期刊文献+
共找到626篇文章
< 1 2 32 >
每页显示 20 50 100
Tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in glioma U87 cells
1
作者 Fei Zhong Xiangyuan Wu +5 位作者 Chunkui Shao Qu Lin Min Dong Jingyun Wen Xiaokun Ma Li Wei 《Neural Regeneration Research》 SCIE CAS CSCD 2010年第17期1319-1323,共5页
Studies have shown that tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)exhibits strong induction of apoptosis in human glioma cells.It remains unclear whether the mitochondrion pathway,an important ap... Studies have shown that tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)exhibits strong induction of apoptosis in human glioma cells.It remains unclear whether the mitochondrion pathway,an important apoptosis signaling pathway,is involved in TRAIL-induced glioma cell apoptosis.In the present study,in vitro cultured human glioma U87 cells were treated with human recombinant soluble TRAIL.Apoptosis of glioma U87 cells,mitochondrial transmembrane potential(Δψm),cytoplasmic cytochrome c concentration and changes in caspase-3,-8 and-9 activity following human recombinant soluble TRAIL treatment were investigated to determine the mechanism of glioma U87 cell apoptosis induced by TRAIL.Additionally,blocking caspase-8resulted in TRAIL-induced mitochondrion pathway activation,suggesting that TRAIL,through activating caspase-8,initiated a series of mitochondrial events and resulted in apoptosis of glioma U87 cells. 展开更多
关键词 tumor necrosis factor-related apoptosis-inducing ligand GLIOMA apoptosis MITOCHONDRIA neural regeneration
下载PDF
Antitumor effect of tumor necrosis factor-related apoptosis inducing ligand combined with mevastatin on a human glioma cell line SWO-38
2
作者 Fei Zhong Jing Yang +1 位作者 Xiaogan Jin Guoping Sun 《Neural Regeneration Research》 SCIE CAS CSCD 2010年第5期396-400,共5页
BACKGROUND: Previous studies have reported that statins are less toxic to the human body and have greater antitumor activity; however, few studies have addressed the antitumor effect of statins combined with tumor ne... BACKGROUND: Previous studies have reported that statins are less toxic to the human body and have greater antitumor activity; however, few studies have addressed the antitumor effect of statins combined with tumor necrosis factor-related apoptosis inducing ligand (TRAIL). OBJECTIVE: To explore the effect of TRAIL combined with mevastatin on the proliferation and apoptotic cell death of a human glioma cell line SWO-38, and to study its mechanism of action. DESIGN, TIME AND SETTING: An in vitro control experiment was performed at the Central Laboratory of the Third Hospital Affiliated to Sun Yat-sen University, between January and April 2009. MATERIALS: The human SWO-38 cell line was provided by Cell Research, Department of Animal Experimental Center of Sun Yat-sen University; human recombinant soluble TRAIL by R&D, USA; and mevastatin by Sigma, USA. METHODS: SWO-38 cells were separately incubated in TRAIL (100, 200, 300, 400, and 500 tJg/L) and mevastatin (5, 10, 20, 30, and 40 pmol/L) for 72 hours. In addition, SWO-38 cells were incubated in TRAIL (300 μg/L), mevastatin (30 μmol/L), and a solution containing both TRAIL and mevastatin for 12, 24, 48 and 72 hours. MAIN OUTCOME MEASURES: Cell proliferation was detected using methyl thiazolyl tetrazolium assay; cell apoptosis was observed using Hoechst 33258 staining and fluorescence microscopy and was measured using Annexin V/propidium iodide flow cytometry; TRAIL R1/DR4 and TRAIL R2/DR5 protein expressions levels were measured using indirect immunofluorescence staining combined with flow cytometry in the recombinant soluble TRAIL (rsTRAIL, 300 tJg/L), mevastatin (30 IJmol/L) and combination groups; TRAIL R1/DR4 and TRAIL R2/DR5 mRNA expression was detected using real-time polymerase chain reaction. RESULTS: rsTRAIL, mevastatin and their combination inhibited tumor proliferation in a time- and dose-dependent manner. The proliferation inhibitory rate and apoptosis rate of human SWO-38 cells in the combined group were significantly greater than the rsTRAIL or mevastatin alone group (P 〈 0.01). TRAIL R1/DR4 and TRAIL R2/DR5 protein and mRNA expressions were increased in the combination group compared with mevastatin or rsTRAIL alone after 72 hours (P 〈 0.01). CONCLUSION: Both rsTRAIL and mevastatin inhibit the proliferation and apoptosis of the human glioma cell line SWO-38, while their combination enhances the anti-tumor effect. The mechanism of action possibly correlates to the upregulation of TRAIL R1/DR4 and TRAIL R2/DR5 mRNA expression by mevastatin, thereby enhancing the cell sensitivity to rsTRAIL. 展开更多
