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姜黄素通过激活 NRF2/抗氧化反应元件通路保护 BEAS-2B 细胞免受 PM 诱导的氧化应激和炎症。

Curcumin protects BEAS‑2B cells from PM‑induced oxidative stress and inflammation by activating NRF2/antioxidant response element pathways.

机构信息

Department of Pulmonary and Critical Care Medicine, Wuhan No. 1 Hospital, Wuhan, Hubei 430000, P.R. China.

出版信息

Int J Mol Med. 2021 Apr;47(4). doi: 10.3892/ijmm.2021.4878. Epub 2021 Feb 8.

Abstract

Fine particulate matter (PM) with an average aerodynamic diameter of <2.5 µm can cause severe lung injury. Oxidative stress and inflammation are considered the main outcomes of PM exposure. Curcumin is a well‑known antioxidant; however, its effect on PM‑induced oxidative injury in airway epithelial cells remains unclear. In the present study, it was demonstrated that pre‑treatment with curcumin significantly reduced the PM‑induced apoptosis of BEAS‑2B human bronchial epithelial cells by decreasing the level of intercellular reactive oxygen species. Western blot analysis revealed that curcumin increased the expression of nuclear factor erythroid 2‑related factor 2 (NRF2) and regulated the transcription of downstream genes, particularly those encoding antioxidant enzymes. Moreover, curcumin reduced the PM‑induced expression and production of inflammatory factors, and induced the expression of the anti‑inflammatory factors, interleukin (IL)‑5 and IL‑13. Taken together, the present study demonstrates that curcumin protects BEAS‑2B cells against PM‑induced oxidative damage and inflammation, and prevents cell apoptosis by increasing the activation of NRF2‑related pathways. It is thus suggested that curcumin may be a potential compound for use in the prevention of PM‑induced tissue injury.

摘要

细颗粒物(PM)的平均空气动力学直径小于 2.5µm,可导致严重的肺部损伤。氧化应激和炎症被认为是 PM 暴露的主要后果。姜黄素是一种众所周知的抗氧化剂;然而,其对气道上皮细胞中 PM 诱导的氧化损伤的影响尚不清楚。在本研究中,研究表明姜黄素通过降低细胞间活性氧的水平,显著减少 PM 诱导的 BEAS-2B 人支气管上皮细胞凋亡。Western blot 分析显示,姜黄素增加了核因子红细胞 2 相关因子 2(NRF2)的表达,并调节下游基因的转录,特别是那些编码抗氧化酶的基因。此外,姜黄素降低了 PM 诱导的炎症因子的表达和产生,并诱导抗炎因子白细胞介素(IL)-5 和 IL-13 的表达。综上所述,本研究表明姜黄素通过增加 NRF2 相关途径的激活,保护 BEAS-2B 细胞免受 PM 诱导的氧化损伤和炎症,并防止细胞凋亡。因此,姜黄素可能是预防 PM 诱导的组织损伤的潜在化合物。

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