05),M组凋亡率显著低于S+M组(P
Objective Inactivated Sendai virus particle[hemagglutinating virus of Japan envelope(HVJ-E)]has a potential oncolytic effect due to its ability to induce apoptosis in tumor cells.However,the molecular mechanism of apoptosis induction in cancer cells mediated by HVJ-E has not been fully elucidated.This Baricitinib 价格 paper aims to investigate the underlying mechanism of apoptosis induction by HVJ-E in prostate cancer cells(PC3).Methods PC3 cells were treated with HVJ-E at various MOI,and then interferon-6(IFN-S) production,and the cell viability and

apoptosis were detected by ELISA,MTT-based assay and flow cytometry,respectively.Next,the roles of Jak-Stat,MAPK and Akt pathways played in HVJ-E-induced apoptosis in PC3 cells were analyzed by immunoblot assay.To further evaluate the cytotoxic effect of HVJ-E on PC3 cells,HVJ-E was intratumorally injected into prostate cancers on BALB/c-nude mice,and the tumor volume was monitored for 36 days.Results HVJ-E induced IFN-β production and activated Jak-Stat signaling pathway,which resulted

in the activation of caspase-8,caspase-3,and Selleck BAY806946 PARP in PC3 prostate cancer cells post HVJ-E treatment.Furthermore,we observed for the first time that p38 and Jnk MAPKs in PC3 cells contributed to HVJ-E-induced apoptosis.In addition,intratumoral HVJ-E treatment displayed a direct inhibitory effect in an in vivo BALB/c nude mouse prostate cancer model.Conclusion Our findings have provided novel insights into the underlying mechanisms by which HVJ-E induces apoptosis in tumor

cells.
饮酒对中枢神经系统有重大影响,小胶质细胞是脑内原位免疫效应细胞,它在乙醇引起的神经毒性中有重要作用,可导致神经元死亡与退行性变;小胶质细胞有利于维持稳态而不是导致神经退行性变,小胶质细胞活化是乙醇引起损害的结果而不是损害的原因。本文对乙醇引起的神经元死亡和退行性变中小胶质细胞的反应及相应机制作一综述。
目的:探讨NDRG2在热疗诱导的热应激抗肝癌细胞侵袭中所发挥的作用和机制研究。方法:构建NDRG2过表达和干涉表达的HepG-2细胞稳转细胞株,通过Transwell和Western-blot方法检测了和细胞侵袭力和细胞内NDRG2、MMP-2和MMP-9的表达量变化;构建荷瘤鼠模型,通过HE染色及免疫组化方法检测并对比了热对肿瘤细胞向周围肌肉组织的侵袭抑制作用。结果:给予NDRG2过表达的HepG-2细胞45℃、30min热处理后,细胞内NDRG2的表达明显增高,同时伴随细胞侵袭力、MMP-2和MMP-9的表达明显降低(P
目的:研究血小板源性生长因子(PDGF-BB)对血管平滑肌细胞(VSMC)G0S2基因mRNA表达的调控,并初步探讨其机制。方法:体外培养大鼠胸主动脉平滑肌细胞,逆转录实时定量聚合酶联反应(RT-QPCR)法测定PDGF-BBJVSMC中G0S2 这个 mRNA表达影响的时效关系和量效关系;运用不同细胞信号通路阻断剂处理,研究PDGF-BB影响G0S2 mRNA表达的信号途径;转染含有G0S2基因启动子的荧光素酶报告基因质粒pGL3-G0S2-Promotor,检测PDGF-BB对G0S2基因启动子活性的影响。结果:PDGF-BB能够增加平滑肌细胞G0S2 mRNA表达,PDGF-BB诱导VSMC表达G0S2mRNA在12h后达峰值[20ng/ml增加(2.83±0.81)倍;10ng/ml增加(2.99±0.