关键词 tumor necrosis factor-related apoptosis inducing ligand mevastatin neuroglioma cell apoptosis cell proliferation SWO-38 human glioma cells nerve factor neural regeneration
下载PDF
TNF related apoptosis-inducing ligand and its receptors in ocular tumors 被引量:1
3
作者 Qian Ning, Xin-Han Zhao 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2011年第5期552-557,共6页
Most of the ocular tumors have poor prognosis, and they remain a difficult problem in the area of ophthalmology. With the rapid development of molecular biology and immunologic techniques and the deep research on ocul... Most of the ocular tumors have poor prognosis, and they remain a difficult problem in the area of ophthalmology. With the rapid development of molecular biology and immunologic techniques and the deep research on ocular tumor related genes, it becomes possible to diagnose and treat malignant tumors from the molecular level. The tumor necrosis factor related apoptosis-inducing ligand (TRAIL), a member of the tumor necrosis factor (TNF) super family, is a promising candidate, either alone or in combination with established cancer therapies, since it can initiate apoptosis through the activation of their death receptors. The ability of TRAIL to selectively induce apoptosis of transformed, virus-infected or tumor cells but not normal cells promotes the development of TRAIL-based cancer therapy. Here, we will review TRAIL and its receptors' structure, function, mechanism of action and application in ocular tumors therapy. 展开更多
关键词 tumor necrosis factor related apoptosis-inducing ligand ocular tumors apoptosis
下载PDF
Expression of tumor necrosis factor related apoptosis inducing ligand receptor in glioblastoma
4
作者 Dongling Gao Zhongwei Zhao Hongxin Zhang Lan Zhang Kuisheng Chen Yunhan Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2008年第5期538-541,共4页
BACKGROUND: Receptors for tumor necrosis factor related apoptosis inducing ligand (TRAIL) include death receptor 4, death receptor 5, decoy receptor 1, and decoy receptor 2. Activation of death receptor 4 and 5 sel... BACKGROUND: Receptors for tumor necrosis factor related apoptosis inducing ligand (TRAIL) include death receptor 4, death receptor 5, decoy receptor 1, and decoy receptor 2. Activation of death receptor 4 and 5 selectively kills tumor cells. OBJECTIVE: To detect TRAIL receptor expression in glioblastoma by immunohistochemistry and RT-PCR, and to compare this expression to that in normal brain tissue. DESIGN: Observational analysis. SETTING: Department of Pathology, the First Affiliated Hospital of Zhengzhou University; Henan Tumor Pathology Key Laboratory. PARTICIPANTS: Twenty-five patients (17 males and 8 females) who received glioblastoma resection were selected from the Fifth Affiliated Hospital of Zhengzhou University, between September 2003 to June 2004. All glioblastoma samples were diagnosed pathologically. Twenty patients (12 males and 8 females) with craniocerebral injury who received normal brain tissue resection were selected in the same time period. There were no significant differences in sex and age between glioblastoma patients or between craniocerebral injury patients (P 〉 0.05). All patients and appropriate relatives provided informed consent, and this study was approved by the local research ethics committee. METHODS: Polyclonal antibody against TRAIL receptors and an immunohistochemical kit (batch number: 200502) were purchased from Boster Company, Wuhan. Immunohistochemistry: Expression of death receptor 4, death receptor 5, decoy receptor l, and decoy receptor 2 were observed in both glioblastoma and normal brain tissue. The experiment was