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Fas/Fas配体途径并不介导小鼠弹性蛋白酶诱导的肺气肿中的细胞凋亡。

The Fas/Fas-ligand pathway does not mediate the apoptosis in elastase-induced emphysema in mice.

作者信息

Sawada Masahiro, Ohno Yasushi, La Bu Lin Bai, Funaguchi Norihiko, Asai Toshihiro, Yuhgetsu Hideyuki, Takemura Genzou, Minatoguchi Shinya, Fujiwara Hisayoshi, Fujiwara Takako

机构信息

Second Department of Internal Medicine, Regeneration and Advanced Medical Science, Graduate School of Medicine, Gifu University, Gifu, Japan.

出版信息

Exp Lung Res. 2007 Aug;33(6):277-88. doi: 10.1080/01902140701509458.

Abstract

Porcine pancreatic elastase (PPE), which induces emphysema via apoptosis, was administered to wild-type and Fas-deficient (lpr) mice. On days 3 and 28 after administration, the mean linear intercepts within lung tissues were significantly higher in PPE-treated wild-type and lpr mice than in control mice, though there were no significant differences between the PPE-treated groups. Likewise, the numbers of TUNEL-positive cells were increased in the lungs of PPE-treated wild-type and lpr mice, and again the effect was similar in the two PPE-treated groups. These findings suggest that apoptosis associated with PPE-induced emphysema is not mediated via the Fas/Fas-ligand pathway.

摘要

通过凋亡诱导肺气肿的猪胰腺弹性蛋白酶(PPE)被施用于野生型和Fas缺陷(lpr)小鼠。给药后第3天和第28天,PPE处理的野生型和lpr小鼠肺组织内的平均线性截距显著高于对照小鼠,尽管PPE处理组之间没有显著差异。同样,PPE处理的野生型和lpr小鼠肺中TUNEL阳性细胞数量增加,并且在两个PPE处理组中效果再次相似。这些发现表明,与PPE诱导的肺气肿相关的凋亡不是通过Fas/Fas配体途径介导的。

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