P19细胞

摘要： 目的 深入心脏发育相关基因表达层面,研究视黄酸代谢中的关键基因视黄醛脱氢酶2 (retinaldehyde dehydrogenase 2,Raldh2)在P19细胞中的表达并探讨对其心肌样分化的影响机制.方法 构建miRNA干扰质粒转染P19细胞以使Raldh2表达降低,qPCR检测miRNA对Raldh2在P19细胞中的敲低效率,利用杀稻瘟菌素筛选出稳定低表达Raldh2的细胞株,加入二甲基亚砜以诱导P19细胞分化为心肌样细胞,qPCR检测心肌发育相关基因在心肌样分化各时期的表达水平.结果 成功构建Raldh2低表达的稳定P19细胞株MiRaldh2,敲低效率达91％(t=25.52,P＜0.000 1,95％CI:0.81～1.01);在整个分化过程中,MiRaldh2组部分心脏相关转录因子的mRNA水平普遍低于P19组,尤其在第7天,MiRaldh2组Gata 4、Tef-1、N-myc、α-mhc和Ctnt的相对表达率分别为P19组的0.16±0.01(t=17.29,P＜0.000 1)、0.51±0.02(t=3.564,P=0.023 5)、0.23±0.01(t=13.17,P=0.000 2)、0.20±0.02(t=17.76,P＜0.000 1)和0.59±0.06 (t=3.642,P=0.021 9),然而对于Nkx2.5和Hand2的mRNA水平,MiRaldh2组在第2～7天显著升高,第7天的表达率分别为P19组的2.25±0.35(t=3.526,P=0.024 3)和3.58±0.20(t=9.214,P=0.011 6).结论 敲低Raldh2基因可抑制P19细胞向心肌样细胞的分化,Raldh2可能对心脏早期发育具有重要作用,其低表达可能是维甲酸缺乏引起心脏畸形的原因之一.

摘要： Objective: To investigate the function of pATMtide in the heart development of zebra fish and differentiation of P19 cells. Methods: An obvious up-regulated polypeptide pATMtide was found from our previous study. In vitro experiment, the effect of pATMtide on P19 cells differentiation were detected; and in vivo experiment, after microinjecting the zygotes zebra fish with pATMtide, the cardiac development of zebra fish was observed. Results: The differentiation and related cardiac biomarkers of P19 cells are reduced as well as the heart development of zebrafish after adding pATMtide. Conclusion: The differentiation and development are influenced after adding pATMtide. It indicates that pATMtide may play an important role in congenital heart disease.%目的:研究多肽pATMtide在P19细胞(小鼠畸胎瘤细胞)的分化及斑马鱼心脏发育中的作用,探讨其与先天性心脏病(congenital heart disease,CHD)之间的关系.方法:从已报道的CHD羊水多肽图谱中筛选出1条表达明显上调的多肽pATMtide.在体外实验中,通过加入外源性多肽pATMtide,检测其对P19细胞分化的影响;在体内实验中,将多肽pATMtide通过显微注射技术注入到斑马鱼受精卵,观察其对斑马鱼心脏发育的影响.结果:与对照组相比,加入外源性多肽pATMtide明显抑制了P19细胞的分化,心脏发育各相关标志物表达水平明显下调.斑马鱼实验表明:多肽pATMtide可造成斑马鱼心脏发育畸形.结论:多肽pATMtide可影响P19细胞分化并导致斑马鱼心脏发育畸形,表明多肽pATMtide与CHD的形成有一定的关系.

