中国细胞生物学学报(原名:细胞生物学杂志)
分子细胞生物学报 Journal of Molecular Cell Biology
Congenital kidney maldevelopment and molecular biology research The abstract kidney maldevelopment is the kidney has theunusual clinical consequence, its typical histo-pathologycharacteristic is appears originally Beginning kidney pellet and 肾小管, 软骨样 metaplasia andso on. In recent years through application molecular technology and soon target gene and home position clone Has the molecular regulation mechanism research to the normalmammal kidney, has to the congenital kidney maldevelopmentpathogenesis More understandings. This article will make a discussion to thecongenital kidney maldevelopment molecular biology research recentsituation, and will be right Including the growth factor several kind of gene mutation,copies the regulative barrier and the expression change and the kidneysends the good relations Carries on the discussion. The kidney maldevelopment is the kidney has not been able to carry onthe congenital disease which the normal growth growth forms, in thepast arose to it The mechanism understanding are really few, along with themember biological technology development and the application, expoundsthe kidney occurrence from the member study mechanism Had a more thorough understanding from the molecular biologylevel to the kidney maldevelopment occurrence. This article onshort-term regarding this question The research progress makes an introduction. 1 kidney occurs with the kidney maldevelopment Before the normal mammalia kidney is located between liesbetween 中胚层, 中胚层 the differentiation forms the kidneydrive pipe, after further tempts Leads forms 中肾 the drive pipe to the ureter bud, under theureter bud induction, end the embrionic body two sides fresh reninssplits up into after The kidney 胚基, the kidney embryonic development isprecisely completes by the ureter bud and the latter kidney 胚基 twoparts, former gradually grows Becomes 肾盂, 肾盏 and 集合管, latter grows肾小管and the kidney pellet, finally 肾小管and集合管docking, Constitutes normally 肾单位. If the ureter bud and thelatter kidney 胚基 two parts cannot grow according to the normaldegree and implement rightly Meets namely creates the kidney maldevelopment. The kidneymaldevelopment may be partial, also may be complete. Most types The kidney maldevelopment partner has the cyst, prompts themaldevelopment each kind of form to have machine-made together in theformation. On clinical common congenital kidney maldevelopment including multi-pouches, obstruction kidney maldevelopment as well as with gene The related kidney growth is unusual. The histo-pathologyimportant characteristic appears primitive 肾小管and the metaplasiacartilage. Complete list The side kidney maldevelopment, may display for does not havethe symptom. In most maldevelopment case of illness, the kidney flawis the double side, prompts Gene mutation in normal kidney growth vital role. Shan Cexingdisease then possibly is one kind of obtaining damage is the resultof, This damage destroyed the gene normal expression, thenaffected maturely had the vital significance to the kidney the proteinproduction. 2 kidneys maldevelopment common type 2.1 congenital multi- pouches kidneys maldevelopment The multi- pouches kidney maldevelopment (multiple cystichypoplastic) is one common completeness The kidney maldevelopment, are many for the single sidepathological change (14-20% for double side nature), contracts thekidney to lose the normal shape, irregular The size cyst replaces, the kidney function loses and oftenthe partner has the ureter obstruction, is newborn abdomen Bao Kuaizuicommon One of reasons. The multi- pouches maldevelopment kidney outlook assumes thekidney-shaped structure, the most case of illness partner has a 闭锁ureter. Pregnancy The early polycystic kidney includes the normal growth to havethe ingredient, loses the urine including the induction after kidney胚基 island and the branch The tube drive pipe, may distinguish the pouch change in thisstage 肾单位 each Duan Yijun [ 1 ]. After lives the multi- pouchesmaldevelopment kidney The histo-pathology variation including the primitive肾小管pouch change, expands also the disarrangement of thestructure, has around