scholarly journals Cigarette smoke extract enhances oxytocin-induced rhythmic contractions of rat and human preterm myometrium

Reproduction ◽  
2006 ◽  
Vol 132 (2) ◽  
pp. 343-353 ◽  
Author(s):  
Tsuyoshi Nakamoto ◽  
Katsuhiko Yasuda ◽  
Masahiro Yasuhara ◽  
Tatsuya Nakajima ◽  
Tomomi Mizokami ◽  
...  
Keyword(s):  
Preterm Delivery ◽  
Cigarette Smoke ◽  
Contractile Activity ◽  
Underlying Mechanism ◽  
Cigarette Smoke Extract ◽  
Control Group ◽  
Smoking During Pregnancy ◽  
Expression Levels ◽  
Uterine Contractions ◽  
Uterine Contractile

Although smoking during pregnancy is a major risk factor for preterm delivery, the underlying mechanism by which smoking stimulates uterine contractions is still poorly understood. In the present study, we tried to clarify the effects of smoking on myometrial contractility induced by oxytocin (OT) using cigarette smoke extract (CSE). Myometrial strips, which were taken from the rat on day 16 of pregnancy, and from human preterm and term delivery groups, were incubated overnight with several doses of CSE at 37 ° C under non-hormonal conditions. The uterine contractile sensitivity and activity (force and frequency) upon exposure to OT were investigated. Furthermore, the expression levels of oxytocin receptor (OTR) mRNA in the myometrial strips were investigated by real-time PCR. Contractile sensitivity to OT in the rat CSE (10−7pieces/ml) group was found to be significantly higher than in the control group (P< 0.05). Contractile activity did not differ between the CSE and control groups. The expression levels of rat OTR mRNA in the CSE (10−7pieces/ml) group were significantly higher than in the control group (P< 0.01). Similarly, in preterm myometrial strips, the expression levels of human OTR mRNA in the CSE (10−7pieces/ml) group were significantly higher than in the control group (P< 0.05). These findings suggest that CSE directly increases the contractile sensitivity of preterm myometrium in response to OT by upregulating the expression of OTR mRNA and thereby increases the risk of preterm delivery in women, who smoke during pregnancy.

scholarly journals Cigarette Smoke Exposure Inhibits Bacterial Killing via TFEB-Mediated Autophagy Impairment and Resulting Phagocytosis Defect

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Garrett Pehote ◽  
Manish Bodas ◽  
Kathryn Brucia ◽  
Neeraj Vij
Keyword(s):  
Cigarette Smoke ◽  
Therapeutic Potential ◽  
Underlying Mechanism ◽  
Cigarette Smoke Extract ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Bacterial Clearance ◽  
Bacterial Killing ◽  
Bactericidal Activities ◽  
Autophagy Inhibition

Introduction. Cigarette smoke (CS) exposure is the leading risk factor for COPD-emphysema pathogenesis. A common characteristic of COPD is impaired phagocytosis that causes frequent exacerbations in patients leading to increased morbidity. However, the underlying mechanism is unclear. Hence, we investigated if CS exposure causes autophagy impairment as a mechanism for diminished bacterial clearance via phagocytosis by utilizing murine macrophages (RAW264.7 cells) and Pseudomonas aeruginosa (PA01-GFP) as an experimental model. Methods. Briefly, RAW cells were treated with cigarette smoke extract (CSE), chloroquine (autophagy inhibitor), TFEB-shRNA, CFTR(inh)-172, and/or fisetin prior to bacterial infection for functional analysis. Results. Bacterial clearance of PA01-GFP was significantly impaired while its survival was promoted by CSE (p<0.01), autophagy inhibition (p<0.05; p<0.01), TFEB knockdown (p<0.01; p<0.001), and inhibition of CFTR function (p<0.001; p<0.01) in comparison to the control group(s) that was significantly recovered by autophagy-inducing antioxidant drug, fisetin, treatment (p<0.05; p<0.01; and p<0.001). Moreover, investigations into other pharmacological properties of fisetin show that it has significant mucolytic and bactericidal activities (p<0.01; p<0.001), which warrants further investigation. Conclusions. Our data suggests that CS-mediated autophagy impairment as a critical mechanism involved in the resulting phagocytic defect, as well as the therapeutic potential of autophagy-inducing drugs in restoring is CS-impaired phagocytosis.