摘要： 目的:探讨microRNA-29c(miR-29c)过表达对P19细胞增殖、凋亡和分化的影响及机制.方法:体外传代培养P19细胞,利用细胞转染技术构建miR-29c过表达细胞(mimic组).CCK-8试剂盒检测细胞增殖,流式细胞技术检测细胞周期;Hoechst染色结合流式细胞技术检测细胞凋亡情况,定量PCR和蛋白质免疫印迹(Western blot)检测凋亡相关因子Bax/Bcl-2表达情况;二甲亚砜(DMSO)诱导P19细胞分化,定量PCR检测心肌特异性标志基因肌球蛋白重链(α-myosin heavy chain, αMHC),转录因子GATA4和心肌增强因子2c(myocyte enhancer factor 2c,Mef2c)表达情况,明确miR-29c过表达对P19细胞分化的影响;生物信息学分析结合荧光素酶报告实验和Western blot明确miR-29c的靶基因.结果:与对照组相比,miR-29c过表达组细胞增殖速率较慢,细胞周期S期比例降低;miR-29c过表达组细胞凋亡率增高,Bax表达水平增高,而Bcl-2表达无明显差异;P19细胞分化第6天和第8天miR-29c过表达组αMHC、GATA4和Mef2c的表达水平显著高于对照组;Akt3被证实为miR-29c的靶基因.结论:miR-29c过表达可能是通过调控Akt3来抑制P19细胞增殖、促进P19细胞的凋亡和分化.%Objective:To explore the effect of miR-29c overexpression on P19 cell proliferation, apoptosis and differentiation. Methods:P19 cells were cultured and transfected with miR-29c mimics. Proliferation was examined with CCK-8 kit and cell cycle was examined with flow cytometey. Apoptosis rate was checked with Hoechst staining and flow cytometry. The mRNA and protein expression of Bax/Bcl-2 was tested with qPCR and Western blot. P19 cells were induced to differentiate with DMSO and the mRNA expression level of αMHC, GATA4, Mef2c was checked with methods of qPCR. We used bioinformatic analysis, lucierase assays and Western blot to find target gene of miR-29c. Results:Compared with the control group, cells in the miR-29c overexpression group showed a lower proliferation rate and lower S cycle percentage. Apoptosis rate of the miR-29c overexpression group was higher than that of the control group. Expression of Bax of the miR-29c overexpression group was significantly higher than that of the control group, while there was no difference seen in Bcl-2 expression. About The mRNA expression level of αMHC, GATA4, Mef2c, the miR-29c overexpression group was significantly higher than those of the control group at day 6 and day 8. Akt3 was proved to be a target gene of miR-29c. Conclusion:Overexpression of miR-29c can inhibits proliferation and promotes apoptosis and differentiation in P19 embryonal carcinoma cells with Akt3.

摘要： 背景:内皮素1作为一种来源于心内膜和动脉血管内皮的旁分泌信号,能够诱导心脏传导细胞的分化成熟.目的:探讨内皮素1在体外诱导P19细胞向心脏传导细胞分化的作用.方法:P19 细胞分别与1%二甲基亚砜和100 nmol/L浓度内皮素1孵育,通过Western blot、免疫荧光和qRT-PCR鉴定早期心肌细胞特征性转录因子GATA4、MEF2C和心肌细胞分化标志物MHC-α、cTnT,以及重要的传导细胞转录因子Nkx2.5、Tbx5和分化标志物Cx40、ANP的变化.qRT-PCR鉴定内皮素1特异性受体阻断剂和阻断PI3K-AKT-mTOR信号通路对内皮素1诱导P19细胞分化的影响.结果与结论:①内皮素1能够上调P19细胞早期心肌转录因子、心肌结构基因和传导系统特征表型表达;②与二甲基亚砜相比,内皮素1能够确实诱导P19细胞向心脏传导细胞分化;③内皮素1主要通过ETA通路上调 Nkx2.5 和 Cx40表达水平从而诱导 P19细胞向传导细胞分化,ETB通路可能还参与了一条负反馈调节通路;④内皮素1能够通过PI3K-AKT-mTOR信号通路调控Nkx2.5表达进而影响传导细胞分化.%BACKGROUND: Endothelin-1, as a paracrine cytokine derived from endocardium and vascular endothelial cells, can promote the differentiation and maturation of cardiac conduction cells. OBJECTIVE:To explore the effect of endothelin-1 on P19 cells differentiating into cardiac conduction cells in vitro. METHODS: P19 cells were cultured with 1% dimethyl sulfoxide or 100 nmol/L endothelin-1. Afterwards, the changes of early cardiomyocyte transcription factors MEF2C and GATA4, differentiation markers MHC-α and cTnT, important conduction cell transcription factors Nkx2.5 and Tbx5, and differentiation markers Cx40 and ANP were identified by western blot assay, immunofluorescence and real-time PCR. Specific antagonists of endothelin-1 receptors, and blocking PI3K-AKT-mTOR signaling pathway on the differentiation of P19 cells induced by endothelin-1 were evaluated by real-time PCR. RESULTS AND CONCLUSION: Endothelin-1 significantly up-regulated the levels of early cardiac transcription factors, cardiomyocyte structure factors and characteristic conduction system markers. Compared with dimethyl sulfoxide, endothelin-1 was prone to enhance the differentiation of cardiac conduction cells derived from P19 cells. Up-regulation of Nkx2.5 and Cx40 by endothelin-1 was mainly attributed to the ETAsignaling pathway. ETBsignaling pathway may be also involved in a negative feedback regulation pathway. The PI3K-AKT-mTOR signaling pathway can play an important role in the differentiation from P19 cells to cardiac conduction cells triggered by endothelin-1.

