抑制肿瘤细胞的生长。临床研究显示,索拉非尼对人肿瘤的动物移植模型有广泛的抗肿瘤活性,包括结肠癌、胰腺癌、肺癌、乳腺癌和卵巢癌,其抗肿瘤作用与抑制RAF/MEK/ERK通路有关[1]。     

达沙替尼体外抗鼻咽癌细胞增殖与转移的作用

目的SRC作为酪氨酸蛋白激酶在多种实体肿瘤中存在高表达,通过激活RAS/RAF/MEK/ERK、P13K/AKT通路促进肿瘤细胞的生长与增殖,并通过激活FAK促进肿瘤细胞的转移。此外,SRC还参与了EGFR抑制剂耐药的发生。本研究旨在研究SRC的抑制剂达沙替尼在体外对鼻咽癌细胞的抑制作用。方法采用M1Tr方法绘制细胞生长曲线,并计算达沙替尼对鼻咽癌细胞的半数抑制浓度（IC50值）;PI/AnnexinV双染法检测达沙替尼诱导鼻咽癌细胞凋亡的作用;WesternBlot检测达沙替尼引起鼻咽癌细胞中信号通路的改变;Transwell实验检测达沙替尼对鼻咽癌细胞迁移的影响。结果达沙替尼能明显在体外抑制鼻咽癌细胞的增殖,诱导鼻咽癌细胞的凋亡,并且呈浓度依赖性;应用达沙替尼处理CNE2后发现,能明显抑制RAS/RAF/MEK/ERK、P13K/AKT通路活性表现为phospho-AKT、Phospho．MEK、Phospho-ERK的表达水平明显减低;达沙替尼还能明显抑制CNE2的迁移能力和Phospho-FAK的表达水平。结论SRC的抑制剂达沙替尼能在体外明显抑制鼻咽癌细胞中RAS/RAF/MEK/ERK、P13K/AKT通路的活性和FAK蛋白的表达,进一步抑制鼻咽癌细胞的增殖与转移,促进细胞凋亡。     

苦参碱对骨肉瘤细胞凋亡的影响

目的 探讨苦参碱在MG-63细胞中促凋亡的作用及机制。方法 实验分为0浓度组和10%苦参碱组,分别灌胃生理盐水和10%苦参碱制备大鼠含药血清,干预人成骨肉瘤细胞株MG-63。采用CCK-8法检测细胞增殖,流式细胞术检测细胞凋亡,荧光定量聚合酶链式反应（PCR）检测c-myc、胱天蛋白酶9(caspase-9)基因的表达,采用免疫印迹（Western blot）法检测细胞外信号调节激酶5(ERK5)信号通路中相关蛋白Nur77、丝裂原激活蛋白激酶5(MEK5)及凋亡相关蛋白c-myc,caspase-9的表达水平。结果 与0浓度组相比,10%苦参碱组能显著抑制MG-63细胞增殖,并促进其凋亡;荧光定量PCR实验结果表明,10%苦参碱组能抑制c-myc转录,并促进caspase-9转录;Western blot实验结果表明,在ERK5信号通路中,10%苦参碱组Nur77、MEK5及c-myc蛋白表达下调,而caspase-9蛋白表达上调。结论 苦参碱可能通过干扰ERK5信号通路,调控c-myc,caspase-9等蛋白的表达,从而抑制MG-63细胞增殖,并促进其凋亡。     

新型低氧还原剂Q39通过阻断HIF-1α转运引起肝癌Bel-7402细胞凋亡

目的 评价Q39低氧条件下诱导肝癌细胞Bel-7402细胞凋亡的抗肿瘤活性及其机制。方法 MTT法测定Q39对人肝癌细胞Bel-7402增殖抑制作用。PI染色法检测Q39诱导人肝癌细胞凋亡作用。免疫荧光法检测HIF-1α蛋白的转运和表达。结果 Q39在常氧和低氧下均抑制肝癌Bel-7402细胞的生长。Q39在低氧条件下促进Bel-7402肿瘤细胞凋亡。Q39通过抑制ERK1/2的磷酸化,明显抑制HIF-1α的转运。结论 Q39在低氧条件下通过抑制ERK1/2信号通路引起Bel-7402肿瘤细胞凋亡。     