performed according to the kit instructions, and positive staining was brown-yellow. Assessment: There were no positive signals (-); weakly positive signals, positive cells 〈 25% (+); weakly positive signals, positive cells 25%-50% (++); strongly positive signals, positive cells 50%-75% (+++); strongly positive signals, positive cells 〉 75% (++++). Evaluation: Expression levels of TRAIL receptors were estimated in both normal brain tissue and glioblastoma. Expression of decoy receptor 1 and decoy receptor 2 mRNA in glioblastoma were detected by reverse transcription polymerase chain reaction, and expression of decoy receptor in glioblastoma was estimated. MAIN OUTCOME MEASURES: Comparison of death receptor and decoy receptor protein expression between glioblastoma and normal brain tissue; decoy receptor mRNA expression in glioblastoma. RESULTS: Death receptor protein expression was strongly positive (+++) in glioblastoma, while it was weakly positive (+, ++) in normal brain tissue. Therefore, expression rate of death receptor protein in the glioblastoma was significantly higher than that in the normal brain tissue (.~ 2 = 18.48, 23.03, P 〈 0.01). Decoy receptor protein expression in the glioblastoma was significantly lower than that in the normal brain tissue ( x2 = 6.65, 18.76, P 〈 0.01). The level of decoy receptor mRNA expression in glioblastoma was significantly higher than those of protein expression ( x 2 = 9.82, 10.09, P〈 0.01). CONCLUSION: High expression of death receptor and low expression of decoy receptor are frequently observed in glioblastoma, suggesting that TRAIL receptor genes show an anti-tumor and expressive response during the initiation and development of the tumor. There are significant differences in decoy receptor expression between normal brain tissue and glioblastoma, suggesting that the restricted expression of decoy receptor in glioblastoma is regulated at the post-transcriptional level. 展开更多
关键词 GLIOBLASTOMA tumor necrosis factor related apoptosis inducing ligand apoptosis IMMUNOHISTOCHEMISTRY reverse transcription polymerase chain reaction
下载PDF
Brain-derived neurotrophic factor protects PC12 cells from beta-amyloid-induced neurotoxicity through the tropomyosin-related kinase B receptor pathway
5
作者 Zhikun Sun Xingrong Ma +2 位作者 Hongqi Yang Jiahua Zhao Jiewen Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第32期2485-2489,共5页
The present study utilized beta amyloid (Aβ)-induced cell apoptosis in PC12 cells as a cell model of Alzheimer's disease to investigate the interaction between brain-derived neurotrophic factor (BDNF) and the tr... The present study utilized beta amyloid (Aβ)-induced cell apoptosis in PC12 cells as a cell model of Alzheimer's disease to investigate the interaction between brain-derived neurotrophic factor (BDNF) and the tropomyosin-related kinase B receptor. Results showed that Aβ(25-35) can reduce survival of PC12 cells and increase cleaved caspase-3 expression in PC12 cells. However, BDNF inhibited Aβ(25-35)-induced cytotoxicity and cleaved casapase-3 expression. Interestingly, pretreatment with the tropomyosin-related kinase receptor inhibitor K252a for 20 minutes prior to BDNF blocked the neuroprotective effect of BDNF on PC12 cells. 展开更多
关键词 Β-AMYLOID apoptosis brain-derived neurotrophic factor Alzheimer's disease caspase-3 tropomyosin-related kinase B
下载PDF
姜酮通过激活Nrf2/HO-1信号通路减轻OGD/R后氧化应激损伤对HT22细胞凋亡的抑制作用 被引量:2
6
作者 侯玮琛 张桂美 张舒石 《吉林大学学报(医学版)》 CAS CSCD 北大核心 2024年第1期97-105,共9页
目的:探讨姜酮对氧糖剥夺/复糖复氧(OGD/R)后小鼠海马神经元HT22细胞的保护作用,阐明其相关作用机制。方法:培养HT22细胞,设置不同OGD/R时间梯度,建立OGD/R细胞损伤模型。HT22细胞分为对照组、OGD/R组、OGD/R+1μmol·L^(-1)姜酮组... 目的:探讨姜酮对氧糖剥夺/复糖复氧(OGD/R)后小鼠海马神经元HT22细胞的保护作用,阐明其相关作用机制。方法:培养HT22细胞,设置不同OGD/R时间梯度,建立OGD/R细胞损伤模型。HT22细胞分为对照组、OGD/R组、OGD/R+1μmol·L^(-1)姜酮组、OGD/R+10μmol·L^(-1)姜酮、OGD/R+100μmol·L^(-1)姜酮组和OGD/R+0.2%二甲亚枫(DMSO)组,CCK-8法检测各组细胞活性并计算各组细胞存活率,确定姜酮最适药物浓度。细胞分为对照组、OGD/R组、OGD/R+姜酮组和OGD/R+姜酮+核因子E2相关因子2(Nrf2)抑制剂(ML385)组,OGD/R+姜酮组细胞经姜酮给药处理4 h后予以OGD 8 h和复糖复氧8 h处理,OGD/R+姜酮+ML385组细胞在姜酮给药前予以10μmol·L^(-1)ML385预处理6 h,CCK-8法检测各组细胞活性,Western blotting法检测各组细胞中Nrf2、血红素加氧酶1(HO-1)、B细胞淋巴瘤2(Bcl-2)和Bcl-2相关X蛋白(Bax)蛋白表达水平,酶联免疫吸附试验(ELISA)法检测各组细胞培养上清中超氧化物歧化酶(SOD)活性和丙二醛(MDA)水平。