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目的研究宿主细胞感染马尔尼菲青霉后细胞凋亡、凋亡途径与该菌胞内寄生的相关性。方法马尔尼菲青霉接种于小鼠腹腔内,采用流式细胞术检测4 h、36h的小鼠腹腔细胞凋亡率,用RT-PCR法测定Capase-3、Mcl-1的mRNA水平。结果小鼠腹腔内的炎症细胞凋亡率实验组4h是10.22±3.12,36h是8.22±2.64;空白组4h是23.91±4.10,36h是27.72±8.70;凋亡因子Caspase-3的mRNA的表达量实验组4h是0.65±0.04,36h是0.53±0.02,Mcl-1的mRNA的表达量实验组4h是0.81±0.06,36h是0.92±0.06,与空白组比较其4h、36h均有显著差异性(P<0.05);各组内4h与36h间无明显差异(P>0.05)。结论马尔尼菲青霉可能通过下调Caspase-3 mRNA表达及增加Mcl-1的mRNA表达,从而导致宿主细胞凋亡减少,这可能是马尔尼菲青霉得以存活并随宿主细胞游走播散的致病机制之一。
Objective To study the apoptosis of host cells infected with Penicillium marneffei and the correlation between the apoptosis pathway and intracellular parasitism. Methods Penicillium marneffei was inoculated intraperitoneally in mice. Flow cytometry was used to detect the apoptosis rate of peritoneal cells in 4 and 36 hours. The mRNA levels of Capase-3 and Mcl-1 were detected by RT-PCR. Results The apoptosis rate of inflammatory cells in mice peritoneal cavity was 10.22 ± 3.12 in 4h and 8.22 ± 2.64 in experimental group, 23.91 ± 4.10 in 4h and 27.72 ± 8.70 in control group, respectively. The mRNA expression of Caspase-3 The experimental group 4h was 0.65 ± 0.04,36h was 0.53 ± 0.02, Mcl-1 mRNA expression in the experimental group 4h was 0.81 ± 0.06, 36h was 0.92 ± 0.06, compared with the blank group 4h, 36h were significantly different ( P <0.05). There was no significant difference between 4h and 36h in each group (P> 0.05). Conclusion Penicillium marneffei may reduce the apoptosis of host cells by downregulating the expression of Caspase-3 mRNA and increasing the mRNA expression of Mcl-1, which may be caused by the survival of Penicillium marneffei and its spread with host cells One of the pathogenic mechanisms.