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在病毒诱导的急性肝衰竭动物模型中细胞凋亡的死亡观察-GI.2 感染期间。

Apoptotic Cell Death in an Animal Model of Virus-Induced Acute Liver Failure-Observations during /GI.2 Infection.

机构信息

Institute of Biology, University of Szczecin, Felczaka 3c, 71-412 Szczecin, Poland.

Department of Histology and Embryology, Faculty of Medicine and Dentistry, Pomeranian Medical University in Szczecin, Powstańców Wlkp. 72, 70-111 Szczecin, Poland.

出版信息

Int J Mol Sci. 2024 Jan 8;25(2):798. doi: 10.3390/ijms25020798.

DOI:10.3390/ijms25020798
PMID:38255873
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10815770/
Abstract

/GI.2 causes severe and highly fatal Rabbit Hemorrhagic Disease (RHD). Because of its characteristics, this infection is used as an animal model for acute liver failure (ALF). Apoptosis is one of the key processes underlying ALF and has been described as one of the mechanisms of RHD pathogenesis. Apoptotic cell death has been quite well characterized in infection with different variants of GI.1 strains, but so far, the GI.2 genotype has not been widely studied. In this study, we performed an evaluation of apoptotic cell death in hepatocytes of rabbits infected with /GI.2. We analyzed the expression of genes involved in apoptotic cell death by real-time PCR and performed immunohistochemical (IHC) assays. We showed a significant increase in the expression of and the proapoptotic and anti-apoptotic in infected animals. In addition, we recorded increased / ratios. IHC analyses showed the presence of morphological signs of apoptosis in the hepatocytes of infected rabbits. Our results indicate that caspase-3 and proteins from the Bcl-2 families play a key role in apoptosis induced by /GI.2 infection.

摘要

/GI.2 可引起严重且致命性极高的兔出血症(RHD)。由于其特征,这种感染被用作急性肝衰竭(ALF)的动物模型。细胞凋亡是 ALF 发病机制的关键过程之一,被描述为 RHD 发病机制之一。不同 GI.1 株变体感染中的凋亡细胞死亡已得到很好的描述,但迄今为止,GI.2 基因型尚未得到广泛研究。在这项研究中,我们评估了感染 /GI.2 的兔肝细胞中的凋亡细胞死亡。我们通过实时 PCR 分析了参与细胞凋亡的基因的表达,并进行了免疫组织化学(IHC)检测。结果显示,感染动物中 和 的表达显著增加, 和 的促凋亡和抗凋亡作用增强。此外,我们记录了 / 比值的增加。IHC 分析显示感染兔肝细胞中存在凋亡的形态学迹象。我们的结果表明,半胱氨酸天冬氨酸蛋白酶-3 和 Bcl-2 家族蛋白在 /GI.2 感染诱导的细胞凋亡中起关键作用。

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