White tea encompasses a number of teas unique to eastern Fujian in China. Although white tea extracts have been reported to result in cancer cell apoptosis, to date, few studies have evaluated the mechanism of such ap...White tea encompasses a number of teas unique to eastern Fujian in China. Although white tea extracts have been reported to result in cancer cell apoptosis, to date, few studies have evaluated the mechanism of such apoptotic induction. A transcription factor that plays a critical role in cell apoptosis, NF-κB p65, is also likely critical by which white tea extracts induce cancer cell apoptosis. In this study, white tea aqueous extract (WTAE) was added to BEL-7402 and Hela cell media and NF-κB p65 activation was evaluated using western blotting and immunofluorescence. Results revealed that the phosphorylation of IKBα and p65 decreased in both cell lines after WTAE treatment. And the nuclear translocation of NF-κB p65 in both cell lines was also reduced with the WTAE treatment. NF-κB p65 inhibition was noted to accelerate apoptosis. Our findings suggest that NF-κB p65 was an important modulator in WTAE-induced apoptotic signal transduction and it acted as a negative regulator of apoptotic induction in BEL-7402 and Hela cancer cell lines.展开更多
Objective:To investigate the relationship among Pokemon,NF-κB p65 and Bcl-2 in hepatoma cells.Methods:HCC cell HepG2,SMMC7721 and human fetal liver cell line L02 cells were used,and expression of Pokemon,NF-κB p65 a...Objective:To investigate the relationship among Pokemon,NF-κB p65 and Bcl-2 in hepatoma cells.Methods:HCC cell HepG2,SMMC7721 and human fetal liver cell line L02 cells were used,and expression of Pokemon,NF-κB p65 and Bcl-2 in three cells were detected by realtime PCR and western blot.Then siRNA of Pokemon was applied to inhibit the expression of Pokemon and NF-κB p65 and apoptotic rate was determined by flow cytometric analysis. Results:Expressions of Pokemon,NF-κB p65 and Bcl-2 in human hepatoma cell HepG2, SMMC7721 expression were significantly higher than those in human embryonic stem cells L02. siRNA of Pokemon inhibited the expression of Pokemon,NF-κB p65 and Bcl-2 in liver cancer cells,and significantly increased apoptosis of liver cells.While siRNA of NF-κB n65 inhibited the expression of NF-κB p65 and Bcl-2,but Pokemon expression in hepatoma cells had no significant change.Conclusions:The proto-oncogene Pokemon can inhibit PI4ARF by specific transcription regulation of cell cycle and can induce tumors.In addition,Pokemon can regulate NF-κB p65 through the expression of apoptosis repressor,and promote the development of liver cancer.It suggests signal network in the liver include the regulation of new non-classical NF-κB regulatory pathway.展开更多
目的探讨弥漫性大B细胞淋巴瘤(diffuse large B cell lymphoma,DLBCL)组织核转录因子κB(nuclear factor-kappa B,NF-κB)/p65、Bcl-2和Bax蛋白表达及其对临床B症状、国际预后指数(international prognostic index,IPI)得分、临床分期...目的探讨弥漫性大B细胞淋巴瘤(diffuse large B cell lymphoma,DLBCL)组织核转录因子κB(nuclear factor-kappa B,NF-κB)/p65、Bcl-2和Bax蛋白表达及其对临床B症状、国际预后指数(international prognostic index,IPI)得分、临床分期等病理特征和预后的影响。方法组织标本来自于2012年3月至2015年2月我院接受手术治疗的78例DLBCL患者和30例反应增生性淋巴结患者,采用免疫组化方法比较DLBCL患者和反应增生性淋巴结患者淋巴组织NF-κB/p65、Bcl-2和Bax蛋白表达情况,分析它们与病理参数、生存期的关系。结果 DLBCL组织中,NF-κB/p65和Bcl-2阳性率分别为39.74%和51.28%,显著高于反应增生性淋巴结组织(P<0.05),Bax阳性率为32.05%,显著低于反应增生性淋巴结组织(P<0.05);DLBCL组织NF-κB/p65阳性表达与B症状、IPI得分、临床分期有关(P<0.05),Bcl-2阳性表达与IPI得分、临床分期有关(P<0.05),Bax阳性表达与临床分期有关(P<0.05);NF-κB/p65与Bcl-2呈正相关(r=0.53,P<0.05),NF-κB/p65与Bax呈负相关(r=-0.51,P<0.05),Bcl-2与Bax呈负相关(r=-0.62,P<0.05);NF-κB/p65、Bcl-2阳性表达者生存期较短,Bax阳性表达者生存期较长。结论DLBCL组织中NF-κB/p65、Bcl-2高表达,Bax低表达,有助于DLBCL预后评估。展开更多