the obvious tube Response nature, textile fiber myo- link formation, cartilageingredient as symbol organization transformation and so on. 2.2 congenital obstructions kidneys maldevelopment The congenital urine road obstruction in dissects in theposition often to occur to the ureter and urinary bladder 连接处,after congenitalness The urethra valve is the babies and infants uninary systemobstruction important reason. Congenital obstruction kidney histologycharacteristic and multi- pouches The kidney maldevelopment is similar, including 肾单位 eachDuan Rushen the pellet pouch transformation, the nature expands alsothe disarrangement of the structure, the marrow The nature and the straight small blood vessel remarkablehypoplasia, has around the tube the textile fiber myo- link, the manykinds of forms kidney pellet and the growth kidney Unit each section. Is same with the multi- pouches kidneymaldevelopment, the congenital obstruction kidney performance is aseries of diseases, its degree and The embryonic period urine 流阻 related fills the time whichoccurs [ 2 ]. The table partner has the kidney to grow the unusual syndrome ------------------------------------------------------ Syndrome chromosome heredity form ------------------------------------------------------ The tip and refers to (foot) to be abnormal (Apert ' s)常染色体 the dominance Sends chest gallery malnutrition 常染色体 recessivenesswhich suffocates Obese, reproduction hypofunction and so on 常染色体recessiveness Gill - ear - kidney 常染色体 dominance Campomelic growth exceptionally 常染色体 recessiveness Brain - liver - kidney (Passarge ' s) 常染色体recessiveness Fryns ' s 常染色体 recessiveness Goemine ' s X- connection Goldston (hereditary blood capillary expands) 常染色体recessiveness? Hall-Pallster ' s sending out Ivemark ' s 常染色体 recessiveness Marden-Walker ' s 常染色体 recessiveness Mecket-Gruber 常染色体 recessiveness Miranda ' s 常染色体 recessiveness Senlor-Loken ' s 常染色体 recessiveness? Three bodies chromosomes 16-18 (Edwards) Three bodies chromosomes 13-15 (Patau) Three bodies chromosomes 21 (Down) 结节性 hardened 常染色体 dominance Von Hippel-Lindau 常染色体 dominance ------------------------------------------------------ 2.3 kidneys maldevelopment syndrome The kidney maldevelopment syndrome is includes kidney abnormalthe and so on pouch maldevelopment hereditary indication group (seesthe table ). Presently expounds a part of syndromes its special gene andthe protein flaw. The maldevelopment phenotype apparent rate assumes Presently a band, prompts has other gene influence kidneysfinally 表型. The maldevelopment usually all contains the many kindsof organs, Explained the flaw the gene involves the normal organogenesisthe foundation. The histo-pathology discovered that, this kind ofsyndrome light is possible Appears the great pouch to form (for example 结节性hardening), heavy possibly appears the pouch growth exceptionally withthe renal failure (Meckel- Gruber syndrome). 3 kidneys maldevelopment molecular biology The present research discovery has the many kinds of genes andthe kidney maldevelopment related, like WT-1, Pax-2, GDNF, B Gene and so on F-2, BMP-7, PDGF, Wnt-4 in after kidney 胚基expression. Pax-2, c-ret, BMP-7, alpha 3 beta 1 and so on in ureter bud expression. When these genes lack ordestroys, the kidney cannot normally occur with the growth [ 3 ]. Sonnenberg and so on [ 4 ] 补体 RNA and the DNA probeconducts the research with the specificity immune body and theemission mark, the determination Multi- peptides growth factor, heparin structure growth factorand their acceptor, extracellular matrix member and cell surfaceentire Gathers gene and so on element in the kidney growth specificexpression position. For example liver cell growth factor mainly inafter kidney embryo gene Expression, but its acceptor c-met in ureter plumule epidermisexpression. This kind of peptides and its the acceptor are thin in twokind of types On butcher's expression explanation ureter drive pipe formsthe induction to the after 肾间 archery target. Schuchardt and so on[ 5 ] passes Using the gene recombination and the preparation 纯合子invalid sudden change mouse, discovers some influence kidney growththe gene and the multi- peptides, like