结果:与对照组比较,HT22细胞经OGD 8 h和复糖复糖8 h处理后细胞存活率低于50%,以OGD 8 h和复糖复糖8 h建立HT22细胞OGD/R模型。与OGD/R组比较,OGD/R+不同剂量姜酮组细胞存活率均不同程度升高,其中OGD/R+100μmol·L^(-1)姜酮组细胞存活率升高最明显(P<0.01),故选用100μmol·L^(-1)姜酮用于后续实验。与对照组比较,OGD/R组细胞活性明显降低(P<0.01),细胞中Nrf2、HO-1和Bax蛋白表达水平明显升高(P<0.01),Bcl-2蛋白表达水平明显降低(P<0.05),细胞培养上清中SOD活性明显降低(P<0.01),MDA水平明显升高(P<0.01);与OGD/R组比较,OGD/R+姜酮组细胞活性明显升高(P<0.01),细胞中Nrf2、HO-1和Bcl-2蛋白表达水平明显升高(P<0.05或P<0.01),Bax蛋白表达水平明显降低(P<0.05),细胞培养上清中SOD活性明显升高(P<0.01),MDA水平明显降低(P<0.01);与OGD/R+姜酮组比较,OGD/R+姜酮+ML385组细胞活性明显降低(P<0.01),细胞中Nrf2、HO-1和Bcl-2蛋白表达水平明显降低(P<0.01),Bax蛋白表达水平明显升高(P<0.01),细胞培养上清中SOD活性明显降低(P<0.01),MDA水平明显升高(P<0.05)。结论:姜酮可通过激活Nrf2/HO-1信号通路减轻OGD/R后氧化应激损伤对HT22细胞凋亡的抑制作用。 展开更多
关键词 姜酮 糖氧剥夺 HT22神经元 核因子E2相关因子2 血红素加氧酶1 氧化应激 细胞凋亡
下载PDF
肺源性心脏病并发肺动脉高压患者血清β-NGF和TRAIL水平检测在临床诊断及预后评估中的意义
7
作者 唐文慧 应会领 +2 位作者 段静 董卓 尤欣怡 《现代检验医学杂志》 CAS 2024年第4期131-137,共7页
目的探讨肺源性心脏病(pulmonary heart disease,PHD)并发肺动脉高压(pulmonary heart disease,PAH)患者血清β-神经生长因子(β-nerve growth factor,β-NGF)、肿瘤坏死因子相关凋亡诱导配体(tumor necrosis factor-related apoptosis-... 目的探讨肺源性心脏病(pulmonary heart disease,PHD)并发肺动脉高压(pulmonary heart disease,PAH)患者血清β-神经生长因子(β-nerve growth factor,β-NGF)、肿瘤坏死因子相关凋亡诱导配体(tumor necrosis factor-related apoptosis-inducing ligand,TRAIL)表达水平及其在临床诊断及预后评估中的意义。方法采用1∶1病例-对照研究设计选取2019年1月~2022年6月北京市大兴区人民医院86例并发PAH的PHD患者为病例组,86例单纯PHD患者为对照组,进行回顾性分析。将病例组根据肺动脉收缩压(pulmonary arterial systolic pressure,PASP)分为轻度PAH组(n=39)、中度PAH组(n=25)和重度PAH组(n=22),根据出院后一年的结果分为预后良好组(n=75)和预后不良组(n=11)。收集研究对象人口学资料和实验室检查指标,采用酶联免疫吸附(ELISA)法检测血清β-NGF,TRAIL水平。Pearson积矩相关分析β-NGF,TRAIL与PASP的关系,Logistic回归分析PHD患者PAH影响因素,ROC曲线评估β-NGF,TRAIL对PAH的诊断价值,COX比例风险回归分析β-NGF,TRAIL与PHD并发PAH患者预后不良的关系,ROC曲线评估其对预后不良的预测价值。结果与对照组比较,病例组PHD病程长(8.63±1.27年vs 5.49±1.15年),血清β-NGF(26.97±8.25 ng/ml vs 22.14±7.32 ng/ml)和TRAIL(2.83±0.76 ng/ml vs 1.71±0.68 ng/ml)水平升高,差异具有统计学意义(t=17.006,4.064,10.183,均P<0.05)。血清β-NGF,TRAIL对PHD患者PAH有诊断价值,AUC分别为0.842,0.838,二者联合诊断的AUC为0.920,诊断价值高于单一指标(Z=3.416,3.508,均P<0.05)。轻度PAH组、中度PAH组和重度PAH组血清β-NGF(23.26±5.13 ng/ml,27.83±5.57 ng/ml,32.57±6.02 ng/ml),TRAIL(2.24±0.65 ng/ml,2.89±0.71 ng/ml,3.81±0.90 ng/ml)水平依次升高,差异具有统计学意义(F=20.624,31.972,均P<0.05)。病例组血清β-NGF,TRAIL与PASP呈正相关(r=0.673,0.659,均P<0.05)。预后不良组血清β-NGF(36.34±8.05 ng/ml),TRAIL(3.49±1.01 ng/ml)水平高于预后良好组(25.59±7.28 ng/ml,2.73±0.89 ng/ml),差异具有统计学意义(t=4.516,2.604,均P<0.05)。Logistic回归分析结果显示,PHD病程[OR(95%CI):1.784(1.135~2.806)]、β-NGF[OR(95%CI):1.976(1.108~3.523)],TRAIL[OR(95%CI):1.866(1.123~3.101)]是PHD患者发生PAH的独立危险因素(均P<0.05)。多因素COX比例风险回归结果显示,PHD病程[OR(95%CI):1.167(1.082~1.364]、β-NGF[OR(95%CI):1.322(1.134~1.649)],TRAIL[OR(95%CI):1.259(1.087~1.590)]是PHD并发PAH患者预后不良的独立危险因素(均P<0.05)。血清β-NGF,TRAIL可预测PHD并发PAH患者预后不良发生风险,AUC分别为0.863,0.881,二者联合检测的AUC为0.907,诊断价值高于单一指标检测(Z=2.905,3.128,均P<0.05)。结论血清β-NGF和TRAIL升高是PHD患者PAH独立危险因素,并与PAH严重程度有关,早期联合β-NGF和TRAIL检测可提高对PAH的诊断价值及对患者预后不良的预测效果。 展开更多
关键词 Β-神经生长因子 肿瘤坏死因子相关凋亡诱导配体 肺源性心脏病 肺动脉高压
下载PDF
COMBINATION OF γ-INTERFERON WITH TRAIL AND CISPLATIN OR ETOPOSIDE INDUCES APOPTOSIS IN HUMAN NEUROBLASTOMA CELL LINE SH-SY5Y 被引量:9
8
作者 Hai-xia Tong Chun-wei Lu +2 位作者 Ji-hong Zhang Li Ma Jin-hua Zhang 《Chinese Medical Sciences Journal》 CAS CSCD 2007年第1期38-43,共6页
Objective To study the effect of γ-interferon (IFNγ), tumor necrosis factor related apoptosis inducing ligand (TRAIL), and cisplatin or etoposide induced apoptosis in human neuroblastoma cell line SH-SY5Y and it... Objective To study the effect of γ-interferon (IFNγ), tumor necrosis factor related apoptosis inducing ligand (TRAIL), and cisplatin or etoposide induced apoptosis in human neuroblastoma cell line SH-SY5Y and its possible molecular mechanisms. Methods The expressions of Caspase 8 mRNA and protein were detected with RT-PCR and Western blot analysis. The effects of IFNγ, TRAIL, IFNγ + TRAIL, IFNγ + Caspase 8 inhibitor + TRAIL, IFNγ + cisplatin + TRAIL, and IFNγ + etoposide + TRAIL on the growth and apoptosis of SH-SY5Y cells were detected with the methods of MTT and flow cytometry. The relative Caspase 8 activity was measured with colorimetric assay. Results Caspase 8 was undetectable in SH-SY5Y cells but an increased expression of Caspase 8 mRNA and protein was found after treatment with IFNγ. SH-SY5Y ceils themselves were not sensitive to TRAIL, but those expressing Caspase 8 after treatment with IFNγ were. The killing effect of TRAIL on SH-SY5Y cells expressing Caspase 8 was depressed by Caspase 8 inhibitor. Cisplatin and etoposide could enhance the sensitivity of TRAIL on SH-SY5Y cells. The relative Caspase 8 activity of SH-SY5Y cells in IFNγ + TRAIL group was significantly higher than those of control group, IFNγ group, TRAIL group, and inhibitor group ( P 〈 0. 