摘要： 背景:内皮素1作为一种来源于心内膜和动脉血管内皮的旁分泌信号,能够诱导心脏传导细胞的分化成熟。目的:探讨内皮素1在体外诱导P19细胞向心脏传导细胞分化的作用。方法:P19细胞分别与1%二甲基亚砜和100 nmol/L浓度内皮素1孵育,通过Western blot、免疫荧光和qRT-PCR鉴定早期心肌细胞特征性转录因子GATA4、MEF2C和心肌细胞分化标志物MHC-α、cTnT,以及重要的传导细胞转录因子Nkx2.5、Tbx5和分化标志物Cx40、ANP的变化。qRT-PCR鉴定内皮素1特异性受体阻断剂和阻断PI3K-AKT-mTOR信号通路对内皮素1诱导P19细胞分化的影响。结果与结论:①内皮素1能够上调P19细胞早期心肌转录因子、心肌结构基因和传导系统特征表型表达;②与二甲基亚砜相比,内皮素1能够确实诱导P19细胞向心脏传导细胞分化;③内皮素1主要通过ETA通路上调Nkx2.5和Cx40表达水平从而诱导P19细胞向传导细胞分化,ETB通路可能还参与了一条负反馈调节通路;④内皮素1能够通过PI3K-AKT-mTOR信号通路调控Nkx2.5表达进而影响传导细胞分化。

摘要： 目的：研究多肽pATMtide在P19细胞（小鼠畸胎瘤细胞）的分化及斑马鱼心脏发育中的作用,探讨其与先天性心脏病（congenital heart disease,CHD）之间的关系。方法：从已报道的CHD羊水多肽图谱中筛选出1条表达明显上调的多肽pATMtide。在体外实验中,通过加入外源性多肽pATMtide,检测其对P19细胞分化的影响;在体内实验中,将多肽pATMtide通过显微注射技术注入到斑马鱼受精卵,观察其对斑马鱼心脏发育的影响。结果：与对照组相比,加入外源性多肽pATMtide明显抑制了P19细胞的分化,心脏发育各相关标志物表达水平明显下调。斑马鱼实验表明：多肽pATMtide可造成斑马鱼心脏发育畸形。结论：多肽pATMtide可影响P19细胞分化并导致斑马鱼心脏发育畸形,表明多肽pATMtide与CHD的形成有一定的关系。

摘要： 目的：探讨维甲酸（ RA）诱导P19向神经分化的潜在分子机制。方法适当浓度RA诱导 P19细胞4 d，观察是否有神经细胞标志物β-Tubulin产生，同时观察对SIRT1和Notch1的影响。 RT-PCR和Western印迹实验检测敲低SIRT1对β-Tubulin和Notch1的影响。 Western印迹实验检测高表达Notch1是否对β-Tubulin表达水平产生影响。结果 RA诱导P19细胞4 d内β-Tubulin表达水平逐渐升高，SIRT1和Notch1表达水平明显降低，表明RA在4 d内能够明显地刺激P19细胞向神经细胞方向分化，并能够抑制SIRT1和Notch1信号通路。敲低SIRT1后，与对照组比较诱导分化4 d后神经分化标志物β-Tubulin水平升高，Notch1水平下降。高表达Notch1组在诱导神经分化4 d后β-Tubulin 水平相对较低。结论 RA可能通过降低SIRT1而抑制Notch1信号通路，促使P19细胞向神经分化。