The shift growth factor - beta, the liver cell growth factor,the insulin type growth factor - II, according to saw finally shows The inference specific gene has the function in the normalkidney. Tyrosine activating enzyme body acceptor c-ret leads in thebranch ureter The tube as well as matches in the nerve nutrition factorwhich the body - neuroglia grows to express. When the mouse c-ret geneis destroyed, leads Sends the entire kidney maldevelopment. Copies the factor genecode protein to be able with the DNA union, moreover has regulatesother gene tables Reaches function. In the mammal kidney growth, Wilms ' tumorgene WT-1 and Pax2 code copies the factor, Its expression form influence kidney cell differentiation [ 6,7 ]. The gene syndrome and the kidney form exceptionally related, inthe table arranges in order Leaves the disease, some syndromes have the heredity, somewhathas located the specific gene flaw with the home position clonetechnology [ 8 ]. These syndromes are being sick the family members to beable to have the remarkable 表型 variation. This kind of situationand in 纯合子 is invalid The sudden change mouse sees the variation is similar, namelythe kidney finally 表型 is decided by the experimental mouse's genebackground. The kidney maldevelopment occurrence is several kind of differentgenes flaws, perhaps meets in the embryo development period sends 畸the factor And so on many kinds of genes regulation barrier finaloutcome. 肾间 the nature - epidermis transforms process as well asureter branch and growth Is complex and the huge gene system guides by, some genes arethe kidney specificity, some rights and wrongs are special . Certain growth factor genes, although they have the timeexpression in the kidney to be active, but when they are destroyedcertainly not shade The loud kidney normal growth, this meant the growth kidneynormal expression each kind of gene has in the function overlaps [ 9]. Another one Plants the possibility is this kind of normal expression formdestruction in the kidney maldevelopment occurrence development thecertain function, or Is the kidney maldevelopment cause. The latter 肾间 nature flaw may cause the kidney maldevelopment.Moreover, the gene ill should is the dislocation expression, possiblyto kidney The maldevelopment plays the certain role. On clinical hasthe isolation the multi- pouches kidney maldevelopment and theobstruction kidney maldevelopment two Parallel existence case of illness. Congenitalness and theexperimental nature single gene mutation may cause the pouch kidneygrowth to be unusual, these genes The sudden change may change mutually relates. Theoreticallyspeaking, the sudden change may affect: (1) 胚基 proliferation andsplit up ureter drive pipe minute An institute must peptide and matrix protein expression; (2)Ureter drive pipe to after kidney 胚基 signal reaction capacity; (3)Loses After the ureter drive pipe expression starts and maintainsthe kidney 胚基 epidermis induction to need the protein the ability;(4) Latter kidney 胚基 to these letters The number carries on the response the ability; (5) Ureterbud and latter kidney 胚基 cell to signal reaction capacity [ 10 ]. Recently already separated the phosphoric acid glucose phaseomanniteglycoprotein gene, was called the GPC3 gene. The GPC3 flaw and aremany Pouch kidney maldevelopment related [ 11 ]. Although thesingle gene may finally cause the kidney maldevelopment with themulti- genes flaw, but Its 表型 possibly decided to receives the gene regulationwhich affects to be out of balance or the expression change at first,like congenital obstruction and pouch Kidney maldevelopment [ 12, 13 ]. The multi- pouchesmaldevelopment kidney, and in the nature has the growth factor gene inthe pouch epidermis Change. In the mouse obstruction growth kidney, the bloodvessel tense element and the shift growth factor assumes excessivelyexpresses [ 14 ]. Grinds Investigates the proof, in the after kidney growth unusualarea, promotes the acorn tube epidermis to appear the pouch changefactor Pax2 and Bcl-2 same Assumes excessively expresses [ 15, 16 ]. This researchpossibly can provide the important line to each kind of form kidneymaldevelopment pathogenesis Rope.
