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951.
MA Zheng JIAO Guang-mei SHAN Hai-lei ZHANG Xiao-xuan KANG Ling-ling DOU Zhi-jie GAO Yan-jun 《园艺学报》2019,35(10):1776-1781
AIM: To investigate the effects of Kruppel-like factor 6 (KLF6) over-expression on the viability, apoptosis, reactive oxygen species (ROS) level and AKT signaling pathway of THP-1 cell-derived macrophages. METHODS: Human monocyte cell line THP-1 was induced to differentiate into macrophages by phorbol myristate acetate (PMA), and the macrophages were randomly divided into pcDNA3.1 group, oxidized low-density lipoprotein (ox-LDL) group, ox-LDL+pcDNA3.1 group and ox-LDL+pcDNA3.1-KLF6 group. pcDNA3.1 was transfected according to LipofectamineTM 2000 Kit. The cell viability, apoptotic rate and ROS level were detected by MTT assay, flow cytometry with Annexin V-FITC/PI double staining and H2DCF-DA probing, respectively. The protein levels of Bcl-2, Bax and p-AKT were determined by Western blot. RESULTS: After pcDNA3.1-KLF6 was transfected into the macrophages, the expression of KLF6 was increased significantly (P<0.05). ox-LDL significantly inhibited the viability of the macrophages, induced apoptosis and ROS production, up-regulated the protein expression of Bax, and down-regulated the protein levels of Bcl-2 and p-AKT (P<0.05). Over-expression of KLF6 significantly reduced the effects of ox-LDL on cell viability, apoptosis, ROS level and the protein levels of Bcl-2, Bax and p-AKT (P<0.05). CONCLUSION: KLF6 significantly reduces the apoptosis of THP-1 cell-derived macrophages induced by ox-LDL, which may be related to the reduction of ROS level and activation of AKT signaling pathway. 相似文献
952.
AIM: To explore the effect of berbamine(BER) on apoptosis in K562 cells and its possible molecular mechanisms. METHODS: The apoptosis rate was measured by flow cytometry while electron microscopy and DNA electrophoresis were used to evaluate the characteristic changes of apoptosis, RT-PCR and Western blot were used to examine the expression levels of apoptosis related gene bcr/abl and BCR/ABL protein. RESULTS: By FCM, the apoptosis rate of K562 cells treated with 8.0 mg/L BER for 24 h and 72 h increased from (29.20±3.82)% to (61.77±4.35)% (P＜0.01); The typical apoptosis morphologic changes and the DNA ladder were more clearly observed. After treated with BER 0 to 16.0 mg/L for 24 h, the expression levels of bcr/abl mRNA and P210 (semiquantity value) decreased quickly from 1.19±0.02 to 0.73±0.02 (P＜0.01) and from 1.04±0.02 to 0.63±0.01 (P＜0.01), respectively. CONCLUSION: BER induces apoptosis of K562 cells in a time-and-concentration-dependent manner, the decline of bcr/abl mRNA and P210 may play an important role in the apoptotic effect of BER in K562 cells. BER could be used as a new clinical trials for bcr-abl+ diseases such as CML. 相似文献
953.
灵芝水提物（LZ）对8种肿瘤细胞增殖的抑制作用具有剂量依赖关系.通过透析和离子交换凝胶过滤层析方法从LZ中分离出活性组分LZ-DN-2-2和LZ-DW-2-a-3.LZ、LZ-DN-2-2 和LZ-DW-2-a-3可剂量依赖地诱导SW620细胞凋亡,使细胞增殖周期停滞于G0期. 相似文献
954.
研究了云芝子实体氯仿提取物（CVFC）对人肝癌细胞株HepG2的体外抑制作用,并初步探讨了抑瘤机制。MTr结果显示,CVFC对HepG2细胞有明显的抑制作用,并呈明显的量效关系,半数抑制浓度为（75．83±3．96）μg·mL^-1。荧光显微镜和透射电镜形态观察发现CVFC处理可使细胞发生细胞皱缩、核碎裂等凋亡特征;Annexin V/PI双染结果证实有胞膜磷脂酰丝氨酸的翻转,经150μg·mL^-1 CVFC处理HepG2细胞24h后早期凋亡率为17．82％,晚期凋亡率为22．59％,均显著高于对照组5．35％和3．75％。这些结果表明CVFC具有体外抑制HepG2细胞的活性,其抑瘤机制与诱导肿瘤细胞凋亡有关。 相似文献
955.
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957.