01 ). There was no significant difference among IFNγ + TRAIL group, IFNγ + cisplatin + TRAIL group, and IFNγ + etoposide + TRAIL group. Conclusions IFNγ could sensitize SH-SY5Y cells to TRAIL-induced apoptosis and this may be realized by the up-regulation of Caspase 8. Cisplatin and etoposide could enhance the killing effect of TRAIL on SH-SY5Y cells. 展开更多
关键词 NEUROBLASTOMA apoptosis tumor necrosis factor related apoptosis inducing ligand γ-interferon
下载PDF
褪黑素通过下调HIF-1α表达增强卵巢癌细胞OVCAR3顺铂敏感性
9
作者 张海光 杨君 +3 位作者 郭会敏 张雪英 秦学娜 华方方 《现代肿瘤医学》 CAS 2024年第10期1804-1809,共6页
目的:探讨褪黑素对卵巢癌细胞顺铂敏感性的影响及其机制。方法:采用不同浓度褪黑素联合顺铂作用于卵巢癌细胞OVCAR3,MTT法检测细胞增殖,流式细胞术检测细胞凋亡,Western blot检测凋亡相关蛋白及信号通路蛋白AKT及ERK的磷酸化,同时检测... 目的:探讨褪黑素对卵巢癌细胞顺铂敏感性的影响及其机制。方法:采用不同浓度褪黑素联合顺铂作用于卵巢癌细胞OVCAR3,MTT法检测细胞增殖,流式细胞术检测细胞凋亡,Western blot检测凋亡相关蛋白及信号通路蛋白AKT及ERK的磷酸化,同时检测褪黑素对HIF-1α蛋白表达的影响。结果:MTT结果显示,褪黑素和顺铂联合作用能够显著抑制OVCAR3细胞增殖(P<0.05)。流式细胞仪检测结果显示,褪黑素和顺铂联合作用相较于单独顺铂作用或褪黑素作用能够显著增加OVCAR3细胞的凋亡。Western blot结果显示,褪黑素与顺铂联合作用能够增加促凋亡蛋白BAX及Caspase3的表达,抑制抗凋亡蛋白BCL2的表达,检测信号通路结果显示,褪黑素与顺铂联合作用能够促进AKT及ERK的磷酸化,同时褪黑素能够抑制HIF-1α蛋白的表达。结论:褪黑素通过抑制HIF-1α的表达使OVCAR3细胞对顺铂敏感。 展开更多
关键词 卵巢癌 褪黑素 顺铂 缺氧诱导因子1ɑ 凋亡相关蛋白
下载PDF
Targeted anti-cancer therapy: Co-delivery of VEGF siRNA and Phenethyl isothiocyanate (PEITC) via cRGD-modified lipid nanoparticles for enhanced anti-angiogenic efficacy 被引量:1
10
作者 Bao Li Haoran Niu +10 位作者 Xiaoyun Zhao Xiaoyu Huang Yu Ding Ke Dang Tianzhi Yang Yongfeng Chen Jizhuang Ma Xiaohong Liu Keda Zhang Huichao Xie Pingtian Ding 《Asian Journal of Pharmaceutical Sciences》 SCIE CAS 2024年第2期170-187,共18页
Anti-tumor angiogenesis therapy, targeting the suppression of blood vessel growth in tumors, presents a potent approach in the battle against cancer. Traditional therapies have primarily concentrated on single-target ... Anti-tumor angiogenesis therapy, targeting the suppression of blood vessel growth in tumors, presents a potent approach in the battle against cancer. Traditional therapies have primarily concentrated on single-target techniques, with a specific emphasis on targeting the vascular endothelial growth factor, but have not reached ideal therapeutic efficacy. In response to this issue, our study introduced a novel nanoparticle system known as CS-siRNA/PEITC&L-cRGD NPs. These chitosan-based nanoparticles have been recognized for their excellent biocompatibility and ability to deliver genes. To enhance their targeted delivery capability, they were combined with a cyclic RGD peptide (cRGD). Targeted co-delivery of gene and chemotherapeutic agents was achieved through the use of a negatively charged lipid shell and cRGD, which possesses high affinity for integrin αvβ3 overexpressed in tumor cells and neovasculature. In this multifaceted approach, co-delivery of VEGF siRNA and phenethyl isothiocyanate (PEITC) was employed to target both tumor vascular endothelial cells and tumor cells simultaneously. The co-delivery of VEGF siRNA and PEITC could achieve precise silencing of VEGF, inhibit the accumulation of HIF-1α under hypoxic conditions, and induce apoptosis in tumor cells. In summary, we have successfully developed a nanoparticle delivery platform that utilizes a dual mechanism of action of anti-tumor angiogenesis and pro-tumor apoptosis, which provides a robust and potent strategy for the delivery of anti-cancer therapeutics. 展开更多
关键词 ANTI-ANGIOGENESIS Tumor apoptosis Nanoparticles VEGF siRNA Hypoxia inducible factor(HIF)-1 protein Phenethyl isothi ocyanate(PEITC)
下载PDF
EGCG Enhances TRAIL-mediated Apoptosis in Human Melanoma A375 Cell Line 被引量:2
11
作者 沈琴 田芬 +4 位作者 蒋萍 李艳秋 张丽 卢静静 李家文 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2009年第6期771-775,共5页