scholarly journals Prenatal cigarette smoke exposure slightly alters neurobehavioral development in neonatal rats: Implications for developmental origins of health and disease (DoHAD)

2020 ◽  
Vol 107 (1) ◽  
pp. 55-66
Author(s):  
B. Mammel ◽  
T. Kvárik ◽  
Zs. Szabó ◽  
J. Gyarmati ◽  
T. Ertl ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Motor Coordination ◽  
Smoke Exposure ◽  
Whole Body ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Developmental Origins ◽  
Smoking During Pregnancy ◽  
Neurobehavioral Development ◽  
Health And Disease

AbstractNumerous studies indicate that smoking during pregnancy exerts harmful effects on fetal brain development. The aim of this study was to determine the influence of maternal smoking during pregnancy on the early physical and neurobehavioral development of newborn rats. Wistar rats were subjected to whole-body smoke exposure for 2 × 40 min daily from the day of mating until day of delivery. For this treatment, a manual closed-chamber smoking system and 4 research cigarettes per occasion were used. After delivery the offspring were tested daily for somatic growth, maturation of facial characteristics and neurobehavioral development until three weeks of age. Motor coordination tests were performed at 3 and 4 weeks of age. We found that prenatal cigarette smoke exposure did not alter weight gain or motor coordination. Critical physical reflexes indicative of neurobehavioral development (eyelid reflex, ear unfolding) appeared significantly later in pups prenatally exposed to smoke as compared to the control group. Prenatal smoke exposure also resulted in a delayed appearance of reflexes indicating neural maturity, including hind limb grasping and forelimb placing reflexes. In conclusion, clinically relevant prenatal exposure to cigarette smoke results in slightly altered neurobehavioral development in rat pups. These findings suggest that chronic exposure of pregnant mothers to cigarette smoke (including passive smoking) results in persisting alterations in the developing brain, which may have long-lasting consequences supporting the concept of developmental origins of health and disease (DoHAD).

scholarly journals Erythromycin Suppresses the Cigarette Smoke Extract-Exposed Dendritic Cell-Mediated Polarization of CD4+ T Cells into Th17 Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Jifeng Liu ◽  
Xiaoning Zhong ◽  
Zhiyi He ◽  
Jianquan Zhang ◽  
Jing Bai ◽  
...  
Keyword(s):  
T Cells ◽  
Cigarette Smoke ◽  
Th17 Cells ◽  
Mixed Lymphocyte Reaction ◽  
Mononuclear Cells ◽  
Cigarette Smoke Extract ◽  
Exposed Group ◽  
Control Group ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

Cigarette smoke is a major effector of chronic obstructive pulmonary disease (COPD), and Th17 cells and dendritic cells (DCs) involve in the pathogenesis of COPD. Previous studies have demonstrated the anti-inflammatory effects of macrolides. However, the effects of macrolides on the cigarette smoke extract- (CSE-) induced immune response are unclear. Accordingly, in this study, we evaluated the effects of erythromycin (EM) on CSE-exposed DCs polarizing naïve CD4+ T cells into Th17 cells. DCs were generated from bone marrow-derived mononuclear cells isolated from male BALB/c mice and divided into five groups: control DC group, CSE-exposed DC group, CD40-antibody-blocked CSE-exposed DC group, and EM-treated CSE-exposed DC group. The function of polarizing CD4+ T cells into Th17 cells induced by all four groups of DCs was assayed based on the mixed lymphocyte reaction (MLR) of naïve CD4+ T cells. CD40 expression in DCs in the CSE-exposed group increased significantly compared with that in the control group (P<0.05). The Th17 cells in the CSE-exposed DC/MLR group increased significantly compared with those in the control DC/MLR group (P<0.05). Moreover, Th17 cells in the CD40-blocked CSE-exposed DC/MLR group and EM-treated CSE-exposed DC/MLR group were reduced compared with those in the CSE-exposed DC/MLR group (P<0.05). Thus, these findings suggested that EM suppressed the CSE-exposed DC-mediated polarization of CD4+ T cells into Th17 cells and that this effect may be mediated through inhibition of the CD40/CD40L pathway.