甘草查尔酮A通过Akt/ERK信号通路抑制骨肉瘤增殖

目的 探究甘草查尔酮A(licochalcone A,LCA)对骨肉瘤细胞增殖和凋亡的影响及相关分子机制。方法 体外培养骨肉瘤HOS和U2OS细胞,通过MTT实验检测不同浓度LCA处理不同时间对HOS和U2OS细胞增殖的影响;加入终浓度分别为对照组(含0.1%DMSO的培养液)、5、10及20μmol·L^-1的LCA处理细胞48 h,流式细胞术检测LCA对HOS和U2OS细胞凋亡的影响,通过Western blot检测LCA对细胞凋亡相关蛋白cleaved PARP1、Bcl-2、Bax以及Akt和ERK蛋白表达水平的影响;通过裸鼠荷瘤实验从体内水平探究LCA的抗肿瘤作用。结果 MTT实验结果表明,LCA可抑制骨肉瘤HOS和U2OS细胞的增殖,并且呈时间和剂量依赖性;流式细胞术的结果表明,LCA可引起细胞凋亡。Western blot结果显示,ERK和Akt的磷酸化被抑制,cleaved PARP1和Bax的表达量升高,Bcl-2的表达量降低。裸鼠荷瘤实验表明,注射LCA后肿瘤体积明显减小(P<0.05),肿瘤的质量明显减小(P<0.01)。结论 LC...     

二苯乙烯苷调控MAPKs信号通路诱导大肠癌SW116细胞凋亡

目的研究二苯乙烯苷(THSG)对大肠癌SW116细胞凋亡的诱导作用及其可能的分子机制。方法体外常规培养SW116细胞,采用不同剂量(0、5、10、20、40、80、120 mmol/L)THSG处理SW116细胞,CCK8法分析不同剂量药物处理24、48、72 h后细胞的存活率;不同浓度(0、10、20、40 mmol/L)THSG干预SW116细胞24 h后,Annexin/PI双染后流式细胞仪检测SW116细胞凋亡情况,Western blot方法检测SW116细胞中凋亡相关蛋白PARP和Pro-caspase 3的表达及MAPKs信号通路p38、ERK、JNK的磷酸化水平;p38、ERK、JNK特异性抑制剂干预细胞后,Western blot方法检测抑制剂对p38、ERK、JNK磷酸化的抑制作用。结果 THSG呈剂量和时间依赖性地抑制大肠癌SW116细胞的增殖,诱导细胞凋亡;THSG干预SW116细胞后,Cleaved PARP表达显著升高、Pro-caspase 3表达显著降低,胞内p38和JNK磷酸化水平显著升高(P<0.05),然而ERK磷酸化水平显著降低(P<0.05)。结论特异性抑制剂阻断ERK激活,可以增强THSG诱导SW116细胞凋亡,特异性阻断p38、JNK活化,能够部分逆转THSG对p38和JNK磷酸化和细胞凋亡的诱导作用。THSG通过激活p38和JNK信号传导,抑制ERK信号途径,诱导大肠癌SW116细胞凋亡。     

乌头碱通过ROS/JNK信号转导通路诱导骨肉瘤细胞凋亡的机制研究

目的 基于ROS/JNK信号转导通路探讨乌头碱诱导骨肉瘤细胞凋亡的机制.方法 MTT法测定乌头碱对人骨肉瘤143B细胞活力的抑制作用;Western Blot法检测乌头碱处理后143B细胞cleaved caspase-9、cleaved caspase-3和磷酸化JNK的表达水平;采用流式细胞术检测用乌头碱处理后143B细胞的凋亡及活性氧簇(ROS)的产生.结果 乌头碱可显著诱导143B细胞发生凋亡,产生ROS.乌头碱处理后143B细胞cleaved caspase-9、cleaved caspase-3、磷酸化JNK均显著上升.乌头碱有显著的体外抗骨肉瘤作用,能显著抑制143B细胞的活力.结论 乌头碱通过ROS/JNK信号通路诱导人骨肉瘤143B细胞发生凋亡,具有显著的抗肿瘤作用.     

