scholarly journals Peroxiredoxin 6 differentially regulates acute and chronic cigarette smoke–mediated lung inflammatory response and injury

2010 ◽  
Vol 36 (8) ◽  
pp. 451-462 ◽  
Author(s):  
Isaac K. Sundar ◽  
Sangwoon Chung ◽  
Jae-Woong Hwang ◽  
Gnanapragasam Arunachalam ◽  
Suzanne Cook ◽  
...  
Molecules ◽  
2019 ◽  
Vol 24 (6) ◽  
pp. 1159 ◽  
Author(s):  
Zeng Qi ◽  
Zhuo Li ◽  
Xuewa Guan ◽  
Cuizhu Wang ◽  
Fang Wang ◽  
...  

Panax ginseng Meyer cv. Silvatica (PGS), which is also known as “Lin-Xia-Shan-Shen” or “Zi-Hai” in China, is grown in forests and mountains by broadcasting the seeds of ginseng and is harvested at the cultivation age of 15–20 years. In this study, four new dammarane-type triterpenoids, ginsengenin-S1 (1), ginsengenin-S2 (2), ginsenoside-S3 (3), ginsenoside-S4 (4), along with one known compound were isolated from pearl knots of PGS. Ginsengenin-S2 significantly alleviated oxidative damage when A549 cells were exposed to cigarette smoke (CS) extract. In addition, ginsengenin-S2 could inhibit the CS-induced inflammatory reaction in A549 cells. Protective effects of ginsengenin-S2 against CS-mediated oxidative stress and the inflammatory response in A549 cells may involve the Nrf2 and HDAC2 pathways.


2021 ◽  
pp. 096032712199798
Author(s):  
R Reis ◽  
D Orak ◽  
D Yilmaz ◽  
H Cimen ◽  
H Sipahi

Smoking is one of the most important leading death cause worldwide. From a toxicological perspective, cigarette smoke serves hazards especially for the human being exposed to passive smoke. Over the last decades, the effects of natural compounds on smoking-mediated respiratory diseases such as COPD, asthma, and lung cancer have been under investigation, as well as the mechanistic aspects of disease progression. In the present study, the protective mechanism of eucalyptol (EUC), curcumin (CUR), and their combination on BEAS-2B cells were investigated in vitro to understand their impact on cell death, oxidative cell injury, and inflammatory response induced by 3R4F reference cigarette extract (CSE). According to the present findings, EUC, CUR, and their combination improved cell viability, attenuated CSE-induced apoptosis, and LC3B expression. Further, CSE-induced oxidative damage and inflammatory response in human bronchial epithelial cells were remarkably reduced by the combination treatment through modification of enzymatic antioxidant activity, GSH, MDA, and intracellular ROS levels as well as nitrite and IL-6 levels. In addition, nuclear translocation of Nrf2, a regulatory protein involved in the indirect antioxidant response, was remarkably up-regulated with the combination pre-treatment. In conclusion, EUC and CUR in combination might be a potential therapeutic against smoking-induced lung diseases through antioxidant and inflammatory pathways and results represent valuable background for future in vivo pulmonary toxicity studies.


Author(s):  
Ken R. Bracke ◽  
Lennart Zabeau ◽  
Jan Tavernier ◽  
Guy F. Joos ◽  
Emiel F.M. Wouters ◽  
...  

Nutrition ◽  
2006 ◽  
Vol 22 (11-12) ◽  
pp. 1192-1201 ◽  
Author(s):  
Frank Silva Bezerra ◽  
Samuel Santos Valença ◽  
Manuella Lanzetti ◽  
Wagner Alves Pimenta ◽  
Paulo Castro ◽  
...  

2020 ◽  
Vol 21 (3) ◽  
pp. 853 ◽  
Author(s):  
Kentaro Akata ◽  
Stephan F. van Eeden

Chronic obstructive pulmonary disease (COPD) is caused by the chronic exposure of the lungs to toxic particles and gases. These exposures initiate a persistent innate and adaptive immune inflammatory response in the airways and lung tissues. Lung macrophages (LMs) are key innate immune effector cells that identify, engulf, and destroy pathogens and process inhaled particles, including cigarette smoke and particulate matter (PM), the main environmental triggers for COPD. The number of LMs in lung tissues and airspaces is increased in COPD, suggesting a potential key role for LMs in initiating and perpetuating the chronic inflammatory response that underpins the progressive nature of COPD. The purpose of this brief review is to discuss the origins of LMs, their functional properties (chemotaxis, recruitment, mediator production, phagocytosis and apoptosis) and changes in these properties due to exposure to cigarette smoke, ambient particulate and pathogens, as well as their persistent altered functional properties in subjects with established COPD. We also explore the potential to therapeutically modulate and restore LMs functional properties, to improve impaired immune system, prevent the progression of lung tissue destruction, and improve both morbidity and mortality related to COPD.


Sign in / Sign up

Export Citation Format

Share Document