摘要： 背景：既往研究发现，miR-25在向心肌分化的P19细胞中的表达水平显著低于其在未分化的P19细胞中的表达水平，但是其对心脏发育的影响及其机制尚不明确。　　目的：探索miR-25对P19细胞向心肌细胞分化的影响及其机制。　　方法：体外培养P19细胞并向心肌细胞诱导分化。通过实时反转录PCR检测miR-25在向心肌分化的和未分化的P19细胞中的表达水平。通过脂质体转染构建miR-25过表达的P19细胞，观察miR-25对P19细胞向心肌细胞分化的影响。通过miRNA靶基因预测数据库预测miR-25的靶基因，并利用荧光素酶报告基因实验检测miR-25对Pax3的靶向作用，沉默Pax3，观察Pax3对P19细胞向心肌细胞分化的影响。　　结果与结论：miR-25在分化的P19细胞中表达水平较低。miR-25过表达能够促进P19细胞向心肌细胞分化。靶基因预测分析Pax3为miR-25潜在的靶基因，荧光素酶实验进一步证实Pax3是miR-25的直接靶点，Pax3沉默促进P19细胞向心肌细胞分化。提示miR-25通过靶向Pax3促进P19细胞向心肌细胞分化，为心脏发育以及先天性心脏病的防治提供新的线索和理论依据。%BACKGROUND:Previous studies have found that the expression level of miR-25 in differentiated P19 cels is significantly lower than that in undifferentiated P19 cels. However, the effect of miR-25 on cardiomyogenesis and the relevant mechanism remain unclear. OBJECTIVE: To explore the effect and mechanism of miR-25 on the differentiation of P19 cels into cardiomyocytes. METHODS:P19 cels were cultured and differentiated into cardiomyocytesin vitro. The expression of miR-25 in differentiated and undifferentiated P19 cels was detected by real-time PCR. miR-25-overexpressing P19 cels were constructed by lipofection transfection, and were used to investigate the effect of miR-25 on the differentiation of P19 cels into cardiomyocytes. MicroRNA target analysis tools were used to explore potential targets of miR-25, and dual luciferase reporter assay was used to identify whether the 3’UTR of Pax3 mRNA was a binding target of miR-25. In addition, we transfected P19 cels with Pax3 shRNAs to silence the expression of Pax3, and investigated the effect of Pax3 on the differentiation of P19 cels into cardiomyocytes. RESULTS AND CONCLUSION: Expression level of miR-25 in differentiated P19 cels was obviously down-regulated compared with that in undifferentiated P19 cels. miR-25 overexpression promoted the differentiation of P19 cels into cardiomyocytes. By target prediction analysis, we confirmed that Pax3 was a potential target gene of miR-25. Luciferase assay further confirmed that miR-25 targeted Pax3 directly. Moreover, knockdown of Pax3 promoted the differentiation of P19 cels into cardiomyocytes. Taken together, miR-25 promotes the differentiation of P19 cels into cardiomyocytes by targeting Pax3. These findings offer new clues and theoretical basis for cardiomyogenesis and prevention and cure of congenital heart disease.

摘要： BACKGROUND:Previous studies have found that the expression level of miR-2135 in differentiated P19 cel s is significantly higher than that in undifferentiated P19 cel s. However, the effects of miR-2135 on P19 cel proliferation and differentiation into cardiomyocytes as wel as cardiomyogenesis remain unclear. OBJECTIVE:To explore the effect of miR-2135 on P19 cel proliferation and differentiation into cardiomyocytes. METHODS:P19 cel s were transferred with miR-2135 knockdown plasmid or vector plasmid. After 4 days of culture, cel proliferation was detected by MTT assay. Flow cytometry was used to detect cel cycle at 0, 24, 48 hours of culture. P19 cel s in the two groups were induced to differentiate into cardiomyocytes. The expression of miR-2135 in differentiated and undifferentiated P19 cel s was detected by quantitative real-time PCR at 0 and 10 days of induction. Levels of cardiac troponin T, atrial natriuretic peptide and myocardial transcription factor were detected using western blot assay at 10 days of induction. RESULTS AND CONCLUSION:Expression level of miR-2135 in miR-2135-downexpressed P19 cel s was obviously reduced. Compared with control cel s, miR-2135 knockdown significantly upregulated P19 cel proliferation (P<0.05) as wel as induced a cel cycle rest in S stage after 24 and 48 hours of culture (P<0.05). PCR findings showed that in the miR-2135 knockdown group, the expression level of miR-2135 at 10 days of induction was significantly higher than that at 0 day of induction (P<0.01). Western blot assay showed that miR-2135-downexpressed P19 cel s had obvious decreases in the protein levels of cardiac troponin T, atrial natriuretic peptide and myocardial transcription factor at 10 days of induction. Our findings confirm that miR-2135 inhibits P19 cel proliferation, but promotes the differentiation of P19 cel s into cardiomyocytes.%背景：既往研究发现，向心肌分化P19细胞中的miR-2135表达水平显著高于未分化P19细胞，但miR-2135对P19细胞增殖、向心肌细胞分化和心脏发育的影响尚不明确。　　目的：探索miR-2135对P19细胞增殖及向心肌细胞分化的影响。　　方法：分别以miR-2135沉默及空载质粒转染P19细胞，培养0-4 d，MTT法检测细胞增殖；培养0，24，48 h，流式细胞仪检测细胞周期。诱导两组转染的P19细胞向心肌细胞分化，诱导第0，10天，采用qRT-PCR检测P19细胞中miR-2135的表达；诱导第10天，采用蛋白免疫印迹检测心肌分化相关标志物心肌肌钙蛋白T、心房钠尿肽和心肌转录因子的表达。　　结果与结论：①转染结果：转染miR-2135沉默质粒的P19细胞低表达miR-2135；②细胞增殖与周期：miR-2135沉默质粒转染P19细胞的增殖速度快于空载质粒转染P19细胞(P<0.05)，培养24，48 h的S期细胞比例明显高于空载质粒转染P19细胞(P<0.05)；③qRT-PCR检测结果：miR-2135沉默质粒转染P19细胞诱导10 d的miR-2135表达明显高于诱导0 d水平(P<0.01)；④蛋白免疫印迹检测结果：诱导10 d，miR-2135沉默质粒转染P19细胞心肌肌钙蛋白T、心房钠尿肽和心肌转录因子的表达明显低于空载质粒转染P19细胞；⑤结果表明：miR-2135抑制P19细胞的增殖，可促进其向心肌细胞分化。

