ETM study of electroporation influence on cell morphology in human malignant melanoma and human primary gingival fibroblast cells

Objective:To estimate electroporation(EP) influence on malignant and normal cells.Methods: Two cell lines including human malignant melanoma(Me-43) and normal human gingival fibroblast(HCFs) were used.EP parameters were the following:230,1000,1 730,2 300 V/cm;30 μ s by 3 impulses for every case.The viability of cells after EP was estimated by MTT assay. The ullrastructural analysis was observed by transmission electron microscope(Zeiss EM 900). Results:In the current study we observed the intracellular effect following EP on Me-43 and HGF cells.At the conditions applied,we did not observe any significant damage of mitochondrial activity in both cell lines treated by EP.Conversely,we showed that EP in some conditions can stimulate cells to proliferation.Some changes induced by EP were only visible in electron microscopy.In fibroblast cells we observed significant changes in lower parameters of EP(230 and 1 000 V/cm).After applying higher electric field intensities(2 300 V/cm) we detected many vacuoles,myelin-like bodies and swallowed endoplasmic reticulum.In melanoma cells such strong pathological modifications after EP were not observed,in comparison with control cells. The ultrastructure of both treated cell lines was changed according to the applied parameters of EP.Conclusions:We can claim that EP conditions are cell line dependent.In terms of the intracellular morphology,human fibroblasts are more sensitive to electric field as compared with melanoma cells.Optimal conditions should be determined for each cell line.Summarizing our study,we can conclude that EP is not an invasive method for human normal and malignant cells. This technique can be safely applied in chemotherapy for delivering drugs into tumor cells.

MicroRNA changes of bone marrow-derived mesenchymal stem cells differentiated into neuronal-like cells by Schwann cell-conditioned medium

Bone marrow-derived mesenchymal stem cells differentiate into neurons under the induction of Schwann cells. However, key microRNAs and related pathways for differentiation remain unclear. This study screened and identified differentially expressed microRNAs in bone marrow- derived mesenchymal stem cells induced by Schwann cell-conditioned medium, and explored targets and related pathways involved in their differentiation into neuronal-like cells. Primary bone marrow-derived mesenchymal stem cells were isolated from femoral and tibial bones, while primary Schwann cells were isolated from bilateral saphenous nerves. Bone marrow-derived mesenchymal stem cells were cultured in unconditioned (control group) and Schwann cell-conditioned medium (bone marrow-derived mesenchymal stem cell + Schwann cell group). Neuronal differentiation of bone marrow-derived mesenchymal stem cells induced by Schwann cell-conditioned medium was observed by time-lapse imaging. Upon induction, the morphology of bone marrow-derived mesencaymal stem cells changed into a neural shape with neurites. Results of quantitative reverse transcription-polymerase chain reaction revealed that nestin mRNA expression was upregulated from 1 to 3 days and downregulated from 3 to 7 days in the bone marrow-derived mesenchymal stem cell + Schwann cell group. Compared with the control group, microtubule-associated protein 2 mRNA expression gradually increased from 1 to 7 days in the bone marrow-derived mesenchymal stem cell + Schwann cell group. After 7 days of induction, microRNA analysis iden:ified 83 significantly differentially expressed microRNAs between the two groups. Gene Ontology analysis indicated enrichment of microRNA target genes for neuronal projection development, regulation of axonogenesis, and positive regulation of cell proliferation. Kyoto Encyclopedia of Genes and Genomes pathway analysis demonstrated that Hippo, Wnt, transforming growth factor-beta, and Hedgehog signaling pathv/ays were potentially associated with neural differentiation of bone marrow-derived mesenchymal stem cells. This study, which carried out successful microRNA analysis of neuronal-like cells differentiated from bone marrow-derived mesenchymal stem cells by Schwann cell induction, revealed key microRNAs and pathways involved in neural differentiation of bone marrow-derived mesenchymal stem cells. All protocols were approved by the Animal Ethics Committee of Institute of Radiation Medicine, Chinese Academy of Medical Sciences on March 12, 2017 (approval number: DWLI-20170311).

