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Bax抑制肽减轻博来霉素诱导的小鼠肺损伤。

Bax-inhibiting peptide attenuates bleomycin-induced lung injury in mice.

作者信息

Suzuki Kunihiro, Yanagihara Toyoshi, Yokoyama Tetsuya, Maeyama Takashige, Ogata-Suetsugu Saiko, Arimura-Omori Masako, Mikumo Hironori, Hamada Naoki, Harada Eiji, Kuwano Kazuyoshi, Harada Taishi, Nakanishi Yoichi

机构信息

Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.

Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan

出版信息

Biol Open. 2017 Dec 15;6(12):1869-1875. doi: 10.1242/bio.026005.

DOI:10.1242/bio.026005
PMID:29138212
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5769644/
Abstract

Bax is a pro-apoptotic member of the Bcl-2 family of proteins, and plays a central role in mitochondria-dependent apoptosis. Several lines of evidence have implied that Bax is involved in both epithelial apoptosis and fibroblast proliferation in idiopathic pulmonary fibrosis; however, the mechanisms remain unknown. Bax-inhibiting peptide V5 (BIP-V5) exhibits membrane permeability and inhibits the activation of Bax.The purpose of this study was to investigate whether the control of Bax activity by BIP-V5 reduces the degree of bleomycin-induced lung injury. C57BL/6J mice were administered bleomycin and BIP-V5 intratracheally on day 0. Bronchoalveolar lavage fluid and lung tissue were obtained on day 7. Human pulmonary alveolar epithelial cells (A549 cells) and mouse pulmonary alveolar epithelial cells (LA-4 cells) were stimulated with bleomycin to induce apoptosis.Administration of BIP-V5 improved the survival rate and degree of bleomycin-induced lung injury by suppressing Bax activation in mice. BIP-V5 treatment decreased bleomycin-induced apoptosis of alveolar epithelial cell lines (A549 cells and LA-4 cells) by suppressing Bax activation. These results indicate that administration of BIP-V5 may constitute a novel therapeutic strategy against lung injury.

摘要

Bax是Bcl-2蛋白家族中的一种促凋亡成员，在依赖线粒体的细胞凋亡中起核心作用。多项证据表明，Bax参与了特发性肺纤维化中的上皮细胞凋亡和成纤维细胞增殖；然而，其机制仍不清楚。Bax抑制肽V5（BIP-V5）具有膜通透性，并能抑制Bax的激活。本研究的目的是探讨BIP-V5对Bax活性的调控是否能减轻博来霉素诱导的肺损伤程度。在第0天对C57BL/6J小鼠气管内给予博来霉素和BIP-V5。在第7天获取支气管肺泡灌洗液和肺组织。用博来霉素刺激人肺泡上皮细胞（A549细胞）和小鼠肺泡上皮细胞（LA-4细胞）以诱导细胞凋亡。给予BIP-V5可通过抑制小鼠体内Bax的激活来提高博来霉素诱导的肺损伤的存活率和减轻损伤程度。BIP-V5处理通过抑制Bax激活降低了博来霉素诱导的肺泡上皮细胞系（A549细胞和LA-4细胞）的凋亡。这些结果表明，给予BIP-V5可能构成一种针对肺损伤的新型治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/5769644/6f0df103d8d4/biolopen-6-026005-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/5769644/3e00dc8080a6/biolopen-6-026005-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/5769644/7ef6ee13ceae/biolopen-6-026005-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/5769644/8510dc9cb097/biolopen-6-026005-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/5769644/0d414a1f9d71/biolopen-6-026005-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/5769644/f18d45445312/biolopen-6-026005-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/5769644/6f0df103d8d4/biolopen-6-026005-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/5769644/3e00dc8080a6/biolopen-6-026005-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/5769644/7ef6ee13ceae/biolopen-6-026005-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/5769644/8510dc9cb097/biolopen-6-026005-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/5769644/0d414a1f9d71/biolopen-6-026005-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/5769644/f18d45445312/biolopen-6-026005-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/5769644/6f0df103d8d4/biolopen-6-026005-g6.jpg

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本文引用的文献

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Nat Rev Mol Cell Biol. 2014 Jan;15(1):49-63. doi: 10.1038/nrm3722.
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Building blocks of the apoptotic pore: how Bax and Bak are activated and oligomerize during apoptosis.凋亡孔的组成元件：Bax和Bak在凋亡过程中如何被激活并寡聚化。
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Prednisone, azathioprine, and N-acetylcysteine for pulmonary fibrosis.
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泼尼松、硫唑嘌呤和N-乙酰半胱氨酸治疗肺纤维化。
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