摘要： BACKGROUND:Polychlorinated biphenyls inhibit the differentiation of P19 cels into cardiomyocytes. In the meanwhile, microRNAs play an important role in regulating cel differentiation. OBJECTIVE:To explore the effect of microRNA-32(miR-32) on the polychlorinated biphenyls-inhibited differentiation of P19 cels into cardiomyocytes. METHODS:P19 cels were co-cultured with 2.5 μmol/L polychlorinated biphenyls and 1% dimethyl sulfoxide. Afterwards, α-actinin, desmin, cTnI and GATA4 were identified by western blot assay.Wddwxrof polychlorinated biphenyls on the expression of miR-32 was evaluated by real-time PCR. Mouse eukaryotic vector expressing miR-32 was constructed by gene recombination technology,andtransfected into P19 celsfolowed byco-culturedwith2.5 μmol/Lpolychlorinated biphenylsand1% dimethyl sulfoxide. Then, expressions of differentiation-related proteins were detected by western blot assay. RESULTS AND CONCLUSION:Polychlorinated biphenylsinhibited the differentiation of P19 cels into cardio myocytes anddecreased the miR-32 expression. Cel lines overexpressing miR-32 was successfuly established in mice.Furthermore, we found thatoverexpression of miR-32 weakens the inhibition of polychlorinated biphenyls to the differentiation of P19 cels into cardiomyocytes.%背景：多氯联苯对P19细胞分化成心肌细胞有抑制作用。miRNAs在多氯联苯抑制P19细胞分化成心肌细胞过程中发挥了重要的作用。　　目的：探索miR-32在调节多氯联苯对P19细胞分化成心肌细胞中的作用。　　方法：将P19细胞与1%二甲基亚砜和2.5μmol/L多氯联苯共孵育，通过Western blot鉴定分化标志物α-actinin、desmin、cTnI以及早期心脏发育的重要转录因子GATA4的变化。qRT-PCR鉴定多氯联苯对miR-32表达的影响。应用基因重组技术成功构建了小鼠miR-32真核表达载体，将其转染至P19细胞，与2.5μmol/L多氯联苯和1%二甲基亚砜共孵育，通过Western blot实验观察分化相关蛋白表达。　　结果与结论：①多氯联苯降低了 miR-32的表达水平，抑制 P19细胞向心肌细胞的分化；②成功构建了小鼠miR-32真核表达载体，建立了稳定过表达miR-32的P19细胞系；③过表达miR-32发挥了削弱多氯联苯对P19细胞向心肌细胞分化的抑制作用。

