scholarly journals Efficacy of Low Molecular Heparin on Preeclampsia by Inhibiting Apoptosis of Trophoblasts via the p38MAPK Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Dandan Quan ◽  
Li Li ◽  
Manzhen Zuo
Keyword(s):  
Blood Pressure ◽  
Signaling Pathway ◽  
Heparin Group ◽  
Pregnant Rats ◽  
Apoptosis Rate ◽  
Protein Levels ◽  
Fetal Rats ◽  
P38mapk Signaling ◽  
Tissue Cells ◽  
And Migration

Objective. To explore the efficacy of low molecular heparin on preeclampsia by inhibiting apoptosis of trophoblasts via the p38MAPK signaling pathway. Methods. A preeclampsia rat model was established, and the effects of low molecular heparin on preeclampsia via the p38MAPK signaling pathway were analyzed based on intervention of the rats with different combinations of low molecular heparin and p38MAPK signaling pathway activator. Furthermore, a hypoxia/reoxygenation model of trophoblasts in vitro was established to explore the effects of low molecular heparin on trophoblasts via the p38MAPK signaling pathway. Results. After treatment with low molecular heparin, pregnant rats in the heparin group showed significantly decreased blood pressure, 24 h proteinuria, and p38MAPK protein levels in placenta tissues and decreased apoptosis rate of placenta tissue cells (all P < 0.05 ) and showed more fetal rats and lowered weight of them (both P < 0.05 ) but showed no significant change in the weight of placenta (all P > 0.05 ). Pregnant rats treated with low molecular heparin and p38MAPK activator showed significantly higher blood pressure, 24 h proteinuria, and p38MAPK protein levels in placenta tissues and apoptosis rate of placenta tissue cells than those of pregnant rats in the heparin group (all P < 0.05 ) and also showed less fetal rats and lighter fetal rats than those in the heparin group (both P < 0.05 ) but showed no difference with them in the weight of placenta ( P > 0.05 ). Further analysis revealed that low molecular heparin could protect the survival and migration of trophoblasts under hypoxia/reoxygenation conditions and reduce apoptosis of them (all P < 0.05 ). Conclusion. Low molecular heparin can alleviate preeclampsia by inhibiting the p38MAPK signaling pathway and can inhibit apoptosis of trophoblasts and promote proliferation and migration of them.

scholarly journals Magnesium Lithospermate B Downregulates the Levels of Blood Pressure, Inflammation, and Oxidative Stress in Pregnant Rats with Hypertension

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Kaixiang Xu ◽  
Xiaohong Zang ◽  
Mian Peng ◽  
Qian Zhao ◽  
Binbin Lin
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Gestational Hypertension ◽  
Protective Effects ◽  
Urine Protein ◽  
Pregnant Rats ◽  
Protein Levels ◽  
Arterial Blood ◽  
Magnesium Lithospermate B ◽  
And Oxidative Stress

Background. Magnesium lithospermate B (MLB) was shown to suppress oxidative stress and reduce hypertension, but the role of MLB in pregnancy-induced hypertension (PIH) remains unknown. The objective of this study was to demonstrate the effects of MLB on rats with PIH. Methods. A total of 40 pregnant SD rats were selected, and 30 rats were orally given NG-nitro-L-arginine methyl ester (L-NAME, 60 mg/kg/day) to establish PIH rat models. Rats were equally divided into four groups: control, PIH, 5 mg/kg MLB, and 10 mg/kg MLB. MLB was consecutively administered into PIH rats for one week. The effects of MLB on mean arterial blood pressure (MAP), urine protein level, inflammation, and oxidative stress together with angiogenesis were analyzed. Results. MLB prevented the elevation in MAP and urine protein levels induced by L-NAME. The activities of inflammatory cytokines were highly increased in serum and placental tissues of PIH rats, while cotreatment with MLB partially reversed the activities of these cytokines. MLB also recovered the expression of reactive oxygen species (ROS) in plasma of PIH rats together with levels of oxidative stress and antioxidant capacity in the placenta of PIH rats. The decreased expressions of vascular endothelial growth factor (VEGF), endothelial nitric oxide synthase (eNOS), and NO observed in PIH rats were increased by MLB. In addition, 10 mg/kg MLB exhibited higher protective effects as compared to lower doses of 5 mg/kg. Conclusion. This study demonstrated that pretreatment with MLB decreased MAP, inflammation, and oxidative stress in rats with gestational hypertension.

scholarly journals Expression of cytochrome CYP2B1/2 in nonpregnant, pregnant and fetal rats exposed to tobacco smoke.