NIH 3T3 cells malignantly transformed by mot-2 showinactivation and cytoplasmic sequestration of the p53protein

INTRODUCTIONInvolvementandinactivationofp53,atumorsuppressorandcellulartranscriptionfactorincellularimmortalizationhasbeenwelldocumented[1-4].Variousactivitiesofp53proteininvolveitsfunctionaldomains,viz.,anamino--terminustransactivationdomain(aminoac...

Evaluation of the Aurora Kinase Inhibitor, ZM447439, in Canine Malignant Lymphoid Cells <i>in Vitro</i>

Aurora kinases play an important role in the cell cycle. These enzymes help establish mitotic spindles by directing centrosome duplication and separation and by regulating the spindle assembly checkpoint thereby helping control cytokinesis. An over-expression of aurora kinases has been reported in a variety of human tumors. In this study, we identified the expression of aurora-A and aurora-B kinases in canine malignant lymphoid cells. We also evaluated the effects of the aurora kinase inhibitor (ZM447439), and found that this inhibitor decreases cell viability, increases DNA content change, and leads to apoptosis in canine B- and T-cell lymphoid cell lines. The lymphotoxicity induced by ZM447439 in these canine lymphoid cell lines suggests that further in vivo evaluation of aurora kinase inhibitors as a potential treatment for canine malignant lymphoid tumors is warranted.

Training stem cells for treatment of malignant brain tumors

The treatment of malignant brain tumors remains a challenge. Stem cell technology has been applied in the treatment of brain tumors largely because of the ability of some stem cells to infiltrate into regions within the brain where tumor cells migrate as shown in preclinical studies. However, not all of these efforts can translate in the effective treatment that improves the quality of life for pa-tients. Here, we perform a literature review to identify the problems in the field. Given the lack of efficacy of most stem cell-based agents used in the treatment of malignant brain tumors, we found that stem cell distribution(i.e., only a fraction of stem cells applied capable of targeting tumors) are among the limiting factors. We provide guidelines for potential improvements in stem cell distribution. Specifically, we use an engineered tissue graft platform that replicates the in vivo microenvironment, and provide our data to validate that this culture platform is viable for producing stem cells that have better stem cell distribution than with the Petri dish culture system.

Expression of Telomerase Reverse Transcriptase during the Malignant Transformation of Cadmium-Induced Cells

The objective of the present study was to investigate human telomerase reverse transcriptase (hTERT) mRNA and protein expressions during the cadmium chloride-induced malignant transformation of human bronchial epithelial (16HBE) cells. Fluorescence quantitative PCR (FQ-PCR) and Western blot analyses were performed to detect the hTERT mRNA and protein expressions in normal 16HBE cells, cadmium chloride-transformed 16HBE cells, and tumorigenic cells from nude mice inoculated with cadmium chloride-transformed 16HBE cells. Under the inner standard of GAPDH, the hTERT mRNA expression was significantly higher at different stages of malignant transformation (cadmium chloride-transformed 16HBE cells at passages 15 and 35 and tumorigenic cells from nude mice) than in normal 16HBE cells, and increased with the development of malignancy (P < 0.01). In addition, hTERT protein expression increased with the development of malignancy. These findings demonstrate that hTERT expression is related to cadmium chlorideinduced malignant transformation. Cadmium chloride-induced malignant transformation is involved in changes in the hTERT activity, and might be an early event in cadmium chloride-induced malignant transformation.

p53-independent upregulation of p21^(WAF1) in NIH 3T3 cells malignantly transformed by mot-2

Mot-2 protein is shown to interact with p53 and inhibit its transcriptional activation function. Mot-2 overexpressing stable clones of NIH 3T3 cells were malignantly transformed, however, they had a high level of expression of a p53 downstream gene, p21WAF1. The present study was undertaken to elucidate possible molecular mechanism(s) of such upregulation. An inCreased level of p21WAF1, expression was detected in sta- ble transfectants although an exogenous reporter gene driven by p21WAF1, promoter exhibited lower activity in these cells suggesting that some post-transcriptional mechanism contributes to upregulation. Western analyses of transient and stable clones revealed that upregulation of p21WAF1, in stable NIH 3T3/mot-2 cells may be mediated by cyclin D1 and cdk-2.