摘要： 本发明的目的在于，提供能够使T细胞或NK细胞高效地增殖并且维持该细胞的状态(例如未分化性)的T细胞或NK细胞的制造方法、T细胞或NK细胞的培养用培养基、T细胞或NK细胞的培养方法、维持未分化T细胞的未分化状态的方法和T细胞或NK细胞的增殖促进剂。本发明涉及T细胞或NK细胞的制造方法等，其包括如下步骤：在含有式(X‑1)或式(X‑2)所示的双苄基异喹啉生物碱或者其中的1个醚键断裂后的化合物或其药学上可接受的盐的培养基中培养T细胞或NK细胞。

摘要： 提供能保存细胞的组合物。本发明的组合物包含微小气泡。

摘要： 本发明涉及一种红细胞除去装置(100)，具备：血液容器(10)，其容纳血液；以及红细胞除去器(11)，其从血液容器(10)接受血液，并从血液至少部分地除去红细胞。

摘要： 提供一种细胞的培养方法，在细胞培养器内向细胞导入因子，并在与上述细胞培养器相同的细胞培养器内培养导入了上述因子的细胞。另外，提供一种单核细胞的回收方法，其包括：对血液进行处理，制作至少部分地除去了红细胞而得到的处理血液；对处理血液进行稀释；使稀释后的处理血液中所含的单核细胞沉降；除去稀释后的处理血液的上清液；以及回收单核细胞。

摘要： 本申请提供了一种制备NKT细胞刺激性树突细胞的方法，该方法包括：将单个核细胞置于培养容器内并通过保持该培养容器静置而使得所述单个核细胞中的一些沉降于所述容器的底表面上的步骤；将除已沉降于所述培养容器的底表面上的细胞以外的悬浮细胞去除的步骤；通过向所述培养容器内添加预定的因子而使已沉降于所述底表面上的细胞中的单核细胞分化为未成熟树突细胞的步骤；通过向所述培养容器内添加预定的因子而使所述未成熟树突细胞成熟；和通过向所述培养容器内添加α‑半乳糖神经酰胺而将成熟树突细胞诱导为NKT细胞刺激性树突细胞的步骤。

摘要： 含有细胞细胞外基质的制造方法包括：在具有前端开口部的移液管的内部准备含有(i)细胞外基质前体以及(ii)细胞或者细胞团的细胞外基质溶液；排出上述细胞外基质溶液，在上述移液管的前端开口部形成上述细胞外基质溶液的液滴；使上述移液管的前端开口部接近细胞培养容器的培养面，按照使上述移液管的前端开口部不与上述培养面接触的方式将上述液滴载置于上述培养面上；使上述移液管的前端开口部从上述培养面远离，将上述液滴与上述移液管的前端开口部分离；以及使上述细胞外基质溶液凝胶化，形成含有细胞细胞外基质。

摘要： 本发明提供具备适宜的亲水性和强度，细胞接种后的固定性较高，可高效进行细胞增殖的细胞培养用支架材料。本发明的细胞培养用支架材料为含有合成树脂的细胞培养用支架材料，其中，所述合成树脂的氮含量为0.1质量％以上10质量％以下。

摘要： 本发明公开一种以前所未有的效率及功能性从人类iPSC诱导神经祖细胞、寡树突细胞祖细胞、寡树突细胞的新颖方法。本发明的核心是循着多能细胞到外胚层、神经外胚层到NPC到OPC到寡树突细胞路径的多个关键分化决定点处以早先未知的方式使用经实验发现的转录因子。

摘要： 本发明涉及通过引入逆分化因子Bmi1及dNP63a来诱导尿液细胞逆分化为角质形成细胞干细胞的方法以及包含所诱导的逆分化角质形成细胞干细胞条件培养基作为有效成分的用于促进皮肤再生的组合物。

摘要： 本发明涉及包含作为从鸟类的蛋(egg)分离的细胞的胚盘多能干细胞(pluripotent stem cells，PSCs)或神经干细胞(neural stem cell s，NSCs)、胚胎成纤维细胞(embryonic fibroblasts，FBs)条件培养基(conditioned medium)作为有效成分的用于细胞增殖、皮肤再生及皱纹改善的培养基组合物，具体地，蛋(egg)细胞条件培养基可从根本上防止使用动物血清所导致的污染，而且，不存在由于使用支撑细胞而由不同物质之间的感染物质所导致的传染可能性，从而产生包括人干细胞、皮肤细胞在内的多种细胞增殖效果，并且，产生显著的皮肤再生或皱纹改善效果，因此，可将蛋细胞条件培养基有效用作用于细胞增殖的培养基组合物以及用于皮肤再生或皱纹改善的化妆品组合物。