2000 ◽  
Vol 47 (4) ◽  
pp. 1115-1127 ◽  
Author(s):  
P Czekaj ◽  
A Wiaderkiewicz ◽  
E Florek ◽  
R Wiaderkiewicz
Keyword(s):  
Tobacco Smoke ◽  
Adult Liver ◽  
Pregnant Rats ◽  
Protein Levels ◽  
Pregnant Females ◽  
Fetal Rat ◽  
Fetal Rats ◽  
Brain Microsomes ◽  
Female Wistar Rats ◽  
Fetal Rat Liver

Four-month-old female Wistar rats were exposed for 20 days to tobacco smoke obtained from non-filter cigarettes. During the exposure, concentration of tobacco smoke was monitored indirectly by measuring the CO level (1500 mg/m3 air). The efficacy of exposure was assessed by measuring urine nicotine and cotinine levels. Cigarette smoke did not change total cytochrome P450 and b5 protein levels in any of the organs studied, and most of these organs did not show any changes in the activity of reductases associated with these cytochromes. Following exposure to tobacco smoke, fetal rat liver expressed CYP2B1/2 protein; in newborns (day 1) both liver and lung showed CYP2B1/2 protein expression and very low pentoxyresorufin O-dealkylase activity. Western blot analysis of adult liver, lung, heart, but not of brain microsomes, showed that tobacco smoke induced CYP2B1/2 in both nonpregnant and pregnant rats, though its expression was lower in the livers and hearts of pregnant females. In the rat and human placenta, neither rat CYP2B1/2 nor human CYP2B6 showed basal or tobacco smoke-induced expression at the protein level. This study shows clearly that the expression of CYP2B1/2, which metabolizes nicotine and some drugs and activates carcinogens, is controlled in rats by age-, pregnancy-, and tissue-specific regulatory mechanisms.

scholarly journals Neogambogic acid induces apoptosis of melanoma B16 cells via the PI3K/Akt/mTOR signaling pathway

2020 ◽  
Author(s):  
Chunlan Wu ◽  
Jin He ◽  
Zhimin Sun ◽  
Dongxin Tang ◽  
Changhui Wen
Keyword(s):  
Signaling Pathway ◽  
Acid Concentration ◽  
Mtor Signaling ◽  
Dependent Manner ◽  
Proliferation Inhibition ◽  
Inhibition Rate ◽  
Mtor Signaling Pathway ◽  
Apoptosis Rate ◽  
Melanoma B16 ◽  
And Migration

Background: Neogambogic acid, as one of the main components of gamboge, exhibits high activities against various tumors. Objective: To explore the mechanism by which melanoma B16 cell apoptosis was induced by neogambogic acid. Methods: Melanoma B16 cells were treated with different concentrations of neogambogic acid solutions (0, 1.5, 3.0, 6.0 μM). The proliferation inhibition rate was measured by MTT assay. Cell morphology was observed by inverted microscope. Cell migration and invasion were tested by Transwell assay. Flow cytometry was performed to detect the apoptosis rate and cell cycle of B16 cells. The expressions of PI3K/Akt/mTOR signaling pathway-related proteins were detected by Western blot. Results: The proliferation inhibition rate of B16 cells significantly increased with rising neogambogic acid concentration (P<0.05). The invasive and migration capacities of B16 cells decreased significantly after treatment with neogambogic acid (P<0.05). The apoptosis rate also increased with rising concentration of neogambogic acid. After 24 h of treatment, the percentage of G0/G1 phase cells increased gradually as the neogambogic acid concentration rose, whereas those of S phase and G2/M phase cells decreased. With increasing concentration of neogambogic acid, the expressions of p-PI3K, p-Akt and p-mTOR proteins reduced in a time-dependent manner, but those of PI3K and Akt proteins remained basically unchanged. Conclusion: Neogambogic acid can inhibit the proliferation, invasion and migration of melanoma B16 cells and induce their apoptosis, which may be regulated via the PI3K/Akt/mTOR signaling pathway.

scholarly journals Growth arrest-specific protein-6/AXL signaling induces preeclampsia in rats†

2019 ◽  
Author(s):  
Kelsey M Hirschi ◽  
Kary Y F Tsai ◽  
Taylor Davis ◽  
J Christian Clark ◽  
M Nekel Knowlton ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Growth Arrest ◽  
Specific Protein ◽  
Trophoblast Invasion ◽  
Tyrosine Kinase Receptor ◽  
Pregnant Rats ◽  
Enhanced Expression ◽  
And Migration ◽  
Phosphate Buffered Saline