Effects of retinoic acid on proliferation,phenotype and expression of cyclin-dependent kinase inhibitors in TGF-β1-stimulated rat hepatic stellate cells

AIM To study the molecular mechanisms ofretinoic acid(RA)on proliferation andexpression of cyclin-dependent kinase inhibitors(CKI),i.e.p16,p21 and p27 in cultured rathepatic stellate cells(HSC)stimulated withtransforming growth factor beta 1(TGF-β1).METHODS HSC were isolated from healthy ratlivers and cultured.After stimulated with1 mg/L TGF-β1,subcultured HSC were treatedwith or without 1 nmol/L RA.MTT assay,immunocytochemistry(ICC)for p16,p21,p27and α-smooth muscle actin(α-SMA)protein,insitu hybridization(ISH)for retinoic acidreceptor beta 2(RAR-β2)and p16,p21 and p27mRNA and quantitative image analysis(partially)were performed.RESULTS RA inhibited HSC proliferation(41.50%,P【0.05),decreased the protein levelof α-SMA(55.09%,P【0.05),and induced HSCto express RAR-β2 mRNA.In addition,RAincreased the protein level of p16(218.75%,P【0.05)and induced p21 protein expression;meanwhile,p27 was undetectable by ICC in bothcontrol and RA-treated HSC.However,RA hadno influence on the mRNA levels of p16,p21 orp27 as determined by ISH.CONCLISION Up-regulation of p16 and p21 on post-transcriptional level may contribule, in part to RA inhibition of TGF-β1-initiated rat HSC activation in vitro.

丙丁酚抑制氧化型低密度脂蛋白诱导系膜细胞转化生长因子-β_1表达

目的 观察丙丁酚对ox- LDL诱导系膜细胞AP -1活性和TGF -β1 表达的作用 ,探讨抗氧化剂治疗脂质肾损伤的分子机制。方法 大鼠系膜细胞随机分为正常细胞组、ox- LDL处理组和ox- LDL +丙丁酚处理组。运用凝胶迁移率实验检测AP-1活性变化 ,Western杂交检测c- Jun、JNK/SAPK磷酸化及TGF- β1 蛋白表达水平的改变。运用Northern杂交检测TGF- β1- mRNA表达。结果 丙丁酚 5 0 μmol/L预处理系膜细胞 2 0h ,显著降低ox LDL诱导系膜细胞AP 1活性。丙丁酚浓度为 5 0、1 0 0、2 0 0 μmol/L时 ,均显著抑制ox- LDL诱导JNK ,/SAPK磷酸化 ;且ox LDL +丙丁酚处理组的c Jun蛋白表达分别为ox- LDL处理组的 6 0 %、5 1 %和 4 6 %。Northern杂交显示 :ox LDL为 1 0 μg/mL时并不激活TGF- β1 mRNA表达 (P >0 .0 5 ) ;而当ox-LDL浓度增至 5 0、1 0 0 μg/mL时 ,TGF -β1 mRNA表达分别增加 1 .8和 1 .9倍。Western杂交显示ox -LDL呈剂量依赖方式增加TGF β1 蛋白质表达。加入丙丁酚后显著降低ox LDL诱导系膜细胞的TGF -β1- mRNA和蛋白质表达 (P <0 .0 5 )。结论 丙丁酚可能通过抑制JNK1 /SAPK磷酸化和AP 活性下调ox- LDL诱导系膜细胞TGF- β1 表达。

