scholarly journals Effect of Simvastatin on 5-HT and 5-HTT in a Rat Model of Pulmonary Artery Hypertension

2015 ◽  
Vol 37 (5) ◽  
pp. 1712-1724 ◽  
Author(s):  
Xue Jiang ◽  
LinDong Yuan ◽  
Peng Li ◽  
Jia Wang ◽  
Pengyu Wang ◽  
...  
Keyword(s):  
Body Weight ◽  
Pulmonary Artery ◽  
Cigarette Smoke ◽  
Rat Model ◽  
Structural Damage ◽  
Inflammatory Cells ◽  
Pulmonary Artery Hypertension ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Mean Pulmonary Arterial Pressure

Background/Aims: To investigaterole of serotonin (5-HT) and serotonin transporter (5-HTT) in a rat model of cigarette smoke-induced pulmonary artery hypertension (PAH) and the effect of statins on regulating 5HT and 5-HTT. Methods: A rat model of COPD comorbid with PAH was established by cigarette smoke exposure with or without simvastatin administration. The smoking and the simvastatin plus smoking groups were exposed to cigarette smoke daily, and the latter received simvastatin at 5mg/kg, once a day. After 16 weeks of cigarette smoke exposure, body weight and mean pulmonary arterial pressure (mPAP) were measured, bronchoalveolar lavage (BAL) was performed, and lung tissues and blood samples were collected to determine cardiopulmonary pathology, physiological indices, blood levelof 5-HT and expression of 5-HTT in the lung. Results: In addition to alveolar structural damage (COPD-like injury), chronic cigarette smoke exposure lead to pulmonary artery remodeling and PAH as evidenced by significant elevation of mPAP, RVHI, WT%and WA%. Cigarette smoke exposure resulted in significant reduction in animal body weight, and simvastatin significantly prevented smoke-induced weight loss. The number of inflammatory cells in BALF was dramatically increased in smoke exposed rats, and simvastatin dampened the number of leukocytes, neutrophils, lymphocytes, and macrophages. In addition, circulating 5-HTand expression of 5-HTT in the lung were significantly increased in the smoked rats compared to control rats, and it was significantly reduced by simvastatin. Alteration of BALF inflammatory cells, 5-HT and 5-HTT was significantly correlated with changes of mPAP, RVHI, WT% and WA%. Conclusions: Cigarette smoke exposure could result in not only COPD, but also PAH, which may attribute to the alteration of blood 5-HT and lung tissue 5-HTT. Simvastatin could significantly inhibited 5-HT and 5-HTT expression, and by which mechanism, it may protect animals from development of PAH.

scholarly journals A Rat Model to Determine the Biomedical Consequences of Concurrent Ethanol Ingestion and Cigarette Smoke Exposure

2004 ◽  
Vol 28 (7) ◽  
pp. 1120-1128 ◽  
Author(s):  
Martha J. Gentry-Nielsen ◽  
Elizabeth Vander Top ◽  
Mary U. Snitily ◽  
Carol A. Casey ◽  
Laurel C. Preheim
Keyword(s):  
Cigarette Smoke ◽  
Rat Model ◽  
Smoke Exposure ◽  
Ethanol Ingestion ◽  
Cigarette Smoke Exposure

scholarly journals The Effectiveness of Binahong (Anredera cordifolia (Ten.) Steenis) Extract in Promoting Fertility in Male Wistar Rats after Exposure to Cigarette Smoke

2021 ◽  
Vol 9 (A) ◽  
pp. 123-128
Author(s):  
Achmad Ramadhan
Keyword(s):  
Body Weight ◽  
Cigarette Smoke ◽  
Wistar Rats ◽  
Smoke Exposure ◽  
Male Rats ◽  
Male Rat ◽  
Cigarette Smoke Exposure ◽  
Testicular Weight ◽  
Significant Difference ◽  
Male Wistar Rats

BACKGROUND: Cigarette smoke has a variety of dangerous chemicals and free radicals that can potentially cause infertility. One of the plants that are reported to have medicinal properties and have active compounds as antioxidants is Binahong (Anredera cordifolia (Ten.) Steenis). AIM: This study aims to investigate the effectiveness of A. cordifolia leaf extract (ACLE) in increasing the fertility of male Wistar rats after exposure to cigarette smoke. METHODS: Twenty-four adult male rats were divided into six groups (age 8–10 weeks, weight 200–250 g): Group 1 (normal control) received aquades (1 ml/day) without being given cigarette smoke, Group 2 received exposure to smoke without being given ACLE, Group 3 received cigarette smoke exposure + 25 mg/kg ACLE, Group 4 received cigarette smoke exposure + 50 mg/kg ACLE, Group 5 received cigarette smoke exposure + 75 mg/kg ACLE, and Group 6 received exposure to cigarette smoke + 100 mg/kg of ACLE. To produce smoke from cigarettes and expose rats to the smoke, a Smoke chamber is used. Rats in the treatment group were exposed to cigarette smoke for 2 weeks (40–60 s daily for 6 days each week). The evaluation of male rat fertility was carried out by measuring body weight, genital weight (testis and epididymis), and spermatozoa spermogram (velocity, motility, morphology, and total number). RESULTS: The least significance different test results showed no significant difference in the rate of weight gain between treatments, standard control, and negative control groups. The average testicular weight of rats exposed to cigarette smoke for 14 days was significantly different from normal controls and doses of 50, 75, and 100 mg/kg body weight. However, at a dose of 25 mg/kg of body weight had not shown a significant increase compared to control. The average spermatozoa velocity reached 12.43 mm2/s and 13.36 mm2/s. The spermatozoa velocity increased significantly at a dose of 100 mg/kg body weight. CONCLUSIONS: ACLE at a dose of 100 mg/kg body weight was effective in increasing the fertility of male Wistar rats exposed to cigarette smoke.