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising anti-cancer agent. Epigallocatechin-3-gallate (EGCG) is a polyphenolic constituent of green tea. In this study, inhibitory effect of c... Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising anti-cancer agent. Epigallocatechin-3-gallate (EGCG) is a polyphenolic constituent of green tea. In this study, inhibitory effect of combined use of EGCG and TRAIL on human melanoma A375 cells was examined and the possible mechanism investigated. The cells were divided into 4 groups: control group, EGCG group (EGCG: 10, 20 μg/mL), TRAIL group (TRAIL: 25 ng/mL) and EGCG+TRAIL group (combined group). The growth inhibition was measured in the A375 cells treated with different concentrations of TRAIL ((25, 50, 75, 100, 125, 150 ng/mL) by MTT assay. The apoptosis was assessed by flow cytometry. The expressions of DR4 and DR5 were detected by flow cytometry and western blotting. The activities of caspase-8 and caspase-3 were determined by colorimetric assay. The results showed that TRAIL could dose-dependently inhibit the growth of A375 cells and the IC50 of TRAIL was 150 ng/mL. The apoptosis rate was 11.8% in the TRAIL group, 5%–7% in the EGCG group and 48.9%–59.1% in the combined group. Significant difference was found in the apoptosis rate between the combined group and the EGCG or TRAIL group (P〈0.05 for each). The expression of DR4 instead of DR5 was significantly increased in the EGCG group. The activity of caspase-3 rather than caspase-8 was substantially enhanced in the EGCG group. These results suggest that EGCG is useful for the TRAIL-based treatment for melanoma. 展开更多
关键词 epigallocatechin-3-gallate tumor necrosis factor-related apoptosis-inducing ligand death receptor 4 death receptor 5 apoptosis MELANOMA
下载PDF
EGFR inhibitors sensitize non-small cell lung cancer cells to TRAIL-induced apoptosis 被引量:3
12
作者 Fei Xu Ying Tian +4 位作者 Yan Huang Ling-Ling Zhang Zheng-Zheng Guo Jia-Jia Huang Tong-Yu Lin 《Chinese Journal of Cancer》 SCIE CAS CSCD 北大核心 2011年第10期701-711,共11页
Apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand(TRAIL) can be regulated by the epidermal growth factor(EGF) signaling pathway.In this study,recombinant adenoviral vectors that encode TRAIL... Apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand(TRAIL) can be regulated by the epidermal growth factor(EGF) signaling pathway.In this study,recombinant adenoviral vectors that encode TRAIL gene from the hTERT/RGD promoter(AdTRAIL) was combined with drugs including gefitinib,elotinib,and cetuximab that inhibit EGFR and the EGF signaling pathway in non-small cell lung cancer(NSCLC) cell lines to investigate their antitumor activity.In vitro,compared to single reagent,AdTRAIL combined with EGFR inhibitors reduced proliferation and enhanced apoptosis in H460,A549,and SW1573 cell lines.Western blot results suggested that these effects were relative to up-regulation of pro-apoptosis protein BAX and down-regulation of p-AKT.In vivo,AdTRAIL combined with cetuximab resulted in a significant growth reduction in H460 xenografts without damage to the main organs of nude mice.Histological examination and TUNEL analyses of xenografts showed that cetuximab enhanced cell apoptosis induced by AdTRAIL.These results indicate that EGFR inhibitors enhanced AdTRAIL anti-tumor activity in NSCLC cell lines and that inhibiting the AKT pathway played an important role in this enhancement. 展开更多
关键词 肿瘤坏死因子相关凋亡诱导配体 细胞凋亡 TRAIL EGFR 抑制剂 肺癌细胞 表皮生长因子受体 非小细胞肺癌
下载PDF
X-染色体连锁凋亡抑制蛋白相关因子1通过自噬途径调控Caspase 1介导的胃肠道间质瘤细胞焦亡
13
作者 周江浩 谢书海 陈勇 《河北医学》 CAS 2024年第5期744-750,共7页