STUDIES ON THE RELATIONSHIP BETWEEN CHROMOSOME No15 AND THE BIOLOGICAL CHARACTERISTICS OF MALIGNANT TRANSFORMED SYRIAN HAMSTER FIBROBLAST CELL LINES

During the course of malignant transformation of mammalian cells in vitro,a regular varia-tion in chromosome number and structure is usually found.In order to elucidate the rela-tionship between chromosomal changes and maligannt expression,we isolated fire clonesfrom a malignant transformed Syrian hamster fibroblast cell line and analyzed their biologicalcharacteristics,as well as chromosomal changes.A positive correlation betweetn chromosomeNo 15 monosomy and the transformed and malignant phenotype was observed.We suggestthat a suppression gene may be located on chromosome No 15,and its deletion or the lossof the chromosome may result in expression of the malignant phenotype.

Mucosa color and size may indicate malignant transformation of chicken skin mucosa-positive colorectal neoplastic polyps

BACKGROUND Lipid metabolism reprogramming is suspected to exist in pre-cancerous lesions,including colorectal adenoma.Screening colonoscopy frequently reveals chicken skin mucosa(CSM;white or yellow-white speckled mucosa)surrounding colo-rectal polyps,caused by macrophages engulfing and accumulating the lipids decomposed by colon cells or adjacent tumors.CSM-positive colorectal polyps are associated with various diseases;however,their prognosis varies greatly.Cold snare polypectomy is commonly used to resect lesions up to 10 to 15 mm in diameter without signs of submucosal invasion but is controversial for CSM-positive colorectal polyps.Improved imaging is required to diagnose and treat CSM-positive colorectal polyps.METHODS This retrospective cohort study included 177 patients with CSM-positive colorectal polyps diagnosed using endoscopy.All patient-related information was extracted from the Goldisc soft-clinic DICOM system or electronic medical record system.Based on the pathological results,patients were classified as non-neoplastic polyps(five juvenile polyps),neoplastic polyps,non-invasive high-grade neoplasia(NHGN),or submucosal invasive carcinoma(SM stage cancer).We analyzed and compared the clinical features,suspected risk factors for malignant transformation of neoplastic polyps,and early infiltration of sub-mucosal carcinoma.RESULTS The diameters of NHGN and SM polyps were much smaller than those of neoplastic polyps.Most NHGN polyps had a deeper red mucosal color.On logistic regression analyses,diameter and deeper red mucosal color were independent risk factors for malignant transformation of neoplastic polyps.Type 1 CSM was more common in high-grade intraepithelial neoplasia and SM;type 2 CSM was more common in neoplastic polyps.Logistic regression analyses revealed no significant differences in the malignant transformation of neoplastic polyps or early submucosal invasion of CSM-positive colorectal cancer.Changes in the CSM mucosa surrounding neoplastic polyps and submucosal invasion of colorectal cancer disappeared within 12 months.No tumor recurrence was found during either partial or complete endoscopic resection of the CSM.CONCLUSION CSM-positive colorectal polyps>1 cm in diameter or with deeper red mucosa may be related to NHGN.Resection of CSM surrounding colorectal adenomas did not affect tumor recurrence.

Abnormal Expression of Eukaryotic Translation Factors in Malignant Transformed Human Bronchial Epithelial Cells Induced by Crystalline Nickel Sulfide