先天性肾发育不良与分子生物学的研究
摘要 肾发育不良是肾发生异常的临床后果，其典型病理组织学特征是出现原
始肾小球和肾小管、软骨样化生等。近年来通过应用靶基因和原位克隆等分子技术
对正常哺乳动物肾脏发生分子调控机制的研究，对先天性肾发育不良的发病机理有
了更多的了解。本文将对先天性肾发育不良的分子生物学研究近况作一讨论，并对
包括生长因子在内的几种基因突变、转录调控障碍及表达变化与肾发良不良的关系
进行探讨。
肾发育不良是肾脏未能进行正常生长发育形成的先天性疾病，过去对其发病
机理了解甚少，随着分子生物技术的发展和应用，从分子学机理来阐明肾脏的发生
，从分子生物学水平对肾发育不良的发生有了较深入的认识。本文就近期对此问题
的研究进展作一介绍。
1 肾发生与肾发育不良
正常哺乳类肾脏位于间介中胚层，中胚层分化形成前肾导管，经进一步诱
导形成中肾导管至输尿管芽，在输尿管芽诱导下，胚体尾端两侧的生肾素分化为后
肾胚基，肾脏的胚胎发育正是由输尿管芽和后肾胚基二部分完成的，前者逐步发育
成肾盂、肾盏和集合管，后者发育成肾小管和肾小球，最后肾小管和集合管对接，
构成正常的肾单位。如果输尿管芽和后肾胚基二部分不能按正常程度发育和实行对
接即造成肾发育不良。肾发育不良可以是部分性的，也可以是完全性的。多数类型
的肾发育不良伴有囊肿，提示发育不良的各种形式在形成中有共同机制。
临床上常见的先天性肾发育不良包括多囊性、梗阻性肾发育不良以及与基因
有关的肾发育异常。病理组织学重要特征是出现原始肾小管和化生软骨。完全性单
侧肾发育不良，可表现为无症状。多数发育不良病例中，肾缺陷是双侧性的，提示
基因突变在正常肾发育中起重要作用。单侧性疾病则可能是一种获得性损伤所致，
该损伤破坏了基因的正常表达，进而影响了对肾成熟有重要意义的蛋白质的产生。
2 肾发育不良常见类型
2.1 先天多囊性肾发育不良
多囊性肾发育不良（multiple cystic hypoplastic）是一种常见的完全性
肾发育不良，多为单侧病变（14-20%为双侧性），患肾失去正常形态，被不规则的
大小囊肿所代替，肾脏功能丧失并常伴有输尿管梗阻，是新生儿腹部包块最常见的
原因之一。
多囊性发育不良肾外型呈肾形结构，多数病例伴有一个闭锁的输尿管。妊娠
早期的多囊肾含有正常发育所必须的成份，包括未诱导的后肾胚基岛和分支的输尿
管导管，在此阶段肾单位各段已均可鉴别出囊性改变[1]。生后多囊性发育不良肾
的病理组织学变异包括原始肾小管的囊性改变、膨大且结构破坏、具有明显管周围
反应的间质、纤维肌环的形成、软骨成分为标志的组织转化等。
2.2 先天梗阻性肾发育不良
先天性尿路梗阻在解剖位置上常发生于输尿管和膀胱的连接处，先天性后
尿道瓣膜是婴幼儿泌尿系统梗阻的重要原因。先天梗阻性肾的组织学特征与多囊性
肾发育不良相似，包括肾单位各段如肾小球的囊性转化、间质膨大且结构破坏、髓
质和直小血管显著发育不全、发生管周围纤维肌环、多种形式的肾小球和发育的肾
单位各段。与多囊性肾发育不良一样，先天梗阻性肾表现为一系列疾病，其程度与
胚胎期尿流阻塞发生的时间有关[2]。
表 伴有肾发育异常的综合症
------------------------------------------------------
综合症 染色体遗传形式
------------------------------------------------------
尖头并指（趾）畸形（Apert’s） 常染色体显性
致窒息的胸廓营养不良 常染色体隐性
肥胖、生殖机能减退等 常染色体隐性
鳃-耳-肾 常染色体显性
Campomelic发育异常 常染色体隐性
脑-肝-肾（Passarge’s） 常染色体隐性
Fryns’s 常染色体隐性
Goemine’s X-连接的