乌头碱通过ROS/JNK信号转导通路诱导骨肉瘤细胞凋亡的机制研究

目的 基于ROS/JNK信号转导通路探讨乌头碱诱导骨肉瘤细胞凋亡的机制.方法 MTT法测定乌头碱对人骨肉瘤143B细胞活力的抑制作用;Western Blot法检测乌头碱处理后143B细胞cleaved caspase-9、cleaved caspase-3和磷酸化JNK的表达水平;采用流式细胞术检测用乌头碱处理后143B细胞的凋亡及活性氧簇(ROS)的产生.结果 乌头碱可显著诱导143B细胞发生凋亡,产生ROS.乌头碱处理后143B细胞cleaved caspase-9、cleaved caspase-3、磷酸化JNK均显著上升.乌头碱有显著的体外抗骨肉瘤作用,能显著抑制143B细胞的活力.结论 乌头碱通过ROS/JNK信号通路诱导人骨肉瘤143B细胞发生凋亡,具有显著的抗肿瘤作用.     

偶氮鎓二醇盐衍生物抑制肝癌细胞增殖的机制

目的通过体内实验与体外实验探究NO供体前药即偶氮鎓二醇盐衍生物PABA/NO对Bel-7402肝癌细胞增殖与凋亡的影响。方法MTT法检测PABA/NO对Bel-7402细胞增殖的影响;蛋白免疫印迹法检测Bel-7402细胞中抗凋亡蛋白Bcl-2和Bcl-x L、促凋亡蛋白Bax和Bad、细胞色素C(Cyt c)、活化胱天蛋白酶9、活化胱天蛋白酶3、活化聚二磷酸腺苷核糖聚合酶(cleaved-PARP)、胞内磷脂酰肌醇激酶(PI3K)、蛋白激酶B(AKT)、哺乳动物雷帕霉素靶蛋白(mTOR)、MAPK/ERK激酶(MEK)和细胞外调节蛋白激酶(ERK)的表达。分别用PI3K抑制剂LY294002、ERK抑制剂U0126和NO清除剂Carboxy-PTIO预处理Bel-7402细胞,检测对上述因子的影响。用健康雄性BALB/c小鼠建立肝癌H22移植瘤小鼠模型,随机分为对照组、PABA/NO低剂量组(1 mg·kg~(-1))、PABA/NO中剂量组(2 mg·kg~(-1))和PABA/NO高剂量组(4 mg·kg~(-1))。将H22细胞悬液接种于小鼠腋下,第2天各组小鼠开始尾静脉注射药物,3 d注射1次,连续14 d。观察各组小鼠肿瘤的生长状况,计算抑瘤率。Western印迹法检测肿瘤组织中CD34,PI3K,AKT,mTOR,MEK和ERK的表达。结果 PABA/NO可以有效抑制Bel-7402细胞的增殖并诱导细胞凋亡,具有一定的浓度依赖性。PABA/NO可下调Bcl-2和Bcl-x L,上调Bax和Bad的表达,并释放Cyt c,激活胱天蛋白酶9和胱天蛋白酶3,诱导细胞凋亡。与此同时,PABA/NO还可以激活PARP,并抑制PI3K/AKT/m TOR和MEK/ERK信号通路在细胞内的表达。LY294002和U0126可以提高PABA/NO诱导Bel-7402细胞凋亡的发生率,而Carboxy-PTIO通过清除NO而明显降低PABA/NO引起的细胞凋亡。另外,PABA/NO还可以明显降低H22荷瘤小鼠的肿瘤体积、肿瘤重量以及CD34在体内的表达而发挥抗肿瘤作用。此外,经PABA/NO处理的小鼠体内PI3K/AKT/m TOR和MEK/ERK信号通路明显被抑制。结论 PABA/NO可以通过抑制PI3K/Akt/mTOR和MEK/ERK通路诱导肝癌细胞凋亡。     