Objective To study the oncogenic potential of mouse translation initiation factor 3 （TIF3） and elongation factor-1δ （TEF-1δ） in malignant transformed human bronchial epithelial cells induced by crystalline nickel sulfide （NiS）. Methods Abnormal expressions of human TIF3 and TEF-1δ genes in two kinds of NiS-transformed cells and NiS-tumorigenic cell lines were investigated and analyzed by the reverse transcript polymerase chain reaction （RT-PCR） and fluorescent quantitative polymerase chain reaction （FQ-PCR）, respectively. Results RT-PCR analysis primarily showed that both human TIF3 and TEF-1δ mRNA expressions in two kinds of NiS-transformed cells and NiS-tumorigenic cell lines were increased as compared with controls. FQ-PCR assay showed that the levels of TIF3 expressions in the transformed cells and tumorigenic cells were 3 and 4 times higher respectively, and the elevated expressions of TEF-16 eDNA copies were 2.7- to 3.5-fold in transformed cells and 4.1- to 5.2-fold in tumorigenic cells when compared with non-transformed cells, indicating that the over-expressions of human TIF3 and TEF-1δ genes were related to malignant degree of the cells induced by nickel. Conclusions These findings demonstrate that there are markedly abnormal expressions of TIF3 and TEF-1δ genes during malignant transformation of human bronchial epithelial cell lines induced by crystalline NiS. They seem to be the molecular mechanisms potentially responsible for human carcinogensis due to nickel.

Predicting differentiation potential of human pluripotent stem cells:Possibilities and challenges

The capability of human pluripotent stem cell(hPSC)lines to propagate indefinitely and differentiate into derivatives of three embryonic germ layers makes these cells be powerful tools for basic scientific research and promising agents for translational medicine.However,variations in differentiation tendency and efficiency as well as pluripotency maintenance necessitate the selection of hPSC lines for the intended applications to save time and cost.To screen the qualified cell lines and exclude problematic cell lines,their pluripotency must be confirmed initially by traditional methods such as teratoma formation or by highthroughput gene expression profiling assay.Additionally,their differentiation potential,particularly the lineage-specific differentiation propensities of hPSC lines,should be predicted in an early stage.As a complement to the teratoma assay,RNA sequencing data provide a quantitative estimate of the differentiation ability of hPSCs in vivo.Moreover,multiple scorecards have been developed based on selected gene sets for predicting the differentiation potential into three germ layers or the desired cell type many days before terminal differentiation.For clinical application of hPSCs,the malignant potential of the cells must also be evaluated.A combination of histologic examination of teratoma with quantitation of gene expression data derived from teratoma tissue provides safety-related predictive information by detecting immature teratomas,malignancy marker expression,and other parameters.Although various prediction methods are available,distinct limitations remain such as the discordance of results between different assays and requirement of a long time and high labor and cost,restricting their wide applications in routine studies.Therefore,simpler and more rapid detection assays with high specificity and sensitivity that can be used to monitor the status of hPSCs at any time and fewer targeted markers that are more specific for a given desired cell type are urgently needed.

mir-3168 targeted inhibition of TP53 promotes malignant transformation and cisplatin resistance of AGS and AGS/DDP gastric cancer cells

Objective:To investigate the effect of mir-3168 on the malignant transformation and cisplatin resistance of AGS and AGS/DDP gastric cancer cells,and to verify its target gene.Methods:The expression of mir-3168 in AGS and AGS/DDP gastric cancer cells was detected by qPCR,and mir-3168 mimic,inhibitor and negative control were synthesized.They were transfected into AGS and AGS/DDP gastric cancer cells,respectively.The expression of mir-3168 and TP53 mRNA was detected by qPCR.Cell viability was detected by CCK8 under gradient cisplatin treatment and non treatment,apoptosis was detected by flow cytometry,cell invasion was detected by Transwell,and TP53 protein expression was detected by western blot,The database predicted the binding sites of mir-3168 and TP53.According to the binding sites,the double luciferase experiment was used to verify the binding of mir-3168 and TP53.Results:Compared with cisplatin sensitive gastric cancer cell AGS,mir-3168 was significantly overexpressed in cisplatin resistant gastric cancer cell AGS/DDP;mir-3168 mimic promotes cisplatin resistance,proliferation and invasion of AGS and AGS/DDP gastric cancer cells,and inhibits apoptosis of AGS and AGS/DDP gastric cancer cells;mir-3168 inhibitor inhibits cisplatin resistance,proliferation and invasion of AGS and AGS/DDP gastric cancer cells,and promotes apoptosis of AGS and AGS/DDP gastric cancer cells;mir-3168 mimic inhibits the expression of TP53 mRNA and protein,and mir-3168 inhibitor promotes the expression of TP53 mRNA and protein;Targetscan database predicted that there was a binding point between mir-3168 and TP53,and the double luciferase experiment suggested that mir-3168 was bound to TP53 through the predicted binding site.Conclusion:mir-3168 may promote the malignant transformation of AGS and AGS/DDP gastric cancer cells and cisplatin resistance by targeting TP53.