Goldston(遗传性毛细血管扩张) 常染色体隐性？
Hall-Pallster’s 散发的
Ivemark’s 常染色体隐性
Marden-Walker’s 常染色体隐性
Mecket-Gruber 常染色体隐性
Miranda’s 常染色体隐性
Senlor-Loken’s 常染色体隐性？
三体染色体16-18（Edwards）
三体染色体13-15（Patau）
三体染色体21（Down）
结节性硬化 常染色体显性
Von Hippel-Lindau 常染色体显性
------------------------------------------------------
2.3 肾发育不良综合症
肾发育不良综合症是包括囊性发育不良等肾畸形在内的遗传性征候群（见表
）。现阐明一部分综合症其特异的基因和蛋白质缺陷。发育不良表现型的外显率呈
现一个谱带，提示有其他基因影响肾的最终表型。发育不良通常都包含多种器官，
说明缺陷的基因涉及正常器官发生的基础。病理组织学发现，此类综合症轻者可能
出现巨囊形成（如结节性硬化），重者可能出现囊性发育异常和肾衰竭（Meckel-
Gruber综合症）。
3 肾发育不良分子生物学
目前的研究发现有多种基因与肾发育不良有关，如WT-1、Pax-2、GDNF、B
F-2、BMP-7、PDGF、Wnt-4等基因在后肾胚基表达。Pax-2、c-ret、BMP-7、α3β
1等在输尿管芽表达。当这些基因缺乏或被破坏时，肾脏不能正常地发生与发育[3
]。Sonnenberg等[4]用特异性抗体与放射标记的补体RNA和DNA探针进行研究，确定
了多肽生长因子、肝素结构生长因子及它们的受体、细胞外基质分子和细胞表面整
合素等基因在肾发育中的特定表达位置。例如肝细胞生长因子主要在后肾胚基因内
表达，而其受体c-met则在输尿管胚芽上皮表达。这种多肽及其受体在两种类型细
胞上的表达说明输尿管导管对后肾间质的形成起诱导作用。Schuchardt等[5]通过
应用基因重组与制备纯合子无效突变小鼠，发现一些影响肾发育的基因和多肽，如
转移生长因子-β、肝细胞生长因子、胰岛素样生长因子-Ⅱ，根据所见到的最终表
型推断特定基因在正常肾发生中的作用。酪氨酸激酶体受体c-ret在分支输尿管导
管以及配体-神经胶质衍生的神经营养因子上表达。当小鼠c-ret基因被破坏时，导
致全肾发育不良。转录因子基因编码蛋白能与DNA结合，而且具备调控其它基因表
达的功能。在哺乳动物肾发育中，Wilms’肿瘤基因WT-1及Pax2均编码转录因子，
其表达形式影响肾细胞的分化[6，7]。基因性综合症与肾形成异常有关，表中所列
出的疾病，有些综合症有遗传性，有些用原位克隆技术已定位出特定的基因缺陷[
8]。这些综合症在患病家族成员能发生显著的表型变异。这种情况与在纯合子无效
突变小鼠所见的变异相似，即肾的最终表型取决于实验小鼠的基因背景。
肾发育不良的发生是几种不同的基因缺陷，或是在胚胎发育期遇到致畸因子
等多种基因调控障碍的最终结果。肾间质-上皮转化的过程以及输尿管分支和生长
，是由一个复杂而庞大的基因体系来导向，有些基因是肾特异性的，有些是非特异
的。某些生长因子基因，尽管它们在肾发生期表达活跃，但当它们被破坏时并不影
响肾的正常发育，这意味着发育肾正常表达的各种基因在功能上有重叠[9]。另一
种可能性是这种正常表达形式的破坏在肾发育不良的发生发展中起一定作用，或者
就是肾发育不良的起因。
后肾间质缺陷可导致肾发育不良。另外，基因不适应和错位表达，可能对肾
发育不良起一定作用。临床上有孤立的多囊性肾发育不良和梗阻性肾发育不良两者
并行存在的病例。先天性和实验性单基因突变均可导致囊性肾发育异常，这些基因
突变可改变相互联系。从理论上讲，突变可影响：①胚基增生和分化输尿管导管分