Objective: To explore the underlying molecular mechanisms of cellular response to the challenge by 1-methyl-4-phenylpyridinium (MPP+)-induced apoptosis of PC12 cells, an in vitro cell model for Parkinson’s disease, a...Objective: To explore the underlying molecular mechanisms of cellular response to the challenge by 1-methyl-4-phenylpyridinium (MPP+)-induced apoptosis of PC12 cells, an in vitro cell model for Parkinson’s disease, and the effect of NF-κB activation on the protection of Parkinson’s disease by Isoflavone (I). Methods: PC12 cells were used to establish the cell model of Parkinson’s disease, and are divided into five groups: control group;MPP+ group;I (Isoflavone) + MPP+ group;I group;SN-50 + MPP+ group. The content of NF-κB in PC12 cells was determined by immunocytochemistry;The viability of PC12 cells after treated with cell-permeable NF-κB inhibitor SN-50 and cell viability were measured by MTT assay;the expression levels of NF-κB p65 in cytoplasm and nuclear fractions were evaluated by western blot analysis;the mRNA expression of NF-κB p65 was analyzed by in situ hybridization (ISH). Results: Compared with the control group, the protein of NF-κB p65 both in cytoplasm and in nuclei was significantly higher than in I + MPP+ and MPP+ groups;similarly, the mRNA expression level of NF-κB p65 gene was also significantly higher;moreover, the protein expression of NF-κB p65 was much lower in I group (P + group, the protein of NF-κB p65 was significantly lower in I + MPP+ group, the mRNA expression level of NF-κB p65 gene was also significantly lower, and the protein expression level of NF-κB p65 was much lower in I + MPP+ group (P + group (P > 0.05). Conclusion: NF-κB activation is essential to MPP+-induced apoptosis in PC12 cells;but Isoflavone can inhibit the cell damage to some extent to execute its protective function, which may be involved in nigral neurodegeneration in patients with Parkinson’s disease.展开更多
文摘White tea encompasses a number of teas unique to eastern Fujian in China. Although white tea extracts have been reported to result in cancer cell apoptosis, to date, few studies have evaluated the mechanism of such apoptotic induction. A transcription factor that plays a critical role in cell apoptosis, NF-κB p65, is also likely critical by which white tea extracts induce cancer cell apoptosis. In this study, white tea aqueous extract (WTAE) was added to BEL-7402 and Hela cell media and NF-κB p65 activation was evaluated using western blotting and immunofluorescence. Results revealed that the phosphorylation of IKBα and p65 decreased in both cell lines after WTAE treatment. And the nuclear translocation of NF-κB p65 in both cell lines was also reduced with the WTAE treatment. NF-κB p65 inhibition was noted to accelerate apoptosis. Our findings suggest that NF-κB p65 was an important modulator in WTAE-induced apoptotic signal transduction and it acted as a negative regulator of apoptotic induction in BEL-7402 and Hela cancer cell lines.