VARIATION OF ADHESION CAPABILITY OF K-ras TRANSFORMED MALIGNANT CELLS AND CLINICAL IMPLICATIONS

Objective： To investigate the mechanism of carcinogenesis, invasion and metastasis. Methods： The expressions of adhesive molecule and adhesive structure in v-k-ras transformed normal rat kidney cells （KNRK） were detected with a variety of molecular biological techniques, including cell culture, immunofluorescence labeling, electron microscopy, polyacrylamide gel electrophoresis, and protein blotting, and compared with normal rat kidney （NRK） cells. Results： The significantly shortened doubling time, remarkably active proliferation ability in soft agar, and invasive growth in the abdomen of nude rat, demonstrated the malignant biological behaviors of KNRK cells. In KNRK cells, the adhesive molecules, P-cadherin, α and β catenin, actin, and adhesive structures, the adhesive junction and gap junction, were all abnormally expressed. And cell aggregation was significantly decreased. The aggregation ability disappeared at 20℃, and became active with a suitable amount of calcium solution. Conclusion： Following the transfection of virus K-ras gene, normal cells were transformed into malignant cells. In early stage of cancer, the variation of adhesive ability may be one of the vital factors underlying tumorigenesis, invasion and metastasis.

Blockade of CD300A enhances the ability of human NK cells to lyse hematologic malignancies

Objective: The human cluster of differentiation(CD)300A, a type-I transmembrane protein with immunoreceptor tyrosine-based inhibitory motifs, was investigated as a potential immune checkpoint for human natural killer(NK) cells targeting hematologic malignancies(HMs).Methods: We implemented a stimulation system involving the CD300A ligand, phosphatidylserine(PS), exposed to the outer surface of malignant cells. Additionally, we utilized CD300A overexpression, a CD300A blocking system, and a xenotransplantation model to evaluate the impact of CD300A on NK cell efficacy against HMs in in vitro and in vivo settings. Furthermore, we explored the association between CD300A and HM progression in patients.Results: Our findings indicated that PS hampers the function of NK cells. Increased CD300A expression inhibited HM lysis by NK cells. CD300A overexpression shortened the survival of HM-xenografted mice by impairing transplanted NK cells. Blocking PS–CD300A signals with antibodies significantly amplified the expression of lysis function-related proteins and effector cytokines in NK cells, thereby augmenting the ability to lyse HMs. Clinically, heightened CD300A expression correlated with shorter survival and an “exhausted” phenotype of intratumoral NK cells in patients with HMs or solid tumors.Conclusions: These results propose CD300A as a potential target for invigorating NK cell-based treatments against HMs.