支所必需的肽和基质蛋白的表达；②输尿管导管对后肾胚基信号的反应能力；③输
尿管导管表达启动和维持后肾胚基上皮诱导所需蛋白的能力；④后肾胚基对这些信
号进行反应的能力；⑤输尿管芽和后肾胚基细胞对信号的反应能力[10]。
最近已经分离出磷酸葡萄糖肌醇糖蛋白基因，简称GPC3基因。GPC3缺失与多
囊性肾发育不良有关[11]。虽然单基因与多基因缺陷均可最终导致肾发育不良，但
其表型可能决定于最初受影响的基因调控失调或表达改变，如先天性梗阻性和囊性
肾发育不良[12，13]。多囊性发育不良肾，在囊性上皮和间质中均有生长因子基因
的改变。在小鼠梗阻性发育肾中，血管紧张素和转移生长因子呈过度表达[14]。研
究证明，在后肾发育异常区，促进小管上皮出现囊性改变的因子Pax2和Bcl-2同样
呈过度表达[15，16]。此研究可能会对各种形式肾发育不良的发病机制提供重要线
索。
http://dlib.cnki.net/kns50/detail.aspx?filename=SWJS200405001144&dbname=CPFD2004【论文摘要】 肿瘤是危害人类的恶性疾病,人们对此高做了大量研究工作,然对其认识未产生质的飞跃,越来越多证据显示肿瘤发生与干细胞发育异常有密切的关系。本文从干细胞理论概述了干细胞与肿瘤发生的关系及干细胞工程在肿瘤治疗中的应用前景。 【英文论文摘要】 Tumor is one of deadly diseases to mankind. Up to now, it is known little about its mechanism. Stem cell biology has come of age. More and more evidences show the close relationship between tumor genesis and abnormal development of stem cell. This shot view intends to give a general overview on relationship between tumor and stem cells, and prosperity for tumor recovery. 建议你用教育网来下载，是免费的，不然就要收费~~~（是中国知网哦~~） 答案补充 你用教育网上，就可以免费下载了。就是在高校的网络下载
1.1 投稿范围细胞生物学及其相关领域的国内外最新研究科研成果。中国及地方细胞生物学学会的各种会讯和活动消息。1.2 栏目设置设有特约综述、专题介绍、综述、研究论文、研究简报、技术与方法、教学研究、干细胞研究、探索·发现、新星汇、热点评析、学会动态等栏目，并可根据实际需求开辟新的栏目。1.3 栏目要求专题与综述：深入评介细胞生物学及相关学科某一领域研究的新进展。要求选题重要新颖、评述精辟、注重时效性和前瞻性，论文要求配1幅以上图表。尤其欢迎以本实验室研究工作为基础的高水平综述与专论。研究论文：具有重要学术价值、数据完善和创新性的原始研究工作报告。研究简报：具有首报意义、为争取时间以简报形式发表的阶段性原始研究工作报告。技术与方法：针对细胞生物学领域某一研究方法或某项实验技术的有创新性的、实用性的改进报道。教学研究：针对细胞生物学及相关科学领域的创新性教学方法研究成果的交流。探索·发现：对某一领域探索性研究最新发现的阶段性报道。新星汇：为新创建实验室的年轻科学家提供介绍、交流工作的平台。1.4 文字要求可用中文撰写，附较为详细的英文摘要；也可用英文撰写，附中文摘要。无论用何种语言撰写，均要求写作条理清晰，文字简练流畅。1.5 封面论文在封面上选登当期发表论文中的图片。图片一经选用，该论文即被作为封面论文。封面论文要求是文中能提供1张以上制作精良的彩色图片。