Clevudine University of Georgia/Abbott/Bukwang/Triangle/Yale University

The pyrimidine analog, clevudine (L-FMAU: 2'-fluoro-5-methyl-beta-L-arabinofuranosyluridine) is a potent antihepatitis B virus (HBV) and anti-Epstein-Barr virus (EBV) agent, discovered by researchers at the University of Georgia, in collaboration with Yale University and Bukwang. Bukwang transferred its technology to Triangle Pharmaceuticals in 1998 together with a license to develop clevudine worldwide except Korea [279649], [281942]. In June 1999, Triangle and Abbott Laboratories entered into a strategic alliance to copromote antiviral products including L-FMAU [326798]. In September 2000, Triangle Pharmaceuticals Inc initiated a 30-day phase I/II evaluation of clevudine in HBV-infected patients [381755]. Clevudine is a much less toxic derivative of the toxic agent P-D-FMAU. The mechanism of action of clevudine is not yet clear, but the agent induces a rapid decrease in HBV nucleic acid as doses increase from 0.3 to 10 mg/kg [319145]. It is believed that the target for clevudine lies in the viral replication mechanism. Clevudine is phosphorylated to the triphosphate form intracellularly. This is removed slowly from the cells, thus exerting a sustained inhibitory antiviral activity [178173], [320720], [320721].     

Spotlight from the American Society for Preventive Cardiology on Key Features of the 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guidelines on the Management of Blood Cholesterol

The 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol retains focus on recommendations for statin treatment in the original four statin-eligible groups [those with atherosclerotic cardiovascular disease (ASCVD), diabetes, low-density lipoprotein cholesterol (LDL-C) ≥ 190 mg/dL, and higher risk primary prevention] without the use of treatment initiation or target LDL-C levels from the earlier 2013 American College of Cardiology/American Heart Association (ACC/AHA) guideline, but has several new features. First, patients with primary prevention are divided into those who are at low (< 5%), borderline (5% to < 7.5%), intermediate (7.5% to < 20%), and high (≥ 20%) risk based on the ASCVD risk estimator. Moreover, the new guideline goes further to consider a wider range of factors [now called “risk enhancers”—premature family history of ASCVD, persistently high LDL-C, chronic kidney disease (CKD), metabolic syndrome, conditions specific to women, inflammatory diseases, and high-risk ethnicities] that can be used to better inform the treatment decision. Moreover, more detailed recommendations on how the results of coronary calcium scanning can be used to inform the treatment decision are provided, including how it may be used to “de-risk” certain patients for delaying or avoiding the use of statin therapy. There are also specific sections for cholesterol management in other patient subgroups including women, children, certain ethnic groups, those with CKD, chronic inflammatory disorders and HIV, as well as discussion on the management of hypertriglyceridemia. Importantly, for persons with known ASCVD, a distinction is made for those who are at “very high risk” based on having had two major ASCVD events or one major event and two or more other high risk conditions, such as diabetes or other major risk factors, or bypass surgery or percutaneous intervention. Finally, the concept of a threshold LDL-C for initiating a non-statin therapy (after considering highest tolerated statin dosage) is provided, with ezetimibe recommended as the key non-statin to be added if the LDL-C still remains ≥ 70 mg/dL for all ASCVD patients, and in those who are at “very high risk”, further consideration for using a proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor. While the new guideline does have greater detail (and arguably, complexity), the refinements provide a strategy for guiding the clinician to target both statin and non-statin therapy to those most likely to derive benefit.     