Abstract Preeclampsia (PE) is a complicated obstetric complication characterized by increased blood pressure, decreased trophoblast invasion, and inflammation. The growth arrest-specific 6 (Gas6) protein is known to induce dynamic cellular responses and is elevated in PE. Gas6 binds to the AXL tyrosine kinase receptor and AXL-mediated signaling is implicated in proliferation and migration observed in several tissues. Our laboratory utilized Gas6 to induce preeclamptic-like conditions in pregnant rats. Our objective was to determine the role of Gas6/AXL signaling as a possible model of PE. Briefly, pregnant rats were divided into three groups that received daily intraperitoneal injections (from gestational day 7.5 to 17.5) of phosphate buffered saline (PBS), Gas6, or Gas6 + R428 (an AXL inhibitor administered from gestational day 13.5 to 17.5). Animals dispensed Gas6 experienced elevated blood pressure, increased proteinuria, augmented caspase-3-mediated placental apoptosis, and diminished trophoblast invasion. Gas6 also enhanced expression of several PE-related genes and a number of inflammatory mediators. Gas6 further enhanced placental oxidative stress and impaired mitochondrial respiration. Each of these PE-related characteristics was ameliorated in dams and/or their placentae when AXL inhibition by R428 occurred in tandem with Gas6 treatment. We conclude that Gas6 signaling is capable of inducing PE and that inhibition of AXL prevents disease progression in pregnant rats. These results provide insight into pathways associated with PE that could be useful in the clarification of potential therapeutic approaches.

THE FALL OF BLOOD PRESSURE FOLLOWING INDUCTION OF DECIDUOMATA IN STEROID HYPERTENSIVE RATS RECEIVING PROGESTERONE

1968 ◽  
Vol 59 (2) ◽  
pp. 227-234 ◽  
Author(s):  
H. C. Moore ◽  
I. Cserhati ◽  
F. P. Biliczki
Keyword(s):  
Blood Pressure ◽  
Hypotensive Effect ◽  
Hypertensive Rats ◽  
Pregnant Rats ◽  
Hypertensive Rat ◽  
Equivalent Time ◽  
Metrial Gland ◽  
Blood Pressure Responses ◽  
A Minor ◽  
Maternal Decidua

ABSTRACT Experimental deciduomata and progesterone together lower the blood pressure in the steroid hypertensive rat from the 5th to 10th day of decidual growth i. e. from the 10th to 15th day of pseudopregnancy. This would suggest that the fall of blood pressure at an equivalent time of gestation in hypertensive pregnant rats could be due to the maternal decidua under the influence of progesterone. It is further considered that the metrial gland of the deciduoma is more likely to be responsible for the hypotensive effect and by comparison that the metrial gland is implicated in the hypotensive effect of pregnancy. Progesterone alone also exerts a minor hypotensive effect in those animals in which a nephrectomy forms part of the hypertension regimen and indicates one way in which a maternal renal factor could influence blood pressure responses in hypertensive pregnant rats.

The Effect of α1, 2-Fucosyl Transferase Gene Transfection on p38MAPK Signaling Pathway-mediated Apoptosis of Ovarian Carcinoma RMG-I Cells*

2010 ◽  
Vol 37 (2) ◽  
pp. 175-183 ◽  
Author(s):  
Jian-Ping CONG ◽  
Bei LIN ◽  
Juan-Juan LIU ◽  
Qing LIU ◽  
Fei-Fei LI ◽  
...  
Keyword(s):  
Ovarian Carcinoma ◽  
Signaling Pathway ◽  
Gene Transfection ◽  
Transferase Gene ◽  
P38mapk Signaling ◽  
I Cells

SOX4 Serves an Oncogenic Role in the Tumourigenesis of Human Breast Adenocarcinoma by Promoting Cell Proliferation, Migration and Inhibiting Apoptosis

2020 ◽  
Vol 15 (1) ◽  
pp. 49-58
Author(s):  
Junhe Zhang ◽  
Shujie Chai ◽  
Xinyu Ruan
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Caspase 3 ◽  
Breast Adenocarcinoma ◽  
Migration Ability ◽  
Expression Levels ◽  
Apoptosis Rate ◽  
And Migration ◽  
Mcf 7 ◽  
Proliferation And Migration