以蛋黄为对象对细胞增殖过程中卟啉代谢规律的研究

在以鸡胚胎为细胞繁殖模型,对细胞增殖过程中卟啉代谢规律的研究中,为了寻求能够更好的反映原卟啉Ⅸ(PpⅨ)代谢水平的监测对象,采用4 0 5nm的激发波长,分别对鸡胚胎发育进程中的种蛋中的蛋黄、蛋清和尿囊液的荧光光谱进行测量分析。结果表明,和蛋清相比,蛋黄中PpⅨ的荧光峰相对背景更为明显,在整个鸡胚发育过程中存在的时间也较长,是一种更为理想的对鸡胚胎发育进程中卟啉代谢规律进行研究的监测对象;同时发现在胚胎发育的初级阶段,蛋黄中PpⅨ的代谢水平随着发育的进程而逐渐升高,在第10天左右达到最大值,在发育后期代谢水平又逐渐降低。鸡胚胎发育进程中PpⅨ的这一代谢规律与其在恶性肿瘤发展过程中的代谢规律极为相似,进一步支持了卟啉代谢异常与细胞无限的迅速增殖相关的观点。

术后腹腔粘连形成机制及间充质干细胞外泌体的治疗前景

背景:术后腹腔粘连的形成是一个复杂的过程,预防术后粘连是临床上亟待解决的问题。目的:旨在从细胞及分子水平分析粘连的发生机制,为间充质干细胞外泌体预防和治疗粘连提供理论依据。方法:以“腹腔粘连,盆腔粘连,术后粘连,上皮间充质转化,间充质干细胞,干细胞外泌体,间充质干细胞外泌体”为中文检索词,以“Abdominal adhesion,pelvic adhesion,postoperative adhesion,epithelial mesenchymal transformation,mesenchymal stem cell,stem cell exosomes,mesenchymal stem cell exosomes”为英文检索词,检索PubMed、中国知网和中国生物医学文献数据库,筛选各数据库建库至2023年8月发表的术后腹腔粘连及间充质干细胞外泌体干预研究的相关文章,并进行系统的整理分析,最终纳入54篇文献进行综述。结果与结论:(1)任何腹膜炎症、机械损伤、组织缺血和异物植入等病理因素均可引起腹膜表面的损伤,引起术后腹腔粘连;腹腔粘连的形成过程包括腹膜间皮细胞修复、炎性反应、纤溶系统及凝血途径等过程的相互作用,涉及多种细胞因子及信号通路,包括Wnt/β-catenin通路能诱导纤维化和血管生成,并与转化生长因子β/Smads信号通路相互协同,能刺激成纤维细胞增殖,引起腹膜纤维化;同时,核转录因子kB信号通路上调细胞炎症因子的表达,促进成纤维细胞增生,组织纤维化的过程中发挥关键作用。(2)干细胞的旁分泌功能是目前以再生医学为基础的分子干预腹腔粘连的重要方向,可以参与作用于腹腔粘连中的多种复杂细胞因子及信号通路。(3)相对于传统治疗腹腔粘连的方法,间充质干细胞外泌体具有生物活性、使用安全、无需特殊培养和扩增、更低的免疫原性及较长的稳定性等优势,能通过多种途径引导一种正常的修复和愈合。(4)间充质干细胞外泌体在以往研究中均被证明可以参与调节粘连形成的上述各过程,在临床研究中显示出潜在的应用前景,但需要进一步临床研究以探索适当的间充质干细胞外泌体治疗方案,来解决临床转化的问题。

中华芦荟多糖对辐射后非瘤细胞周期改变及周期相关蛋白表达的影响

目的研究中华芦荟多糖(AP)对X射线照射后人非瘤细胞株C.Liver和293细胞周期进程及细胞周期相关蛋白表达的影响。方法流式细胞仪检测细胞周期,Westernblot检测细胞周期相关蛋白的表达。结果辐射后293和C.Liver细胞均出现明显的G2/M期阻滞,G0/G1期细胞比例显著下降,50μg/mlAP能显著改变上述趋势。AP预处理能显著下调辐射所致C.Liver细胞P53蛋白水平,显著升高P21、CyclinB1、pRb蛋白的表达,对P27、CDK4和CyclinD1蛋白表达水平无显著影响。结论AP对X射线辐射后非瘤细胞周期紊乱的改善作用与对周期相关蛋白表达的调节有关。