凡愿意成为封面论文的作者，请在投稿时声明。 科学名词和术语以全国自然科学名词审定委员会公布的为准。除了国际上通用的缩写词，在摘要和正文中首次出现的缩写词，应先写出中文名词，再在括号内写出英文或拉丁文全称和缩写词。限制性内切酶的前3个英文字母用斜体表示。计量单位和符号按国家技术监督局出版的《量和单位》中规定和国际上通用规则的书写，如：(1) 溶液浓度不用M和N，而用mol/L表示。(2) rpm改为r/min，OD改为A。(3) 相对分子量（Mr）用kDa表示。(4) 秒、分钟和小时分别用s，min和h表示。(5) 统计符号均用斜体：概率用大写斜体P； F 检验用大写斜体F；t检验用小写斜体；样本数用英文小写斜体n ；相关系数用英文小写斜体r ；卡方检验用希文小写χ2；自由度用希文小写斜体υ。稿件由文章题目及各级标题、作者姓名、单位、中英文摘要、关键词、正文、图表、参考文献等部分构成。对各部分的要求分别如下：3.1 文章题目 应言简意赅，不使用不规范的别名或缩写，一般不超过20个字。3.2 各级标题 应简短醒目、层次分明，标题不超过三级，字数以不超过15个字为宜。标题编号方式参照以下示例：1 材料与方法1.1 材料1.1.1 质粒、菌种和细胞株3.3 作者姓名和单位 署名人及单位应是对文章全部或部分内容作出主要贡献并能对文章内容负责的人和单位。多作者署名的文章应用“﹡”注明通讯作者。作者姓名与单位应有中英文对照，分别排在中英文题目之下。中国作者姓名英文写法规定为：先写名，后写姓；姓和单、双名首字母大写，双名在两个汉字的拼音字母之间加连字符“-”。例如：“郭礼和”应写作“Li-He Guo”。 单位应写标准全称、所在城市及邮政编码，单位的英文项中还应写明国别。3.4 中英文摘要 应中英文对照，分别排在中英文题目和作者、单位项之下。 摘要应写成报道性文摘，无缩略语和特殊术语。非综述类论文应在摘要中简要地介绍研究目的、方法、结果（主要数据）和结论。中文摘要字数应不超过300个字。中文论文应给出较中文摘要更为详细的英文摘要，英文摘要不超过250个单词。3.5 关键词 不少于3个，不多于8个，中英文对应，分别列在中英文摘要后面。3.6 脚注 脚注应中英文对应，分别排在正文第一页右下方和英文摘要（英文论文为中文摘要）下方，以横线与正文分开。脚注的内容应包括：(1) 收稿日期与接受日期（由本刊编辑部填写）；(2) 经费（基金）资助来源；(3) 通讯作者及其电话、传真、电子信箱（E-mail）；(4) 其他。3.7 正文（1）引言 应包括该研究的目的和该研究与其他相关研究的关系。（2）实验方法 应尽量简短，但应让其他有经验的研究者能够重复该实验。完全新的方法应该详细描述，以前发表过的引用参考文献即可。有关方法的改进只有在必须重复该实验的前提下才需给出详细的论述。（3）结果 应尽量用图表表示，在结果中应避免大量的讨论。（4）讨论 要简明，应集中对所得的结果做出解释而不是重复的叙述。3.8 插图 出现在正文中应该出现的地方，对图像的要求是尽量使用TIFF格式。图必须是高质量的，图像的分辨率必须在350像素(dpi)以上。对只有彩图才能清晰地说明实验结果的，印刷时必须彩印。图应有简明的图题和详尽的图注，以使其容易被读者理解。插图的尺寸要适中，较小图的宽度不超过8 cm，较大图的宽度不超过16 cm。在有分图时，所有数字、字母和符号必须一致，并使用（A）（B）（C）（D）…表示。横、纵坐标必须清楚地标明测量单位。曲线图可按以下顺序：●，○，▲，△，■，□等使用标准的符号。图用中、英文对照表达（图范例）。3.9 表格 使用三线表（不用竖线），直接放在文中适当的位置。 表应有表题并有足够的信息使读者不去查阅正文即可理解该表的内容。表内每一栏均应有表头，表内的缩写应在标注中说明。