Cerebral metabolism of [3H]-p-chloroamphetamine

The time-dependent metabolism of intraventricularly administered $\text{[}{}^3\text{H}\text{]-p-}\text{chloroamphetamine}$ was followed. The parent compound and its metabolites were recovered by high pressure liquid chromatography and characterized by high pressure liquid chromatography, thin-layer chromatography, and gas chromatography-mass spectrometry. By 4 hr after injection, two major toluene-soluble metabolites were present in brain. Their biological half-lives were different from the parent compound. On the basis of their analyses, one of the metabolites is p-chloronorephedrine, the other (P₃) is as yet unidentified. Pretreatment with Lilly 110140 prevented or markedly reduced the synthesis of both p-chloronorephedrine and P₃. Iprindole prevented the synthesis of p-chloronorephedrine. The P₃ appeared first in the brain then in the liver, suggesting that both of these organs can metabolize p-chloroamphetamine to this compound. The metabolites were recovered primarily from the nuclear and microsomal fractions following subcellular fractionation of the brain, with small quantities present in the synaptosomal fraction. The level of metabolites was higher in the brainstem than in the neocortex. Glutathione, administered simultaneously with p-chloroamphetamine either intraventricularly or intraperitoneally failed to alter the toxicity of p-chloroamphetamine.     

Conversion of the N-O-glucuronide and N-O-sulfate conjugates of N-hydroxyphenacetin to reactive intermediates

The N-O-glucuronide of [¹⁴C]acetyl-N-hydroxyphenacetin is sufficiently stable to purify, but slowly breaks down in aqueous solutions to a reactive intermediate that can covalently bind to protein. When the pure compound was incubated in Tris buffer, pH 7.4, at 37°, it decomposed with a half-life of about 8.7 hr to the following compounds: phenacetin, 2-hydroxyphenacetin glucuronide, acetamide and acetaminophen. On addition of glulathione to the systems and allowing the reactions to go to completion, a glutathione-acetaminophen conjugate was formed at the expense of acetamide and acetaminophen: the fraction converted to phenacetin or to the 2-hydroxyphenacetin glucuronide was unchanged. On addition of ascorbic acid to the system and allowing the reactions to go to completion, the fraction converted to acetaminophen was increased at the expense of acetamide: the fractions converted to phenacetin and 2-hydroxyphenacetin glucuronide, however, were again unchanged. When the glucuronide was incubated with bovine serum albumin, covalent binding to the protein occurred at the expense of acetaminophen and acetamide; again, the fraction of the glucuronide converted to phenacetin and 2-hydroxyphenacetin glucuronide was unchanged. Moreover, the covalent binding could be partially prevented by addition of ascorbic acid or glutathione. Since there is formation of covalently bound material, the glutathione conjugate and acetaminophen appear to be interrelated; it seems likely that they are formed from a common intermediate, possibly acetylimidoquinone. However, the data suggest that the formation of phenacetin and 2-hydroxyphenacetin glucuronide occurs by different mechanisms. The N-O-sulfate of [¹⁴C]acetyl-N-hydroxyphenacetin also breaks down to a reactive intermediate that has properties similar to those of the reactive intermediate formed from the N-O-glucuronide and thus may also be N-acetylimidoquinone. By contrast, the relative ability of various nucleophiles to prevent the covalent binding of the reactive intermediate formed from the N-O-sulfate of 2-acetylaminofluorene to protein differs from the relative ability of the nucleophiles to prevent the covalent binding of the reactive intermediate of either the N-O-sulfate or the N-O-glucuronide of phenacetin, suggesting that the relative rates at which these intermediates combine with the different macromolecules may differ markedly.     

