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霍诺醇通过 SIRT3/SOD2 信号通路改善香烟烟雾诱导的气道上皮细胞损伤。

Honokiol ameliorates cigarette smoke-induced damage of airway epithelial cells via the SIRT3/SOD2 signalling pathway.

机构信息

Department of Pulmonary and Critical Care Medicine, Shanxi Provincial People's Hospital, Taiyuan, China.

The Fifth Clinical Medical College of Shanxi Medical University, Taiyuan, China.

出版信息

J Cell Mol Med. 2023 Dec;27(24):4009-4020. doi: 10.1111/jcmm.17981. Epub 2023 Oct 5.

Abstract

Cigarette smoking can cause damage of airway epithelial cells and contribute to chronic obstructive pulmonary disease (COPD). Honokiol is originally isolated from Magnolia obovata with multiple biological activities. Here, we investigated the protective effects of honokiol on cigarette smoke extract (CSE)-induced injury of BEAS-2B cells. BEAS-2B cells were treated with 300 mg/L CSE to construct an in vitro cell injury model, and cells were further treated with 2, 5 and 10 μM honokiol, then cell viability and LDH leakage were analysed by CCK-8 and LDH assay kits, respectively. Apoptosis was detected by flow cytometry analysis. ELISA was used to measure the levels of tumour necrosis factor (TNF)-ɑ, IL-1β, IL-6, IL-8 and MCP-1. The results showed that honokiol (0.5-20 μM) showed non-toxic effects on BEAS-2B cells. Treatment with honokiol (2, 5 and 10 μM) reduced CSE (300 mg/L)-induced decrease in cell viability and apoptosis in BEAS-2B cells. Honokiol also decreased CSE-induced inflammation through inhibiting expression and secretion of inflammatory cytokines, such as TNF-ɑ, IL-1β, IL-6, IL-8 and MCP-1. Moreover, honokiol repressed CSE-induced reactive oxygen species (ROS) production, decrease of ATP content and mitochondrial biogenesis, as well as mitochondrial membrane potential. Mechanistically, honokiol promoted the expression of SIRT3 and its downstream target genes, which are critical regulators of mitochondrial function and oxidative stress. Silencing of SIRT3 reversed the protective effects of honokiol on CSE-induced damage and mitochondrial dysfunction in BEAS-2B cells. These results indicated that honokiol attenuated CSE-induced damage of airway epithelial cells through regulating SIRT3/SOD2 signalling pathway.

摘要

吸烟会导致气道上皮细胞损伤,并促成慢性阻塞性肺疾病(COPD)。和厚朴酚最初从厚朴中分离出来,具有多种生物学活性。本研究旨在探讨和厚朴酚对香烟烟雾提取物(CSE)诱导的 BEAS-2B 细胞损伤的保护作用。用 300mg/L 的 CSE 处理 BEAS-2B 细胞构建体外细胞损伤模型,用 2、5 和 10μM 的和厚朴酚处理细胞,然后用 CCK-8 和 LDH 试剂盒分别分析细胞活力和 LDH 漏出情况,用流式细胞术检测细胞凋亡,用 ELISA 法检测肿瘤坏死因子(TNF)-ɑ、IL-1β、IL-6、IL-8 和 MCP-1 的水平。结果表明,0.5-20μM 的和厚朴酚对 BEAS-2B 细胞无毒性作用。用 2、5 和 10μM 的和厚朴酚处理能减轻 CSE(300mg/L)诱导的 BEAS-2B 细胞活力下降和凋亡。和厚朴酚还能通过抑制 TNF-ɑ、IL-1β、IL-6、IL-8 和 MCP-1 等炎症细胞因子的表达和分泌,减轻 CSE 诱导的炎症。此外,和厚朴酚抑制了 CSE 诱导的活性氧(ROS)产生、ATP 含量减少和线粒体生物发生以及线粒体膜电位降低。机制上,和厚朴酚促进了 SIRT3 及其下游靶基因的表达,SIRT3 及其下游靶基因是线粒体功能和氧化应激的关键调节因子。沉默 SIRT3 逆转了和厚朴酚对 CSE 诱导的 BEAS-2B 细胞损伤和线粒体功能障碍的保护作用。这些结果表明,和厚朴酚通过调节 SIRT3/SOD2 信号通路减轻 CSE 诱导的气道上皮细胞损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e822/10746946/e71f1d27d6dd/JCMM-27-4009-g004.jpg

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