AIM: To evaluate the effect of interfering TGF-β receptor Ⅱ (TβRⅡ) expression on the viability and differentiation of human acute promyelocytic leukemia NB4 cells induced by all-trans retinoic acid (ATRA) and their apoptosis induced by arsenic trioxide (ATO). METHODS: The technique of lentivirus-mediated RNA interference was used to obtain stable NB4 cells with TβRⅡ knockdown, named TβRⅡ-shRNA NB4 cells. CCK-8 assay was used to detect the viability of TβRⅡ-shRNA NB4 cells. The expression level of CD11b was analyzed by flow cytometry, and Wright-Giemsa staining was used to detect the effects of ATRA on the differentiation of TβRⅡ-shRNA NB4 cells. Double staining (Annexin V-FITC/PI) and AO/EB staining were used to detect the effects of ATO on the apoptosis of TβRⅡ-shRNA NB4 cells. RESULTS: The viability of TβRⅡ-shRNA NB4 cells was significantly higher than that of NB4 parental cells. The differentiation was induced in TβRⅡ-shRNA NB4 cells and NB4 parent cells by treatment with ATRA at different concentration (0.01, 0.02, 0.04, 0.08, 0.1 μmol/L) for 96 h. The differentiation rate of TβRⅡ-shRNA NB4 cells was lower than that of NB4 parental cells in a dose-dependent manner. ATO induced apoptosis of TβRⅡ-shRNA NB4 cells and NB4 parent cells at different concentrations (2, 4 and 8 μmol/L) for 24 h. The apoptotic rate of TβRⅡ-shRNA NB4 cells was lower than that of NB4 parental cells dose-dependently. At the concentration of 8 μmol/L for 24 h, the apoptotic rates in TβRⅡ-shRNA NB4 cells and NB4 cells were (49.15±2.05)% and (66.85±2.41)%, respectively (P<0.01). CONCLUSION: Down-regulation of TβRⅡ increases the viability of NB4 cells, inhibits NB4 cell differentiation induced by ATRA, and also inhibits apoptosis induced by ATO. 相似文献
958.
LI Xiang ZHANG Xiao-yan ZHAO Ji-min LIU Kang-dong ZHAO Ming-yao DONG Zi-ming 《园艺学报》2014,30(6):975-981
AIM：To study the effect of p21-activated protein kinase 2 (PAK2) knockdown by RNA interference on the proliferation and apoptosis of human breast cancer cells. METHODS：The short hairpin RNA (shRNA) targeting PAK2 gene was designed and used for packing lentivirus in 293T cells.Human breast cancer MCF-7 cells were infected by the virus particles and PAK2 knockdown stable cell line was established by puromycin selection. The knockdown efficiency was assessed by Western blotting. The proliferation ability of MCF-7 cells was evaluated by CellTiter 96 AQueous and anchorage-independent growth assays. The cell apoptosis induced by staurosporine was detected by flow cytometry. RESULTS：The protein level of PAK2 was significantly suppressed after silencing of PAK2 gene in MCF-7 cells (P<0.01). Furthermore, knockdown of PAK2 caused remarkable inhibition of the cell proliferation and colony formation (P<0.01). Staurosporine induced more apoptosis in the PAK2 knockdown cells compared with the control cells (P<0.01). CONCLUSION：Knockdown of PAK2 inhibits the proliferation of MCF-7 cells and increases the sensitivity of chemotherapeutic drug-induced cell apoptosis, suggesting that PAK2 might be a new therapeutic target in breast cancer treatment. 相似文献
959.
AIM: To observe the effect of rapamycin on the apoptosis of mouse astrocytes in vitro.ME-THODS:The astrocytes from C57BL/6J newborn mouse pups were isolated and primarily cultured. The effect of rapamycin on the viability of astrocytes was assessed by MTT assay. The mean fluorescence intensity of SYTOX® Green stain in the astrocytes was detected by fluorescence microplate reader in order to analyze the effects of rapamycin on the cell death induced by H2O2, ionomycin and/or deferorxamin. DiOC6(3) staining was used to analyze the mitochondrial membrane potential of the astrocytes induced by H2O2. Flow cytometry analysis was used to determine the production of ROS in the astrocytes and mitochondria by staining with H2DCFDA and MitoSOXTM Red reagent, respectively.RESULTS: Rapamycin at concentration of 0.5 μmol/L protected the astrocytes against cell death induced by H2O2 or deferoxamine plus ionomycin. Rapamycin protected the mitochondrial membrane potential of astrocytes from the injury of H2O2. It also reduced the production of ROS in the astrocytes and decreased the level of ROS in the mitochondria.CONCLUSION: Rapamycin reduces the ROS overload in the mitochondria, keeps mitochondrial membrane potential safety and protects the astrocytes against apoptosis in vitro. 相似文献
960.