Journal of traditional and complementary medicine · 2025
Cinnamaldehyde inhibits the NLRP3 inflammasome and inflammatory response by reducing oxidative stress in Neisseria gonorrhoeae-infected macrophages.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Hua Kuo-Feng, Chiu Hsiao-Wen, Chen Miao-Mei, Wong Wei-Ting, Tsai Wen-Chiuan, Lin Wen-Yu, Wu Chun-Hsien, Wang Chien-Chun, Hsu Chung-Hua, Chernikov Oleg V, Rao Yerra Koteswara, Hsu Hsien-Ta, Ho Chen-Lung, Li Lan-Hui
Аннотация
BACKGROUND AND AIM: Gonorrhoea, a common sexually transmitted disease, is caused by Neisseria gonorrhoeae. The NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome regulates interleukin (IL)-1β and IL-18 secretion via caspase-1 activation and plays a critical role in inflammation. Dysregulation of the NLRP3 inflammasome contributes to various diseases, making it a promising therapeutic target. We previously showed that N. gonorrhoeae activates the NLRP3 inflammasome in macrophages. This study aimed to explore the anti-inflammatory potential of cinnamaldehyde (CA), the major aldehyde in Cinnamomum osmophloeum Kaneh essential oil, in N. gonorrhoeae-infected macrophages.
EXPERIMENTAL PROCEDURE: Protein expression was assessed by ELISA and Western blotting. Intracellular H2O2, mitochondrial reactive oxygen species, and membrane integrity were evaluated with fluorescent probes and flow cytometry. NF-κB activity was measured using reporter cells. Cell viability and bacterial survival were determined by lactate dehydrogenase release and colony forming unit counts, respectively. Bacterial morphology was examined via scanning electron microscopy.
RESULTS AND CONCLUSION: CA inhibited caspase-1 activation and reduced IL-1β, IL-18, and NLRP3 secretion, indicating suppression of NLRP3 inflammasome activity. It also decreased N. gonorrhoeae-induced expression of IL-1β precursor, IL-6, and inducible nitric oxide synthase, without affecting NLRP3, tumour necrosis factor-α, or cyclooxygenase-2 levels. Mechanistic analysis revealed that CA suppressed intracellular H2O2, mitochondrial reactive oxygen species, and ERK1/2 phosphorylation. Importantly, CA also demonstrated bactericidal activity against N. gonorrhoeae. These findings suggest that CA may attenuate NLRP3 inflammasome activation and the associated inflammatory response, highlighting its potential as an anti-inflammatory dietary compound.
EXPERIMENTAL PROCEDURE: Protein expression was assessed by ELISA and Western blotting. Intracellular H2O2, mitochondrial reactive oxygen species, and membrane integrity were evaluated with fluorescent probes and flow cytometry. NF-κB activity was measured using reporter cells. Cell viability and bacterial survival were determined by lactate dehydrogenase release and colony forming unit counts, respectively. Bacterial morphology was examined via scanning electron microscopy.
RESULTS AND CONCLUSION: CA inhibited caspase-1 activation and reduced IL-1β, IL-18, and NLRP3 secretion, indicating suppression of NLRP3 inflammasome activity. It also decreased N. gonorrhoeae-induced expression of IL-1β precursor, IL-6, and inducible nitric oxide synthase, without affecting NLRP3, tumour necrosis factor-α, or cyclooxygenase-2 levels. Mechanistic analysis revealed that CA suppressed intracellular H2O2, mitochondrial reactive oxygen species, and ERK1/2 phosphorylation. Importantly, CA also demonstrated bactericidal activity against N. gonorrhoeae. These findings suggest that CA may attenuate NLRP3 inflammasome activation and the associated inflammatory response, highlighting its potential as an anti-inflammatory dietary compound.