Thymoquinone (Tq) protects necroptosis induced by autophagy/mitophagy‐dependent oxidative stress in human bronchial epithelial cells exposed to cigarette smoke extract (CSE).
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| Title: | Thymoquinone (Tq) protects necroptosis induced by autophagy/mitophagy‐dependent oxidative stress in human bronchial epithelial cells exposed to cigarette smoke extract (CSE). |
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| Authors: | Dera, Ayed A.1,2 (AUTHOR), Al Fayi, Majed1,2 (AUTHOR), Otifi, Hassan3 (AUTHOR), Alshyarba, Mishari4 (AUTHOR), Alfhili, Mohammad5 (AUTHOR), Rajagopalan, Prasanna1,2 (AUTHOR) prachu.rg@gmail.com |
| Source: | Journal of Food Biochemistry. Sep2020, Vol. 44 Issue 9, p1-11. 11p. |
| Subjects: | Cigarette smoke, Epithelial cells, Obstructive lung diseases, Oxidative stress, Black cumin, Mitochondrial membranes |
| Abstract: | 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, GR, 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. Practical applications: This study demonstrates Thymoquinone (Tq), a natural plant extract to possess protective properties against human bronchial epithelial cell autophagy/mitophagy‐dependent necroptosis caused by cigarette smoke extract. The demonstrated efficacy of Tq will throw light for further preclinical evaluation of this molecule in CSE‐mediated complications. A detailed in vivo research is recommended. [ABSTRACT FROM AUTHOR] |
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| Database: | Engineering Source |
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| Abstract: | 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, GR, 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. Practical applications: This study demonstrates Thymoquinone (Tq), a natural plant extract to possess protective properties against human bronchial epithelial cell autophagy/mitophagy‐dependent necroptosis caused by cigarette smoke extract. The demonstrated efficacy of Tq will throw light for further preclinical evaluation of this molecule in CSE‐mediated complications. A detailed in vivo research is recommended. [ABSTRACT FROM AUTHOR] |
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| ISSN: | 01458884 |
| DOI: | 10.1111/jfbc.13366 |