目的:探究X-染色体连锁凋亡抑制蛋白相关因子1(XAF1)对人胃肠道间质瘤(GIST)细胞中半胱氨酸蛋白酶-1(Caspase 1)介导的细胞焦亡的影响及机制。方法:实时荧光定量PCR和Western blot检测人正常胃黏膜上皮细胞系(RGM-1)和GIST细胞系(GIST-T... 目的:探究X-染色体连锁凋亡抑制蛋白相关因子1(XAF1)对人胃肠道间质瘤(GIST)细胞中半胱氨酸蛋白酶-1(Caspase 1)介导的细胞焦亡的影响及机制。方法:实时荧光定量PCR和Western blot检测人正常胃黏膜上皮细胞系(RGM-1)和GIST细胞系(GIST-T1、GIST-430、GIST-882)中XAF1的表达水平;采用脂质体介导转染法将pcDNA3.1-XAF1重组质粒染进GIST-882细胞,以构建高表达XAF1的GIST-882细胞。GIST-882细胞分为对照组、pcDNA3.1组(转染pcDNA3.1空载体质粒)、pcDNA3.1-XAF1组(转染pcDNA3.1-XAF1重组质粒)、pcDNA3.1-XAF1+Rap组(转染pcDNA3.1-XAF1重组质粒并给予自噬激活剂雷帕霉素处理),免疫荧光染色检测各组细胞内微管相关蛋白1轻链3(LC3)表达情况,Western blot检测各组细胞中LC3Ⅱ/LC3Ⅰ比值与Beclin1蛋白表达水平,ELISA法检测各组细胞上清中白细胞介素,IL-1β、IL-18含量,乳酸脱氢酶(LDH)释放实验检测各组细胞LDH释放率,Western blot检测各组细胞中Caspase-1及其活化形式cleaved-Caspase-1、NOD样受体热蛋白结构域相关蛋白3(NLRP3)、消皮素D(GSDMD)蛋白表达水平。结果:与RGM-1细胞比较,GIST-T1、GIST-430、GIST-882细胞中XAF1 mRNA和蛋白相对表达量显著减少(P<0.05);细胞转染后,pcDNA3.1-XAF1组GIST-882细胞中XAF1 mRNA和蛋白相对表达量均显著高于pcDNA3.1组、对照组(P<0.05)。与对照组比较,pcDNA3.1-XAF1组GIST-882细胞内LC3荧光强度明显减弱,LC3Ⅱ/LC3Ⅰ比值、Beclin1蛋白相对表达量显著减少(P<0.05),细胞上清液IL-1β、IL-18含量及LDH释放率显著升高(P<0.05),Caspase-1、cleaved-Caspase-1、NLRP3、GSDMD蛋白相对表达量也显著增加(P<0.05);与pcDNA3.1-XAF1组比较,pcDNA3.1-XAF1+Rap组GIST-882细胞内LC3荧光强度明显增强,LC3Ⅱ/LC3Ⅰ比值、Beclin1蛋白相对表达量显著增加(P<0.05),同时,细胞上清液IL-1β、IL-18含量及LDH释放率显著下降(P<0.05),Caspase-1、cleaved-Caspase-1、NLRP3、GSDMD蛋白相对表达量也显著减少(P<0.05)。结论:XAF1在GIST细胞中表达下降,提高XAF1表达能通过抑制自噬从而促进Caspase 1介导的GIST细胞焦亡,发挥抗肿瘤作用。 展开更多
关键词 胃肠道间质瘤 X-染色体连锁凋亡抑制蛋白相关因子1 自噬 半胱氨酸蛋白酶-1 焦亡
下载PDF
SIRT6过表达激活AMPK/Nrf2/HO-1通路抑制AngⅡ诱导的心肌细胞凋亡
14
作者 卢振华 沈静 +2 位作者 黄文军 孙伟 马勇翔 《中国动脉硬化杂志》 CAS 2024年第8期663-668,676,共7页
[目的]探讨沉默调节蛋白6(SIRT6)过表达抑制血管紧张素Ⅱ(AngⅡ)诱导的心肌细胞凋亡是否涉及腺苷酸活化蛋白激酶/核因子E2相关因子2/血红素加氧酶1(AMPK/Nrf2/HO-1)信号通路的激活。[方法]将实验分为4组:对照组、AngⅡ组、AngⅡ+SIRT6组... [目的]探讨沉默调节蛋白6(SIRT6)过表达抑制血管紧张素Ⅱ(AngⅡ)诱导的心肌细胞凋亡是否涉及腺苷酸活化蛋白激酶/核因子E2相关因子2/血红素加氧酶1(AMPK/Nrf2/HO-1)信号通路的激活。[方法]将实验分为4组:对照组、AngⅡ组、AngⅡ+SIRT6组和AngⅡ+空载体(EV)组,通过RT-PCR检测SIRT6的mRNA水平,MTT法检测细胞活性,流式细胞术检测细胞凋亡率,Western blot检测SIRT6、心肌细胞凋亡相关蛋白(Bax、cleaved Caspase-3、Bcl-2)、DNA损伤相关蛋白(γ-H2AX、p-ATM)及AMPK/Nrf2/HO-1信号通路相关蛋白(p-AMPK、Nrf2、HO-1)的表达水平,DCFH-DA染色法测定活性氧(ROS)含量,比较各组间上述指标的变化情况。[结果]与对照组相比,AngⅡ组SIRT6的mRNA、蛋白表达水平及细胞活性明显降低,细胞凋亡率增高,Bax、cleaved Caspase-3表达升高,Bcl-2表达降低,γ-H2AX、p-ATM蛋白表达升高,p-AMPK、Nrf2、HO-1蛋白表达降低,ROS活性增高(均P<0.01)。与AngⅡ+EV组相比,AngⅡ+SIRT6组SIRT6水平及细胞活性增高,细胞凋亡及Bax、cleaved Caspase-3表达降低,Bcl-2表达升高,γ-H2AX、p-ATM蛋白表达降低,p-AMPK、Nrf2、HO-1蛋白表达升高,ROS的活性降低(均P<0.01)。[结论]SIRT6过表达抑制AngⅡ诱导的心肌细胞凋亡与AMPK/Nrf2/HO-1信号通路的激活有关。 展开更多
关键词 沉默调节蛋白6 腺苷酸环化蛋白激酶/核因子E2相关因子2/血红素加氧酶1 氧化应激 DNA损伤 细胞凋亡
下载PDF
黄酮类中药单体干预Nrf2/HO-1通路治疗糖尿病微血管并发症研究进展
15
作者 刘映君 阴永辉 +2 位作者 王文宽 张金涛 孔畅 《山东中医药大学学报》 2024年第2期246-253,共8页
糖尿病微血管并发症是糖尿病最主要的慢性并发症。研究表明,核转录因子红系2相关因子2/血红素加氧酶-1(Nrf2/HO-1)信号通路是治疗糖尿病微血管并发症的重要靶点。黄酮、黄酮醇、二氢黄酮、异黄酮、二氢异黄酮、查耳酮、黄烷醇、花青素... 糖尿病微血管并发症是糖尿病最主要的慢性并发症。研究表明,核转录因子红系2相关因子2/血红素加氧酶-1(Nrf2/HO-1)信号通路是治疗糖尿病微血管并发症的重要靶点。黄酮、黄酮醇、二氢黄酮、异黄酮、二氢异黄酮、查耳酮、黄烷醇、花青素等黄酮类中药单体可以通过调控Nrf2/HO-1信号通路发挥缓解氧化应激、减少炎症反应、抑制细胞凋亡、减轻纤维化、改善血流动力学等作用,从而达到治疗糖尿病视网膜病变、糖尿病心肌病、糖尿病肾病、糖尿病周围神经病变等多种糖尿病微血管并发症的目的。 展开更多
关键词 糖尿病微血管并发症 核转录因子红系2相关因子2/血红素加氧酶-1信号通路 黄酮类中药单体 氧化应激 炎症反应 细胞凋亡 纤维化 血流动力学
下载PDF
CCAT1靶向抑制miR-375-3p通过线粒体途径诱导的人口腔癌SAS细胞凋亡
16
作者 卢泰青 高振杰 +1 位作者 张炜 施鹏伟 《解剖学杂志》 CAS 2024年第2期114-119,189,共7页
目的:探究长链非编码RNA(lncRNA)结肠癌相关转录因子1(CCAT1)靶向miR-375-3p通过线粒体途径诱导人口腔癌SAS细胞凋亡的作用。方法:人口腔癌SAS细胞随机分为空白组、CCAT1下调组、CCAT1上调组、CCAT1下调对照组、CCAT1上调对照组、miR-37... 目的:探究长链非编码RNA(lncRNA)结肠癌相关转录因子1(CCAT1)靶向miR-375-3p通过线粒体途径诱导人口腔癌SAS细胞凋亡的作用。方法:人口腔癌SAS细胞随机分为空白组、CCAT1下调组、CCAT1上调组、CCAT1下调对照组、CCAT1上调对照组、miR-375-3p下调组、miR-375-3p上调组、miR-375-3p下调对照组和miR-375-3p上调对照组。转染48 h后,流式细胞术检测细胞凋亡;RT-qPCR检测miR-375-3p表达、线粒体凋亡通路相关的基因半胱氨酰天冬氨酸特异性蛋白酶3(caspase-3)、半胱氨酰天冬氨酸特异性蛋白酶9(caspase-9)、B淋巴细胞瘤-2(Bcl-2)和Bcl-2相关X蛋白(Bax)的mRNA表达;免疫印迹检测caspase-3、caspase-9、Bcl-2、Bax蛋白表达;双荧光素酶报告实验分析CCAT1与miR-375-3p的靶向关系。结果:与空白组和CCAT1下调对照组比较,CCAT1下调组细胞凋亡率、miR-375-3p表达、caspase-3、caspase-9、Bax mRNA及蛋白表达升高,Bcl-2 mRNA及蛋白表达降低;与空白组和CCAT1上调对照组比,CCAT1上调组细胞凋亡率、miR-375-3p表达、caspase-3、caspase-9、Bax mRNA及蛋白表达降低,Bcl-2 mRNA及蛋白表达升高;与空白组和miR-375-3p下调对照组比较,miR-375-3p下调组细胞凋亡率、miR-375-3p表达、caspase-3、caspase-9、Bax mRNA及蛋白表达降低,Bcl-2 mRNA及蛋白表达升高;与空白组和miR-375-3p上调对照组比较,miR-375-3p上调组细胞凋亡率、miR-375-3p表达、caspase-3、caspase-9、Bax mRNA及蛋白表达升高,Bcl-2 mRNA及蛋白表达降低。双荧光素酶实验结果提示CCAT1可靶向调控miR-375-3p。结论:CCAT1可抑制人口腔癌SAS细胞凋亡,推测是通过靶向抑制miR-375-3p的表达,调控线粒体凋亡通路相关基因及蛋白的表达来实现的。 展开更多
关键词 长链非编码RNA 结肠癌相关转录因子1 miR-375-3p 口腔癌 线粒体途径 凋亡
下载PDF
Role of Notch-1 signaling pathway in PC12 cell apoptosis induced by amyloid beta-peptide(25–35)
17
作者 Huimin Liang Yaozhou Zhang +2 位作者 Xiaoyan Shi Tianxiang Wei Jiyu Lou 《Neural Regeneration Research》 SCIE CAS CSCD 2014年第13期1297-1302,共6页
