scholarly journals Protective Effects of Quercetin on Livers from Mice Exposed to Long-Term Cigarette Smoke

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Pedro A. Machado-Junior ◽  
Natália P. S. Araújo ◽  
Ana B. F. Souza ◽  
Thalles F. Castro ◽  
Michel Oliveira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Cigarette Smoke ◽  
Liver Diseases ◽  
Inflammatory Cells ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Protective Effects ◽  
Histopathological Changes

Cigarette smoke is highly toxic, and it can promote increased production of reactive species and inflammatory response and leads to liver diseases. Quercetin is a flavonoid that displays antioxidant and anti-inflammatory activities in liver diseases. This study aimed at evaluating the protective effects of quercetin on livers from mice exposed to long-term cigarette smoke exposure. Male C57BL/6 mice were divided into five groups: control (CG), vehicle (VG), quercetin (QG), cigarette smoke (CSG), quercetin, and cigarette smoke (QCSG). CSG and QCSG were exposed to cigarette smoke for sixty consecutive days; at the end of the exposures, all animals were euthanized. Mice that received quercetin daily and were exposed to cigarette smoke showed a reduced influx of inflammatory cells, oxidative stress, inflammatory reaction, and histopathological changes in the liver, compared to CSG. These results suggest that quercetin may be an effective adjuvant for treating damage to the liver due to cigarette smoke exposure.

scholarly journals Effect of long-term maternal smoking on the offspring’s lung health

2017 ◽  
Vol 313 (2) ◽  
pp. L416-L423 ◽  
Author(s):  
Surpon Sukjamnong ◽  
Yik Lung Chan ◽  
Razia Zakarya ◽  
Sonia Saad ◽  
Pawan Sharma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Maternal Smoking ◽  
Smoke Exposure ◽  
Male Offspring ◽  
Mitogen Activated Protein Kinase ◽  
Cigarette Smoke Exposure ◽  
Nuclear Factor ◽  
The Impact

Maternal smoking during pregnancy contributes to long-term health problems in offspring, especially respiratory disorders that can manifest in either childhood or adulthood. Receptors for advanced glycation end products (RAGE) are multiligand receptors abundantly localized in the lung, capable of responding to by-products of reactive oxygen species and proinflammatory responses. RAGE signaling is a key regulator of inflammation in cigarette smoking-related pulmonary diseases. However, the impact of maternal cigarette smoke exposure on lung RAGE signaling in the offspring is unclear. This study aims to investigate the effect of maternal cigarette smoke exposure (SE), as well as mitochondria-targeted antioxidant [mitoquinone mesylate (MitoQ)] treatment, during pregnancy on the RAGE-mediated signaling pathway in the lung of male offspring. Female Balb/c mice (8 wk) were divided into a sham group (exposed to air), an SE group (exposed to cigarette smoke), and an SE + MQ group (exposed to cigarette smoke with MitoQ supplement from mating). The lungs from male offspring were collected at 13 wk. RAGE and its downstream signaling, including nuclear factor-κB and mitogen-activated protein kinase family consisting of extracellular signal-regulated kinase 1, ERK2, c-JUN NH2-terminal kinase (JNK), and phosphorylated JNK, in the lung were significantly increased in the SE offspring. Mitochondrial antioxidant manganese superoxide dismutase was reduced, whereas IL-1β and oxidative stress response nuclear factor (erythroid-derived 2)-like 2 were significantly increased in the SE offspring. Maternal MitoQ treatment normalized RAGE, IL-1β, and Nrf-2 levels in the SE + MQ offspring. Maternal SE increased RAGE and its signaling elements associated with increased oxidative stress and inflammatory cytokines in offspring lungs, whereas maternal MitoQ treatment can partially normalize these changes.