表题写在表格上方，表注写在表格下方。表用中、英文对照表达（表范例）。3.10 参考文献 采用“顺序编码制”的著录方法，即以文中出现顺序排序而不是以作者和年份排序，作者应对引用的参考文献的正确性负全责。待发表的论文、未正式公开发表的论文（包括私人通讯、毕业论文等）、会议论文摘要等不能作为文献引用。必须引用时，请在正文中括注。以电子版和印刷版同时发表的文献，在著录时以印刷版为准。使用EndNote软件的作者，请在EndNote软件中采用Acta Pharmacol Sin的式样对参考文献进行编辑书写，即可基本符合本刊的参考文献格式要求。 参考文献的作者不超过6人（含6人）全部列出，多于6人时只写前6人，后加“等”或“et al”。姓名采用姓前名后的形式，作者之间不加“和”或“and”。 引用期刊的格式为：文献序数，作者姓名，论文题名，期刊名称（英文标准缩写参考Medline或CA），年份，卷号(期号)，起止页码。例如：1 黄 霈, 于 超, 刘洪涛, 杨 竹, 丁裕斌, 王应雄, 等。土贝母皂苷甲作用线粒体途径促进人绒毛膜癌Bewo细胞凋亡。中国细胞生物学学报2009; 31(6): 831-6.2 Wei Y, Weng D, Li F, Zou X, Young DO, Ji J, et al. Involvement of JNK regulation in oxidative stress-mediated murine liver injury by microcystin-LR. Apoptosis 2008; 13(8): 1031-42.引用书籍的格式为：文献序数，主编姓名，书名，版本（第1版不著录），出版地，出版社，年份，起止页码。例如：3 翟中和, 王喜忠, 丁明孝。细胞生物学, 第3版。北京: 高等教育出版社, 2007, 101-11.4 Sambrook J, Fritsch EF, Maniatis T. Molecular Cloning: A laboratory Manual, 2nd ed. New York: Cold Spring Harbor Laboratory Press, 1989, 88-108.5 Phillips SJ, Whisnant JP. Hypertension and stroke. In: Laragh JH, Brenner BM, eds. Hypertension: Pathophysiology, Diagnosis, and Management, 2nd ed. New York: Raven Press, 1995, 465-78.另外，结合以往作者的投稿情况，以下几点请广大投稿人特别注意：(1) 请不要引用读者很难查阅的文献，如某某大学的博士生毕业论文、某某会议的论文集等。(2) 图题(表题)、图注(表注)、图(表)中的文字和内容一律用英文表达；(3) 综述文章要求书写流利，减少翻译痕迹；引用的文献要新，应有最近1~2年的文献；尽量图文并茂，增加可读性。引用他人图表要给出文献出处，不能原版照抄（获得原文作者以及出版社同意除外），而是要做适当修饰，加入作者自己东西，这样不会侵犯他人知识产权，最好是“根据文献[1]做适当修改”这样的表达。(4) 名词问题：有中文译名的一律用中文表达。请尽可能使用已统一定名的专业名词；请使用已公开发行的有关专业《词汇》中的名词译名；对尚未统一的和不常见的名词，一定要在其后附上英文名词；尚无译名或难以定名的，请直接用英文原名；除了国际上通用的缩写词，在摘要和正文中首次出现的缩写词，应先写出中文名词，再在括号内写出英文或拉丁文全称和缩写词。(5) 很多蛋白质是以其基因命名的，因此，在书写时，应特别小心，稍有疏忽，将正体变成斜体，于是蛋白质变成了基因，反之亦然。
