Chronic obstructive pulmonary disease (COPD) is characterized by cigarette smoke‐induced emphysema. Herein, we demonstrate protective effects of Thymoquinone (Tq), an active constituent from Nigella sativa, against cigarette smoke extract (CSE)‐induced abnormalities in bronchial epithelial cells. Dose‐dependent reduction in cell viability was observed in BEAS‐2B cells when exposed to different CSE concentrations, which was significantly reversed by Tq evident by LDH release. Levels of SOD, CAT, G_R, GSH, and mitochondrial membrane ATPases were significantly reduced upon CSE exposure, an event, again, antagonized in presence of Tq. Similarly, Tq treatment significantly blocked CSE‐induced 4HNE elevations. Further, Tq‐improved mitochondrial dysfunction caused by CSE and significantly decreased autophagy/mitophagy markers like LC3II and p‐Drp. Tq also reduced necroptosis markers such as p‐MLKL, RIP‐1, and RIP‐3, by stabilizing PINK‐1 levels. In summary, Tq possesses protective properties against human bronchial epithelial cell autophagy/mitophagy‐dependent necroptosis caused by CSE, which warrants considerable attention for further preclinical evaluations.

中文翻译：

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胸腺醌（Tq）保护暴露于香烟烟雾提取物（CSE）的人支气管上皮细胞中自噬/有丝分裂依赖的氧化应激诱导的坏死病。

慢性阻塞性肺疾病（COPD）的特征是香烟烟雾引起的肺气肿。在本文中，我们证明了百里香（Nigella sativa）的活性成分胸腺醌（Tq）对香烟烟雾提取物（CSE）诱导的支气管上皮细胞异常的保护作用。当暴露于不同的CSE浓度时，在BEAS-2B细胞中观察到剂量依赖性的细胞活力降低，而LDH释放可明显通过Tq逆转。SOD，CAT，G _R的水平CSE暴露后，GSH，GSH和线粒体膜ATP酶显着降低，这再次在Tq存在下被拮抗。同样，Tq治疗显着阻断了CSE诱导的4HNE升高。此外，Tq改善了CSE引起的线粒体功能障碍，并显着降低了自噬/线粒体标记物，如LC3II和p-Drp。通过稳定PINK-1的水平，Tq还减少了诸如p-MLKL，RIP-1和RIP-3的坏死病标记。总之，Tq对CSE引起的人支气管上皮细胞自噬/线粒体依赖性坏死病具有保护作用，值得进一步临床前评估。