scholarly journals L-Leucine Improves Metabolic Disorders in Mice With in-utero Cigarette Smoke Exposure

2021 ◽  
Vol 12 ◽  
Author(s):  
Yunxin Zeng ◽  
Taida Huang ◽  
Nan Wang ◽  
Yi Xu ◽  
Chunhui Sun ◽  
...  
Keyword(s):  
Body Weight ◽  
Cigarette Smoke ◽  
Fat Mass ◽  
Metabolic Disorders ◽  
Fasting Blood Glucose ◽  
Female Offspring ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Leucine Supplementation ◽  
Increased Risk

Objectives: Maternal cigarette smoke exposure (SE) causes intrauterine undernutrition, resulting in increased risk for metabolic disorders and type 2 diabetes in the offspring without sex differences. L-leucine supplementation has been shown to reduce body weight and improve glucose metabolism in both obese animals and humans. In this study, we aimed to determine whether postnatal L-leucine supplementation in female offspring can ameliorate the detrimental impact of maternal SE.Methods: Female Balb/c mice (6-week) were exposed to cigarette smoke (SE, 2 cigarettes/day) prior to mating for 5 weeks until the pups weaned. Sham dams were exposed to air during the same period. Half of the female offspring from the SE and SHAM dams were supplied with L-leucine via drinking water (1.5% w/w) after weaning (21-day) for 10 weeks and sacrificed at 13 weeks (adulthood).Results: Maternal SE during pregnancy resulted in smaller body weight and glucose intolerance in the offspring. L-leucine supplement in Sham offspring reduced body weight, fat mass, and fasting blood glucose levels compared with their untreated littermates; however somatic growth was not changed. L-leucine supplement in SE offspring improved glucose tolerance and reduced fat mass compared with untreated littermates.Conclusions: Postnatal L-leucine supplement could reduce fat accumulation and ameliorate glucose metabolic disorder caused by maternal SE. The application of leucine may provide a potential strategy for reducing metabolic disorders in offspring from mothers who continued to smoke during pregnancy.

scholarly journals Dual interleukin-17A/F deficiency protects against acute and chronic response to cigarette smoke exposure in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hiroo Wada ◽  
Masuo Nakamura ◽  
Shin-Ichi Inoue ◽  
Akihiko Kudo ◽  
Tomoko Hanawa ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Cigarette Smoke ◽  
Inflammatory Responses ◽  
Inflammatory Cells ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Inflammatory Protein ◽  
Interleukin 17A ◽  
Macrophage Colony ◽  
Environmental Air

AbstractIL-17A and IL-17F are both involved in the pathogenesis of neutrophilic inflammation observed in COPD and severe asthma. To explore this, mice deficient in both Il17a and Il17f and wild type (WT) mice were exposed to cigarette smoke or environmental air for 5 to 28 days and changes in inflammatory cells in bronchoalveolar lavage (BAL) fluid were determined. We also measured the mRNA expression of keratinocyte derived chemokine (Kc), macrophage inflammatory protein-2 (Mip2), granulocyte–macrophage colony stimulating factor (Gmcsf) and matrix metalloproteinase-9 (Mmp9 ) in lung tissue after 8 days, and lung morphometric changes after 24 weeks of exposure to cigarette smoke compared to air-exposed control animals. Macrophage counts in BAL fluid initially peaked at day 8 and again on day 28, while neutrophil counts peaked between day 8 and 12 in WT mice. Mice dual deficient with Il17a and 1l17f showed similar kinetics with macrophages and neutrophils, but cell numbers at day 8 and mRNA expression of Kc, Gmcsf and Mmp9 were significantly reduced. Furthermore, airspaces in WT mice became larger after cigarette smoke exposure for 24 weeks, whereas this was not seen dual Il17a and 1l17f deficient mice. Combined Il17a and Il17f deficiency resulted in significant attenuation of neutrophilic inflammatory response and protection against structural lung changes after long term cigarette smoke exposure compared with WT mice. Dual IL-17A/F signalling plays an important role in pro-inflammatory responses associated with histological changes induced by cigarette smoke exposure.

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