文摘Objective:To investigate the relationship among Pokemon,NF-κB p65 and Bcl-2 in hepatoma cells.Methods:HCC cell HepG2,SMMC7721 and human fetal liver cell line L02 cells were used,and expression of Pokemon,NF-κB p65 and Bcl-2 in three cells were detected by realtime PCR and western blot.Then siRNA of Pokemon was applied to inhibit the expression of Pokemon and NF-κB p65 and apoptotic rate was determined by flow cytometric analysis. Results:Expressions of Pokemon,NF-κB p65 and Bcl-2 in human hepatoma cell HepG2, SMMC7721 expression were significantly higher than those in human embryonic stem cells L02. siRNA of Pokemon inhibited the expression of Pokemon,NF-κB p65 and Bcl-2 in liver cancer cells,and significantly increased apoptosis of liver cells.While siRNA of NF-κB n65 inhibited the expression of NF-κB p65 and Bcl-2,but Pokemon expression in hepatoma cells had no significant change.Conclusions:The proto-oncogene Pokemon can inhibit PI4ARF by specific transcription regulation of cell cycle and can induce tumors.In addition,Pokemon can regulate NF-κB p65 through the expression of apoptosis repressor,and promote the development of liver cancer.It suggests signal network in the liver include the regulation of new non-classical NF-κB regulatory pathway.
文摘目的探讨弥漫性大B细胞淋巴瘤(diffuse large B cell lymphoma,DLBCL)组织核转录因子κB(nuclear factor-kappa B,NF-κB)/p65、Bcl-2和Bax蛋白表达及其对临床B症状、国际预后指数(international prognostic index,IPI)得分、临床分期等病理特征和预后的影响。方法组织标本来自于2012年3月至2015年2月我院接受手术治疗的78例DLBCL患者和30例反应增生性淋巴结患者,采用免疫组化方法比较DLBCL患者和反应增生性淋巴结患者淋巴组织NF-κB/p65、Bcl-2和Bax蛋白表达情况,分析它们与病理参数、生存期的关系。结果 DLBCL组织中,NF-κB/p65和Bcl-2阳性率分别为39.74%和51.28%,显著高于反应增生性淋巴结组织(P<0.05),Bax阳性率为32.05%,显著低于反应增生性淋巴结组织(P<0.05);DLBCL组织NF-κB/p65阳性表达与B症状、IPI得分、临床分期有关(P<0.05),Bcl-2阳性表达与IPI得分、临床分期有关(P<0.05),Bax阳性表达与临床分期有关(P<0.05);NF-κB/p65与Bcl-2呈正相关(r=0.53,P<0.05),NF-κB/p65与Bax呈负相关(r=-0.51,P<0.05),Bcl-2与Bax呈负相关(r=-0.62,P<0.05);NF-κB/p65、Bcl-2阳性表达者生存期较短,Bax阳性表达者生存期较长。结论DLBCL组织中NF-κB/p65、Bcl-2高表达,Bax低表达,有助于DLBCL预后评估。
文摘Objective: To explore the underlying molecular mechanisms of cellular response to the challenge by 1-methyl-4-phenylpyridinium (MPP+)-induced apoptosis of PC12 cells, an in vitro cell model for Parkinson’s disease, and the effect of NF-κB activation on the protection of Parkinson’s disease by Isoflavone (I). Methods: PC12 cells were used to establish the cell model of Parkinson’s disease, and are divided into five groups: control group;MPP+ group;I (Isoflavone) + MPP+ group;I group;SN-50 + MPP+ group. The content of NF-κB in PC12 cells was determined by immunocytochemistry;The viability of PC12 cells after treated with cell-permeable NF-κB inhibitor SN-50 and cell viability were measured by MTT assay;the expression levels of NF-κB p65 in cytoplasm and nuclear fractions were evaluated by western blot analysis;the mRNA expression of NF-κB p65 was analyzed by in situ hybridization (ISH). Results: Compared with the control group, the protein of NF-κB p65 both in cytoplasm and in nuclei was significantly higher than in I + MPP+ and MPP+ groups;similarly, the mRNA expression level of NF-κB p65 gene was also significantly higher;moreover, the protein expression of NF-κB p65 was much lower in I group (P + group, the protein of NF-κB p65 was significantly lower in I + MPP+ group, the mRNA expression level of NF-κB p65 gene was also significantly lower, and the protein expression level of NF-κB p65 was much lower in I + MPP+ group (P + group (P > 0.05). Conclusion: NF-κB activation is essential to MPP+-induced apoptosis in PC12 cells;but Isoflavone can inhibit the cell damage to some extent to execute its protective function, which may be involved in nigral neurodegeneration in patients with Parkinson’s disease.