scholarly journals Antiaging effect of a Jianpi-yangwei formula in Caenorhabditis elegans

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Liling Zeng ◽  
Zhimin Yang ◽  
Tianchan Yun ◽  
Shaoyi Fan ◽  
Zhong Pei ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Target Genes ◽  
Underlying Mechanism ◽  
Control Group ◽  
Wild Type ◽  
Survival Times ◽  
Expression Levels ◽  
C Elegans ◽  
Heat Stress Resistance ◽  
Increased Activity

Abstract Background Jianpi-yangwei (JPYW), a traditional Chinese medicine (TCM), helps to nourish the stomach and spleen and is primarily used to treat functional declines related to aging. This study aimed to explore the antiaging effects and mechanism of JPYW by employing a Caenorhabditis elegans model. Methods Wild-type C. elegans N2 worms were cultured in growth medium with or without JPYW, and lifespan analysis, oxidative and heat stress resistance assays, and other aging-related assays were performed. The effects of JPYW on the levels of superoxide dismutase (SOD) and the expression of specific genes were examined to explore the underlying mechanism of JPYW. Results Compared to control worms, JPYW-treated wild-type worms showed increased survival times under both normal and stress conditions (P < 0.05). JPYW-treated worms also exhibited enhanced reproduction, movement and growth and decreased intestinal lipofuscin accumulation compared to controls (P < 0.05). Furthermore, increased activity of SOD, downregulated expression levels of the proaging gene clk-2 and upregulated expression levels of the antiaging genes daf-16, skn-1, and sir-2.1 were observed in the JPYW group compared to the control group. Conclusion Our findings suggest that JPYW extends the lifespan of C. elegans and exerts antiaging effects by increasing the activity of an antioxidant enzyme (SOD) and by regulating the expression of aging-related genes. This study not only indicates that this Chinese compound exerts antiaging effects by activating and repressing target genes but also provides a proven methodology for studying the biological mechanisms of TCMs.

scholarly journals Endoplasmic Reticulum Stress Induces HRD1 to Protect Alveolar Type II Epithelial Cells from Apoptosis Induced by Cigarette Smoke Extract

2017 ◽  
Vol 43 (4) ◽  
pp. 1337-1345 ◽  
Author(s):  
Shuang-xiang Tan ◽  
Di-xuan Jiang ◽  
Rui-cheng Hu ◽  
Ai-guo Dai ◽  
Gui- xiang Gan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Er Stress ◽  
Cigarette Smoke ◽  
Fold Increase ◽  
Underlying Mechanism ◽  
Cigarette Smoke Extract ◽  
Physiological Characteristic ◽  
Chronic Obstructive ◽  
Alveolar Type ◽  
Type Ii

Background/Aims: Cigarette smoking is a major risk factor of chronic obstructive pulmonary disease. This study aimed to examine the effects of cigarette smoke extract (CSE) on alveolar type II epithelial cells (AECII) and investigate the underlying mechanism. Methods: Primary AECII were isolated from rat lung tissues and exposed to CSE. Apoptosis was detected by flow cytometry. Protein expression was detected by Western blot analysis. Results: Primary rat AECII maintained morphological and physiological characteristic after 3 passages. CSE increased the expression of ER specific pro-apoptosis factors CHOP and caspase 12, and the phosphorylation of JNK in AECII. CSE activated ER stress signaling and increased the phosphorylation of PERK, eIF2α and IRE1. Furthermore, CSE induced the expression of Hrd1, a key factor of ER-associated degradation, in AECII. Knockdown of Hrd1 led to more than 2 fold increase of apoptosis, while overexpression of Hrd1 attenuated CSE induced apoptosis of AECII. Conclusions: Our results suggest that ER stress induces HRD1 to protect alveolar type II epithelial cells from apoptosis induced by CSE.

scholarly journals Hypoxia and its possible relationship with endometrial receptivity in adenomyosis: a preliminary study

