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Apoptotic genes expression in mice hepatocytes during malaria infection

机译:疟疾感染小鼠肝细胞凋亡基因的表达。

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Malaria represents a major global health problem by causing multi-cellular dysfunctions in the infected host. The aim of the present study was to investigate the apoptotic gene expression in liver of mice during malaria disease by mRNA expression of three genes involved in apoptosis; Bax, Bcl-2 and Caspase-3 and other parameters at different time points after infection with Plasmodium chabaudi in the liver cells of female C57BL/6 mice. Mice were injected intraperitoneally (ip) with 10 6 P. chabaudi -infected erythrocytes and then scarified at days (0, 1, 4 and 8, respectively). Quantitative real-time PCR and immunoblotting were used to quantify apoptotic genes and protein kinetic, respectively. The levels of Bax, Bcl-2 and Caspase-3 were significantly ( P 0.05) increased only at days 1 and 8 compared with day 0 in both the liver cells and protein. The levels of parasitemia was significantly ( P 0.01) increased at day 8 compared with day 0 in the blood. These results have shown that P. chabaudi induced apoptosis in the liver cells. Thus, this study suggests that the induced apoptotic gene expression was due to the out come of malaria.
机译:疟疾在受感染的宿主中引起多细胞功能障碍,这是一个主要的全球性健康问题。本研究的目的是通过三个参与凋亡的基因的mRNA表达来研究疟疾小鼠在肝脏中的凋亡基因表达。雌性C57BL / 6小鼠肝细胞中的沙巴氏疟原虫感染后不同时间点的Bax,Bcl-2和Caspase-3等参数。给小鼠腹膜内(ip)注射感染了10 6沙巴氏杆菌的红细胞,然后在第几天(分别为0、1、4和8)将其清除。实时定量PCR和免疫印迹分别用于定量凋亡基因和蛋白质动力学。肝细胞和蛋白质中,与第0天相比,仅在第1天和第8天,Bax,Bcl-2和Caspase-3的水平显着增加(P <0.05)。与血液中的第0天相比,第8天的寄生虫血症水平显着增加(P <0.01)。这些结果表明,沙巴假单胞菌诱导肝细胞凋亡。因此,该研究表明诱导的凋亡基因表达是由于疟疾的发作。

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