Recent studies have demonstrated that Notch-1 expression is increased in the hippocampus of Alzheimer's disease patients. We speculate that Notch-1 signaling may be involved in PC12 cell apoptosis induced by amyloid ... Recent studies have demonstrated that Notch-1 expression is increased in the hippocampus of Alzheimer's disease patients. We speculate that Notch-1 signaling may be involved in PC12 cell apoptosis induced by amyloid beta-peptide (25-35) (Aβ25-35). In the present study, PC12 cells were cultured with different doses (0, 0.1, 1.0, 10 and 100 nmol/L) of N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester, a Notch-1 signaling pathway inhibitor, for 30 minutes. Then cultured cells were induced with Aβ25-3s for 48 hours. Pretreatment of PC12 cells with high doses of N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (〉 10 nmol/L) prolonged the survival of PC12 cells after Aβ25-35 induction, decreased the expression of apoptosis-related proteins caspase-3, -8, -9, increased the activity of oxidative stress-related superoxide dismutase and catalase, inhibited the production of active oxygen, and reduced nuclear factor kappa B expression. This study indicates that the Notch-1 signaling pathway plays a pivotal role in Aβ25-35-induced PC12 apoptosis. 展开更多
关键词 nerve regeneration Alzheimer's disease amyloid beta-peptide (25-35) Notch-l PC12cells apoptosis oxidative stress nuclear factor kappa B neural regeneration
下载PDF
逍遥丸对代谢相关脂肪性肝炎CYP2E1及FasL/TNF-α信号通路的影响
18
作者 张馨月 张玉伟 +3 位作者 李梦琪 孟雅楠 李若瑜 苗宇船 《安徽医科大学学报》 CAS 北大核心 2024年第7期1218-1224,共7页
目的研究逍遥丸治疗代谢相关脂肪性肝炎(MASH)大鼠的机制。方法24只雄性SD大鼠随机分为对照组(CON组,n=8)和模型组(n=16),模型组给予高脂饮食+四氯化碳背部皮下注射+饥饱失常+夹尾,联合刺激4周建立MASH模型,再随机分为MOD组和逍遥丸组(... 目的研究逍遥丸治疗代谢相关脂肪性肝炎(MASH)大鼠的机制。方法24只雄性SD大鼠随机分为对照组(CON组,n=8)和模型组(n=16),模型组给予高脂饮食+四氯化碳背部皮下注射+饥饱失常+夹尾,联合刺激4周建立MASH模型,再随机分为MOD组和逍遥丸组(XYW组),每组各8只。XYW组大鼠给予逍遥丸灌胃,其他两组给予0.9%氯化钠溶液灌胃。给药4周后,对不同组别大鼠的血清生化及氧化应激指标进行检测。HE染色和油红O染色对大鼠肝组织进行病理切片观察。Western blot对大鼠肝脏中细胞色素P4502E1(CYP2E1)、凋亡相关因子配体(FasL)、肿瘤坏死因子-α(TNF-α)、转化生长因子-β1(TGF-β1)的表达进行检测。RT-qPCR检测肝组织CYP2E1、FasL、TNF-α、TGF-β1 mRNA相对含量。结果XYW组大鼠的一般情况较MOD组有显著改善,肝指数较MOD组下降(P<0.01),体质量指数较MOD组上升(P<0.01);XYW组血清中三酰甘油、总胆固醇、低密度脂蛋白胆固醇、天冬氨酸氨基转氨酶、丙氨酸氨基转移酶、丙二醛、单核细胞趋化蛋白-1、TNF-α、白细胞介素(IL)-18水平较MOD组降低(均P<0.05),高密度脂蛋白胆固醇、超氧化物歧化酶、IL-10水平较MOD组升高(均P<0.05);光镜下可观察到XYW组肝细胞内脂滴含量较MOD组明显减少;XYW组肝组织CYP2E1、FasL、TNF-α、TGF-β1的蛋白水平较MOD组降低(均P<0.05),CYP2E1、FasL、TNF-α、TGF-β1 mRNA相对含量较MOD组降低(均P<0.05)。结论逍遥丸通过调节CYP2E1、FasL、TNF-α、TGF-β1在MASH大鼠肝组织中的转录表达,减少肝脏脂肪酸蓄积,从而达到治疗MASH的目的。 展开更多
关键词 逍遥丸 代谢相关脂肪性肝炎 细胞色素P4502E1 凋亡相关因子配体 肿瘤坏死因子-α 转化生长因子-β1
下载PDF
肾炎汤联合西药对急性肾小球肾炎患者t-PA、PAI-1、sFas、sFasL的影响
19
作者 彭婷 丁瑜 +1 位作者 郝冬阳 谭会 《中国中医急症》 2024年第9期1612-1615,共4页
目的观察肾炎汤联合西药对急性肾小球肾炎(AGN)患者组织型纤溶酶原激活物(t-PA)、纤溶酶原激活物抑制剂-1(PAI-1)、可溶性凋亡相关因子(sFas)及可溶性凋亡相关因子配体(sFasL)的影响。方法AGN患者92例按奇偶数分组法设为对照组与研究组... 目的观察肾炎汤联合西药对急性肾小球肾炎(AGN)患者组织型纤溶酶原激活物(t-PA)、纤溶酶原激活物抑制剂-1(PAI-1)、可溶性凋亡相关因子(sFas)及可溶性凋亡相关因子配体(sFasL)的影响。方法AGN患者92例按奇偶数分组法设为对照组与研究组各46例。对照组行西医常规治疗,研究组在此基础上联合肾炎汤治疗,两组均治疗14 d。比较两组疗效及临床指标恢复时间,并对两组肾功能及血清t-PA、PAI-1、sFas、sFasL水平进行对比。结果研究组总有效率为95.65%,高于对照组的80.43%(P<0.05)。研究组血尿消退时间、血沉恢复时间、水肿消退时间及血压恢复时间短于对照组(P<0.05)。治疗后,两组24 h尿蛋白定量、血尿素氮、血肌酐比治疗前低,且研究组比对照组低(P<0.05)。治疗后,两组t-PA较治疗前升高,PAI-1、sFas、sFasL较治疗前降低,且研究组改善优于对照组(P<0.05)。结论肾炎汤联合西药治疗AGN患者可有效缩短其临床指标恢复时间,提升疗效,可能与上调t-PA水平及下调PAI-1、sFas、sFasL水平有关。 展开更多
关键词 急性肾小球肾炎 肾炎汤 组织型纤溶酶原激活物 可溶性凋亡相关因子
下载PDF
罗哌卡因对胃癌BGC-823细胞生物学行为及AMPK/Nrf2信号通路的影响
20
作者 袁风雷 张丽霞 +1 位作者 李民 李贵宾 《国际检验医学杂志》 CAS 2024年第6期653-658,共6页
目的探究罗哌卡因对胃癌BGC-823细胞生物学行为及腺苷酸活化蛋白激酶(AMPK)/核因子E2相关因子2(Nrf2)信号通路的影响。方法体外培养胃癌BGC-823细胞,取培养至对数生长期的BGC-823细胞分为对照组(常规培养)、顺铂组(培养基含5 mg/L顺铂)... 目的探究罗哌卡因对胃癌BGC-823细胞生物学行为及腺苷酸活化蛋白激酶(AMPK)/核因子E2相关因子2(Nrf2)信号通路的影响。方法体外培养胃癌BGC-823细胞,取培养至对数生长期的BGC-823细胞分为对照组(常规培养)、顺铂组(培养基含5 mg/L顺铂)及罗哌卡因低水平(培养基含25 mg/L罗哌卡因)、中水平(培养基含50 mg/L罗哌卡因)、高水平(培养基含100 mg/L罗哌卡因)组,培养48 h。采用细胞计数试剂-8(CCK-8)检测BGC-823细胞存活率;Transwell小室实验检测BGC-823细胞侵袭能力;流式细胞仪检测BGC-823细胞凋亡率;实时荧光定量PCR(qPCR)法检测BGC-823细胞中AMPK、Nrf2信使RNA(mRNA)水平;Western blot法检测BGC-823细胞中AMPK、Nrf2蛋白水平。结果与对照组比较,顺铂组及罗哌卡因低、中、高水平组BGC-823细胞存活率、侵袭数量、AMPK、Nrf2 mRNA和蛋白水平均下降(P<0.05),而凋亡率升高(P<0.05);与顺铂组比较,罗哌卡因低、中、高水平组BGC-823细胞存活率、侵袭数量、AMPK、Nrf2 mRNA和蛋白水平均升高(P<0.05),而凋亡率下降(P<0.05);与罗哌卡因低水平组比较,罗哌卡因中、高水平组BGC-823细胞存活率、侵袭数量、AMPK、Nrf2 mRNA和蛋白水平均依次下降(P<0.05),而凋亡率依次升高(P<0.05)。结论罗哌卡因能抑制BGC-823细胞存活和侵袭,促进BGC-823细胞凋亡,其机制可能与抑制AMPK/Nrf2信号通路有关。 展开更多
关键词 罗哌卡因 胃癌BGC-823细胞 腺苷酸活化蛋白激酶/核因子E2相关因子2信号通路 细胞存活 侵袭 凋亡
下载PDF
上一页 1 2 32 下一页 到第
使用帮助 返回顶部