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Song Guo ◽  
Di Zhang ◽  
Xiaowei Lu ◽  
Qian Zhang ◽  
Ruihuan Gu ◽  
...  
Keyword(s):  
Real Time ◽  
Western Blotting ◽  
Real Time Pcr ◽  
Underlying Mechanism ◽  
Endometrial Receptivity ◽  
Control Group ◽  
Expression Levels ◽  
Preliminary Study

Abstract Background Adenomyosis (AM) is an important cause of female infertility. However, the underlying mechanism remains unclear. This report describes a preliminary study of hypoxia and its possible association with endometrial receptivity in AM. Methods The study was divided into in vitro and in vivo experiments. In vitro, expression levels of the endometrial receptivity markers HOXA10 and HOXA11 in the implantation period were examined using real-time PCR and western blotting. Endometrial expression of hypoxia-inducible factor (HIF)-1α, HIF-2α, and HIF-3α was determined using immunohistochemistry. In vivo, using an AM mouse model established by oral administration of tamoxifen, we inhibited expression of HIF-2α using an HIF-2α antagonist (PT2399; 30 mg/kg body weight, twice daily by oral gavage for 2 days) and then examined expression levels of Hoxa10 and Hoxa11 using real-time PCR and western blotting. Results Endometrial mRNA and protein expression levels of HOXA10 and HOXA11 were significantly lower in patients with AM than in control patients. Expression of HIF-2α was significantly higher in the AM group than in the control group, whereas that of HIF-1α and HIF-3α was equivalent in both groups. In vivo analysis showed that administration of the HIF-2α antagonist resulted in increased expression of Hoxa10 and Hoxa11 at both the mRNA and protein levels in AM model mice. Conclusions HIF-2α overexpression may be one reason for decreased endometrial receptivity in AM. The current findings provide insight into HIF-2α-mediated AM-related infertility and suggest that PT2399 has potential as a treatment for AM. Trial registration This trial was retrospectively registered.

Effect of cigarette smoke on TNF-a and IL-1b mRNA expression in lung tissues and cells of rats

2015 ◽  
Author(s):  
Mingli Ji ◽  
Yuxia Wang ◽  
Xiaopeng Li ◽  
Zhibi Qian
Keyword(s):  
Carbon Dioxide ◽  
Mrna Expression ◽  
Cigarette Smoke ◽  
Lung Tissue ◽  
Control Group ◽  
Expression Levels ◽  
Arterial Partial Pressure ◽  
Experimental Group ◽  
Mrna Expression Levels ◽  
Pro Inflammatory Cytokines

We investigated lung tissue expression of the pro-inflammatory cytokines TNF-a and IL-1b in response to cigarette smoke exposure and the ensuing effects on arterial oxygen and carbon dioxide as indices of respiratory function. Experimental group rats were exposed to cigarette smoke twice daily (30 min per exposure) for 28 consecutive days. Arterial partial pressure of oxygen (PO2), arterial partial pressure of carbon dioxide (PCO2), and both mRNA and protein expression levels of TNF-a and IL-1b were compared to a control group. Contents of TNF-a and IL-1b in bronchoalveolar lavage fluid (BALF) and lung homogenate were detected by enzyme linked immunosorbent assays while TNF-a mRNA and IL-1b mRNA expression levels in lung tissue were detected by reverse transcription-polymerase chain reaction. Arterial PO2 was significantly lower in the experimental group than the control group, while the arterial PCO2 was significantly higher. BALF levels of TNF-a and IL-1b were significantly higher in the experimental group than the control group, as were TNF-a mRNA and IL-1b mRNA expression levels in lung tissue. Cigarette smoke may activate inflammatory cells in the pulmonary circulation and increase the expression of the pro-inflammatory cytokines TNF-a and IL-1b in lung tissue, leading to lung injury and respiratory dysfunction.

scholarly journals Effects of Cigarette Smoke and Opium on the Expression of CD9, CD36, and CD68 at mRNA and Protein Levels in Human Macrophage Cell Line THP-1

2020 ◽  
Author(s):  
Mohammad Amin Momeni-Moghaddam ◽  
Gholamreza Asadikaram ◽  
Mohammad Hadi Nematollahi ◽  
Mojdeh Esmaeili Tarzi ◽  
Sanaz Faramarz-Gaznagh ◽  
...  
Keyword(s):  
Protein Expression ◽  
Cell Line ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Scavenger Receptors ◽  
Human Macrophage ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Expression Levels ◽  
Protein Levels

