依贝地农和peimisine可抑制香烟烟雾提取物诱导的BEAS-2B细胞氧化应激损伤和凋亡。

IF 3.3 3区 生物学 Q3 CELL BIOLOGY
Chuanlan Liu , Xiaomu Zhu , Erbu Aga , Wai Ming Tse , Kathy Wai Gaun Tse , Yanyong Liu , Bengui Ye
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引用次数: 0

摘要

Ebeiedinone 和 peimisine 是 Fritillariae Cirrhosae Bulbus 的主要活性成分。在本研究中,我们考察了这两种异甾体生物碱如何保护人支气管上皮 BEAS-2B 细胞免受香烟烟雾提取物(CSE)引起的氧化应激和细胞凋亡。首先,利用 CCK8 试验测定了细胞毒性,并建立了氧化应激模型。然后通过酶联免疫吸附试验、流式细胞术和 Western 印迹法研究了烟草烟雾提取物的抗氧化活性和机制。通过 CCK-8 检测法,暴露于 CSE(20%、40% 和 100%)会降低 BEAB-2S 细胞的活力。流式细胞术的结果表明,CSE 诱导了 ROS 的产生(0.5% 至最大值),而 10μM 依贝地农和 20μM 培米星的处理可减轻 ROS 的产生。Western印迹检测结果表明,依贝酮和培米星通过NRF2/KEAP1和JNK/MAPK依赖途径抑制ROS,上调SOD和GSH/GSSG,下调MDA、4-HNE和8-OHdG,从而减少CSE诱导的氧化应激、DNA损伤、细胞凋亡和自噬失调,从而延缓CS导致的慢性阻塞性肺病的病理进展。我们的数据表明,CSE 会导致 BEAS-2B 细胞氧化应激、DNA 损伤和细胞凋亡,并导致慢性阻塞性肺病的进展。依贝地农和peimisine通过抑制自噬失调和细胞凋亡来对抗CSE诱导的慢性阻塞性肺病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Ebeiedinone and peimisine inhibit cigarette smoke extract-induced oxidative stress injury and apoptosis in BEAS-2B cells

Ebeiedinone and peimisine inhibit cigarette smoke extract-induced oxidative stress injury and apoptosis in BEAS-2B cells
Ebeiedinone and peimisine are the major active ingredients of Fritillariae Cirrhosae Bulbus. In this study, we looked at how these two forms of isosteroidal alkaloids protect human bronchial epithelial BEAS-2B cells from oxidative stress and apoptosis caused by cigarette smoke extract (CSE). First, the cytotoxicity was determined using the CCK8 assay, and an oxidative stress model was established. Then the antioxidative stress activity and mechanism were investigated by ELISA, flow cytometry, and Western blotting. By the CCK-8 assay, exposure to CSE (20%, 40%, and 100%) reduced the viability of BEAB-2S cells. The flow cytometry findings indicated that CSE-induced production of ROS (0.5% to maximum) and treatments with 10 μM ebeiedinone and 20 μM peimisine attenuated the production of ROS. The western blot assay results indicate that ebeiedinone and peimisine reduce CSE-induced oxidative stress, DNA damage, apoptosis, and autophagy dysregulation by inhibiting ROS, upregulating SOD and GSH/GSSG, and downregulating MDA, 4-HNE, and 8-OHdG through the NRF2/KEAP1 and JNK/MAPK-dependent pathways, thereby delaying the pathological progression of COPD caused by CS.Our data suggest that CSE causes oxidative stress, DNA damage, and apoptosis in BEAS-2B cells, as well as the progression of COPD. Ebeiedinone and peimisine fight CS-induced COPD by suppressing autophagy deregulation and apoptosis.
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来源期刊
Cell Stress & Chaperones
Cell Stress & Chaperones 生物-细胞生物学
CiteScore
7.60
自引率
2.60%
发文量
59
审稿时长
6-12 weeks
期刊介绍: Cell Stress and Chaperones is an integrative journal that bridges the gap between laboratory model systems and natural populations. The journal captures the eclectic spirit of the cellular stress response field in a single, concentrated source of current information. Major emphasis is placed on the effects of climate change on individual species in the natural environment and their capacity to adapt. This emphasis expands our focus on stress biology and medicine by linking climate change effects to research on cellular stress responses of animals, micro-organisms and plants.
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