Comparison of Oxidative Effects of Electronic Cigarette and Tobacco Smoke Exposure Performed Experimentally

2021 ◽  
pp. 1-7
Author(s):  
Oktay Aslaner
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Smoke Exposure ◽  
Electronic Cigarette ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Exposure Group ◽  
Oxidative Effects

<b><i>Objective:</i></b> Cigarette smoking is a life-threatening habit that has rapidly spread in every socioeconomic part of the public worldwide. There exist mechanisms of nicotine delivery available to use in the hope of halting cigarette smoking, and the electronic cigarette (EC) is one of the common methods used for tobacco smoking replacement. This study aimed to investigate experimentally the oxidative effects of tobacco smoke and EC smoke which contain nicotine. <b><i>Method:</i></b> We constructed smoke circuit rooms for exposing the rats to EC or tobacco smoke. Three groups were created, the control group (<i>N</i> = 8); the electronic cigarette group (<i>N</i> = 8), exposure to electronic cigarette smoke for 2 h per day; and the tobacco group (<i>N</i> = 8), exposure to traditional cigarette smoke for 2 h per day. After the first and second week of exposure, blood samples were obtained, and serum oxidative stress index (OSI), paraoxonase 1 (PON1) activity, and prolidase levels were evaluated. <b><i>Results:</i></b> Higher values of OSI and prolidase levels were detected in the first week of EC or tobacco smoke exposure in both study groups (<i>p</i> &#x3c; 0.001) when compared with the control group, and partial decrements were observed in the second week. By contrast, elevated PON1 levels were observed in the second week after EC or tobacco smoke exposure. The highest OSI levels were observed in the tobacco smoke group (<i>p</i> &#x3c; 0.001). The lowest values of PON1 levels were detected in the first week of the electronic cigarette smoke group, and this decremental value was statistically different than normal, the second week of the electronic cigarette smoke group, the first week of the traditional cigarette smoke exposure group, and the second week of the traditional cigarette smoke exposure group values (<i>p</i> &#x3c; 0.000). <b><i>Conclusion:</i></b> Our results indicate that EC smoke induced oxidative stress. Therefore, ECs are potentially risky for human health and can lead to important health problems.

Increased Bone Resorption by Long-Term Cigarette Smoke Exposure in Animal Model

2021 ◽  
Author(s):  
Jader Joel Machado Junqueira ◽  
Juliana Dias Lourenço ◽  
Kaique Rodrigues da Silva ◽  
Vanda Jorgetti ◽  
Rodolfo Vieira ◽  
...  
Keyword(s):  
Animal Model ◽  
Bone Resorption ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure

scholarly journals Four Novel Dammarane-Type Triterpenoids from Pearl Knots of Panax ginseng Meyer cv. Silvatica

Molecules ◽  
2019 ◽  
Vol 24 (6) ◽  
pp. 1159 ◽  
Author(s):  
Zeng Qi ◽  
Zhuo Li ◽  
Xuewa Guan ◽  
Cuizhu Wang ◽  
Fang Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Oxidative Damage ◽  
Cigarette Smoke ◽  
Panax Ginseng ◽  
Inflammatory Reaction ◽  
A549 Cells ◽  
Protective Effects

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.

scholarly journals Long-Term Cigarette Smoke Exposure in a Mouse Model of Ciliated Epithelial Cell Function

2010 ◽  
Vol 43 (6) ◽  
pp. 635-640 ◽  
Author(s):  
Samantha M. Simet ◽  
Joseph H. Sisson ◽  
Jacqueline A. Pavlik ◽  
Jane M. DeVasure ◽  
Craig Boyer ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Mouse Model ◽  
Cigarette Smoke ◽  
Cell Function ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Ciliated Epithelial Cell

scholarly journals Impact of maternal cigarette smoke exposure on brain inflammation and oxidative stress in male mice offspring

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Yik Lung Chan ◽  
Sonia Saad ◽  
Carol Pollock ◽  
Brian Oliver ◽  
Ibrahim Al-Odat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Brain Inflammation ◽  
Cigarette Smoke Exposure ◽  
Male Mice ◽  
And Oxidative Stress
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