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再次感染华支睾吸虫并再次接受吡喹酮治疗的仓鼠中凋亡相关基因的表达

Apoptosis-related gene expressions in hamsters re-infected with Opisthorchis viverrini and re-treated with praziquantel.

作者信息

Boonmars T, Srisawangwong T, Srirach P, Kaewsamut B, Pinlaor S, Sithithaworn P

机构信息

Department of Parasitology, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand.

出版信息

Parasitol Res. 2007 Dec;102(1):57-62. doi: 10.1007/s00436-007-0724-3. Epub 2007 Sep 13.

Abstract

Our objective was to reveal whether host immune response in hamster opisthorchiasis post-praziquantel treatment could induce apoptotic cell death in inflammatory cells. We, therefore, investigated apoptosis-related gene expression in hamsters re-infected with Opisthorchis viverrini (OV) and re-treated with praziquantel. Hamsters were re-infected with OV metacercariae then re-treated with praziquantel. The expression of apoptosis-related genes (i.e. apoptosis gene Bcl-2 associated protein X [BAX], caspase 9, p53 and protein kinase B [PKB]) was detected by real-time reverse transcription-polymerase chain reaction. Histopathological analyses of liver tissues were performed by staining the sections with haematoxylin and eosin using light microscopy. The results show that BAX, Akt/PKB, p53 and caspase 9 expression levels were significantly increased on day 30 post-infection and at 6 h post-treatment and gradually decreased to a level near the uninfected control and at 24 h post-treatment, perhaps because of a decrease in inflammatory cells. Apoptotic cell death was observed at the nuclei of epithelial cells of the bile ducts and of T cells. Our results suggest that repeated infection with OV and re-treatment with praziquantel induces a host immune response that increases inflammatory cells, which in turn leads to increase, apoptosis-related gene expression in the short term post-treatment.

摘要

我们的目的是揭示在吡喹酮治疗后的仓鼠华支睾吸虫病中,宿主免疫反应是否能诱导炎症细胞发生凋亡性细胞死亡。因此,我们研究了再次感染华支睾吸虫(OV)并再次接受吡喹酮治疗的仓鼠中凋亡相关基因的表达情况。仓鼠再次感染OV尾蚴后,再用吡喹酮进行治疗。通过实时逆转录聚合酶链反应检测凋亡相关基因(即凋亡基因Bcl-2相关蛋白X [BAX]、半胱天冬酶9、p53和蛋白激酶B [PKB])的表达。肝组织切片用苏木精和伊红染色后,使用光学显微镜进行组织病理学分析。结果显示,感染后第30天和治疗后6小时,BAX、Akt/PKB、p53和半胱天冬酶9的表达水平显著升高,在治疗后24小时逐渐降至接近未感染对照组的水平,这可能是由于炎症细胞减少所致。在胆管上皮细胞和T细胞的细胞核中观察到凋亡性细胞死亡。我们的结果表明,再次感染OV并再次用吡喹酮治疗会诱导宿主免疫反应,增加炎症细胞,进而导致治疗后短期内凋亡相关基因表达增加。

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