甘草配伍大戟的体外肝毒性研究

目的 研究甘草和大戟配伍的体外肝毒性。方法 采用显微观察法和MTT法检测不同浓度的甘草单煎液、大戟单煎液、甘草-大戟合煎液和甘草-大戟单煎混合液对人肝癌细胞HepG2增殖的影响,并比较大戟单煎液、甘草-大戟合煎液和甘草-大戟单煎混合液相当浓度下细胞毒性的大小。结果 大戟单用及大戟与甘草配伍均有细胞毒性,且呈剂量相关性;与大戟单煎液相比,甘草-大戟单煎混合液细胞毒性无明显差异,甘草-大戟合煎液细胞毒性减小。结论 甘草和大戟配伍导致大戟的体外肝毒性减小。     

刺五加的研究进展

刺五加含有苷类、黄酮、多糖等多种活性成分,具有免疫调节、抗肿瘤、抗衰老、抗疲劳等药理作用。对国内外刺五加相关文献进行总结,为刺五加进一步的研究和开发提供参考资料。     

Structure-activity relationships of met5- and leus-enkephalin analogues

1. The effect of various analogues of met5- and leu5-enkephalin were determined on the reduction in twitch height of the electrically-stimulated longitudinal muscle preparation of the guinea-pig ileum and of the isolated mouse vas deferens. 2. In the guinea-pig ileum, D-alanine2-met5-enkephalin was the most potent whereas leu5-enkephalin was the most potent in the mouse vas deferens. 3. The met5-enkephalin analogues were more effective in reducing the twitch height of the ileum than they were in depressing that of the vas deferens preparation. The leu5-enkephalin analogues were more potent in their effects on the mouse vas deferens than they were on the guinea-pig ileum. 4. When a peptide bond is replaced by a glycol bond as in glycol2-3-leu5-enkephalin there is a marked reduction in opiate-like activity. 5. Substitution of a D-alanine residue for the glycine2 residue, as in D-alanine2-met5-enkephalin, increases the duration and potency of opiate-like activity. 6. These results confirm that modification of either met5- or leu5-enkephalin can alter the opiate-like potency of the resulting analogues. It appears that an intact tyrosyl residue of leu5-enkephalin is essential for such activity and that substitution of a D-alanine2 residue for the glycine2 residue confers resistance to enzymatic degradation on the met5-enkephalin peptide. In addition, the glycine2-3 peptide bond is essential for opiate-like activity.     

Quantitative histochemical studies of striatal dopamine depletion following dl-α-methyl-p-tyrosine administration

This study investigated the use of a microfluorimetric histochemical method for the measurement of the depletion of dopamine in the rat caudate nucleus, following α-methyl-p-tyrosine (α-MT) administration. The depletion in three behavioral situations was compared with that of a control group which remained in a cage.The results of the control group indicate that there had been a reduction of approximately 50% in the intensity of the formaldehyde-induced fluorescence derived from dopamine in a region of the neuropil of the caudate nucleus, during the interval (3 hr 40 min) between α-MT, 300 mg/kg i.p., and killing. Disruption of conditioned avoidance response (CAR) performance after α-MT administration was confirmed, but in this study CAR performance in previously trained rats did not have a significant effect on the depletion of formaldehyde-induced fluorescence of the striatal neuropil after α-MT administration. The levels of α-MT-induced depletion of formaldehyde-induced fluorescence in the striatal neuropil following a period of muscular co-ordination/activity and following a period of CAR training were also not significantly different from those shown by a control group.     

Nampt/Visfatin/PBEF研究进展

尼克酰胺磷酸核糖转移酶(nicotinamide phosphoribosyltransferase,Nampt)是生物合成NAD的关键限速酶,又被称为前B细胞克隆增强因子(pre-B cell colony enhancing factor,PBEF)和内脏脂肪素(visfatin).最近研究发现,Nampt/Visfatin/PBEF在NAD生物合成、代谢、炎症反应和细胞增殖、分化、凋亡等诸多领域发挥作用,可能影响2型糖尿病、急性肺损伤、恶性肿瘤等疾病发生、发展和预后.本文主要对Nampt/Visfatin/PBEF的生理功能及临床意义进行综述.