Cigarette smoking and opium use are risk factors for coronary artery disease (CAD). It has been known that scavenger receptors such as CD36 and CD68 play critical roles in the pathogenesis of CAD. CD9, as a member of the tetraspanin, has been shown to interact with scavenger receptors. The aim of this study was to investigate the effects of these risk factors on expression levels of CD9, CD36, and CD68 on the THP-1 cell line. The THP-1 cell line treated with cigarette smoke extract (CSE( and opium, both individually and combinatory, in 24 h incubation. The protein and mRNA levels of CD9, CD36, and CD68 were evaluated by flow cytometry and quantitative reverse transcription-Polymerase Chain Reaction (qRT-PCR) techniques, respectively. CD36 and CD68 mRNA and protein expression levels were significantly increased in the cells treated with cigarette smoke extract compared to the control (p<0.001 in mRNA expression levels and p=0.016 and p=0.012 in protein expression levels, respectively). The CSE increased the level of CD9 protein expression compared to the control group (p=0.041) on the human macrophage cell line THP-1. No significant differences were observed in the CD9, CD36, and CD68 gene expression and at the protein levels between opium-treated THP-1 cells and controls. In conclusion, cigarettes by increasing the levels of CD36, CD68, and CD9 can be a risk factor in the development of many inflammatory diseases, including cardiovascular diseases, chronic obstructive pulmonary disease (COPD) and lung carcinoma.

Efficacy and safety assessment of viburcol drug for preparation of uterine cervix for childbirth and prevention of labor anomalies

2016 ◽  
pp. 73-78
Author(s):  
T.V. Avramenko ◽  
◽  
A.P. Moschich ◽  
Keyword(s):  
Uterine Cervix ◽  
Contractile Function ◽  
Contractile Activity ◽  
Anxiolytic Effect ◽  
Cervical Ripening ◽  
Control Group ◽  
Uterine Contractile ◽  
Regulatory Approach ◽  
Rectal Suppositories ◽  
Reflex Reactions

The objective is to compare the effectiveness of complex bio-regulatory medication (CBRM) Viburcol, produced by «Biologishe Haylmittel Heel GmbH», Germany, with the reference product No-X-sha, produced by «Lekhim-Kharkov», which are used as antispasmodics, for preparation of uterine cervix for childbirth and prevention of labor anomalies. Patients and methods. 92 pregnant women aged 18 to 45 years, who were randomized into 2 groups: the main group (n=46) and the control (n=46) one, were involved in the study. Viburcol was used for the treatment of pathological preliminary period and prevention of development of labor anomalies. It was prescribed at the end of pregnancy and in the 1st stage of labor, in the morning and in the evening. Two Viburcol suppository every 3-4 hours were given at the onset of labor. Antispasmodic No-X-sha was used in the control group. It was studied the functional state of the sympathetic-adrenal system with fluorometric method, the concentration of noradrenaline (NA) and adrenaline (A) in the urine, to assess the neurohormonal regulation of labor. The plasma levels of b-estradiol and progesterone were determined to identify the risk of discoordination of labor activity and the state of uterine contractile function. Also, the parameters of uterine contractile activity were analyzed according to cardiotocography. Results. Usage of complex bio-regulatory medication Viburcol promotes adequate cervical ripening and incidence of discoordination of labor activity decreased by 1.5 times. CDRM Viburcol administration in childbirth facilitated the elimination of pathological levels of catecholamines, which led to the development of discoordination of labor activity. Conclusion. The results show the effectiveness of CDRM Viburcol (rectal suppositories) for the prevention of discoordination of labor activity. The medicine meets all modern requirements for antispasmodics and analgesics used during labor: it has analgesic, antispasmodic, anxiolytic effect, eliminates side reflex reactions, reduces the severity of birth stress, it has no adverse effect on the contractile activity of uterus and the fetus condition. Key words: complex bio-regulatory medications, bio-regulatory approach, labor amoralities, preparation of uterine cervix, Viburcol.

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