Background: Breast cancer is among the most common malignant cancers worldwide, and breast adenocarcinoma in glandular tissue cells has excessive metastasis and invasion capability. However, little is known on the molecular process by which this disease develops and progresses. Objective: In this study, we explored the effects of sex-determining region Y-box 4 (SOX4) protein on proliferation, migration, apoptosis and tumourigenesis of breast adenocarcinoma and its possible mechanisms. Methods: The SOX4 overexpression or knockdown Michigan Cancer Foundation-7 (MCF-7) cell lines were established. Among the SOX4 overexpression or MCF-7 knockdown cell lines, proliferation, migration ability and apoptosis rate were detected. The expression levels of apoptosis-related proteins (Bax and Cleaved caspase-3) were analysed using Western blot. The effect of SOX4 on tumourigenesis was analysed using the clone formation assay in vitro and tumour xenograft experiment in nude mice. Results: Compared with the overexpression of control cells, proliferation and migration ability of SOX4 overexpression cells significantly increased, the apoptosis rate significantly decreased in addition to the expression levels of Bax and Cleaved caspase-3 (P < 0.05). Compared with the knockdown of control cells, proliferation and migration ability of SOX4 knockdown cells significantly decreased, and the apoptosis rate and expression levels of Bax and Cleaved caspase-3 significantly increased (P < 0.05). Clone formation and tumour growth abilities of SOX4 overexpression cells were significantly higher than those of the control cells (P < 0.05), whereas SOX4 knockdown cells had the opposite effect. Conclusion: SOX4 plays an oncogenic role in breast adenocarcinoma tumourigenesis by promoting cell proliferation, migration and inhibiting apoptosis. It can be used as a potential molecular target for breast cancer gene therapy.

Inhibition of 11β-Hydroxysteroid Dehydrogenase in Pregnant Rats and the Programming of Blood Pressure in the Offspring

Hypertension ◽  
1996 ◽  
Vol 27 (6) ◽  
pp. 1200-1204 ◽  
Author(s):  
Robert S. Lindsay ◽  
R. Mark Lindsay ◽  
Christopher R.W. Edwards ◽  
Jonathan R. Seckl
Keyword(s):  
Blood Pressure ◽  
Hydroxysteroid Dehydrogenase ◽  
Pregnant Rats

scholarly journals Regorafenib-Attenuated, Bleomycin-Induced Pulmonary Fibrosis by Inhibiting the TGF-β1 Signaling Pathway

2021 ◽  
Vol 22 (4) ◽  
pp. 1985
Author(s):  
Xiaohe Li ◽  
Ling Ma ◽  
Kai Huang ◽  
Yuli Wei ◽  
Shida Long ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Signaling Pathway ◽  
Transforming Growth Factor ◽  
Kinase Inhibitor ◽  
In Vivo Experiments ◽  
Age Related ◽  
And Migration ◽  
Tgf Β1

Idiopathic pulmonary fibrosis (IPF) is a fatal and age-related pulmonary disease. Nintedanib is a receptor tyrosine kinase inhibitor, and one of the only two listed drugs against IPF. Regorafenib is a novel, orally active, multi-kinase inhibitor that has similar targets to nintedanib and is applied to treat colorectal cancer and gastrointestinal stromal tumors in patients. In this study, we first identified that regorafenib could alleviate bleomycin-induced pulmonary fibrosis in mice. The in vivo experiments indicated that regorafenib suppresses collagen accumulation and myofibroblast activation. Further in vitro mechanism studies showed that regorafenib inhibits the activation and migration of myofibroblasts and extracellular matrix production, mainly through suppressing the transforming growth factor (TGF)-β1/Smad and non-Smad signaling pathways. In vitro studies have also indicated that regorafenib could augment autophagy in myofibroblasts by suppressing TGF-β1/mTOR (mechanistic target of rapamycin) signaling, and could promote apoptosis in myofibroblasts. In conclusion, regorafenib attenuates bleomycin-induced pulmonary fibrosis by suppressing the TGF-β1 signaling pathway.

scholarly journals The Nuclear Zinc Finger Protein Zfat Maintains FoxO1 Protein Levels in Peripheral T Cells by Regulating the Activities of Autophagy and the Akt Signaling Pathway

2016 ◽  
Vol 291 (29) ◽  
pp. 15282-15291 ◽  
Author(s):  
Shuhei Ishikura ◽  
Yuri Iwaihara ◽  
Yoko Tanaka ◽  
Hao Luo ◽  
Kensuke Nishi ◽  
...  
Keyword(s):  
T Cells ◽  
Signaling Pathway ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Protein Levels ◽  
Finger Protein ◽  
Peripheral T Cells
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