Robinin modulates doxorubicin-induced cardiac apoptosis by TGF-β1 signaling pathway in Sprague Dawley rats

2014 ◽  
Vol 68 (8) ◽  
pp. 989-998 ◽  
Author(s):  
P.A. Janeesh ◽  
A. Abraham
Keyword(s):  
Signaling Pathway ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Cardiac Apoptosis ◽  
Tgf Β1

scholarly journals 24-Week Exposure to Oxidized Tyrosine Induces Hepatic Fibrosis Involving Activation of the MAPK/TGF-β1 Signaling Pathway in Sprague-Dawley Rats Model

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Zhuqing Leslie Li ◽  
Yonghui Shi ◽  
Guowei Le ◽  
Yinyi Ding ◽  
Qi Zhao
Keyword(s):  
Oxidative Damage ◽  
Signaling Pathway ◽  
Hepatic Fibrosis ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Liver And Kidney ◽  
Biological Impacts ◽  
Dose Dependent ◽  
Tgf Β1 ◽  
Masson Staining

Scope. Oxidized tyrosine (O-Tyr) has been widely detected in many consumer protein products. O-Tyr products such as dityrosine (Dityr) and 3-nitrotyrosine (3-NT) are universal biomarkers of protein oxidation and have been demonstrated to be associated with metabolic disorders in biological system. Evaluation of potential intracorporal effects of dietary O-Tyr is important since the mechanism of biological impacts induced by oral oxidized protein products (OPPs) is still limited although we have proved that some dietary OPPs would induce oxidative injury to liver and kidney.Methods and Results. The present study aimed to investigate the dose-dependent hepatic injury caused by oral O-Tyr in rats. 24-week feeding of O-Tyr enhanced aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, increased total bilirubin (TBiL) content, and led to oxidative damage in rats liver. Besides, O-Tyr distinctly increased the phosphorylation of p38 and ERK2 MAPKs and enhanced fibrosis-related TGF-β1 and Smad2/3 levels. Higher extracellular matrix (ECM) indexes (ICTP, PIIINP) and histological examination (HE and Masson staining) also supported dose-dependent hepatic fibrosis caused by O-Tyr.Conclusion. These findings reveal that O-Tyr may induce oxidative damage and hepatic fibrosis via MAPK/TGF-β1 signaling pathway, in which ROS together with malondialdehyde (MDA) and OPPs act as the pivotal mediators.

Hypothalamic nesfatin-1 mediates feeding behavior via MC3/4R-ERK signaling pathway after weight loss in obese Sprague-Dawley rats

Peptides ◽  
2019 ◽  
Vol 119 ◽  
pp. 170080 ◽  
Author(s):  
Tianyi Zhang ◽  
Mofei Wang ◽  
Lei Liu ◽  
Bing He ◽  
Jingyao Hu ◽  
...  
Keyword(s):  
Weight Loss ◽  
Feeding Behavior ◽  
Signaling Pathway ◽  
Erk Signaling ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

scholarly journals eNAMPT neutralization reduces preclinical ARDS severity via rectified NFkB and Akt/mTORC2 signaling

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Tadeo Bermudez ◽  
Saad Sammani ◽  
Jin H. Song ◽  
Vivian Reyes Hernon ◽  
Carrie L. Kempf ◽  
...  
Keyword(s):  
Lung Injury ◽  
Signaling Pathway ◽  
Unmet Need ◽  
Serum Lactate ◽  
Sprague Dawley ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Molecular Pattern ◽  
Sprague Dawley Rats ◽  
Pathway Activation ◽  
Nfkb Pathway

AbstractDespite encouraging preclinical data, therapies to reduce ARDS mortality remains a globally unmet need, including during the COVID-19 pandemic. We previously identified extracellular nicotinamide phosphoribosyltransferase (eNAMPT) as a novel damage-associated molecular pattern protein (DAMP) via TLR4 ligation which regulates inflammatory cascade activation. eNAMPT is tightly linked to human ARDS by biomarker and genotyping studies in ARDS subjects. We now hypothesize that an eNAMPT-neutralizing mAb will significantly reduce the severity of ARDS lung inflammatory lung injury in diverse preclinical rat and porcine models. Sprague Dawley rats received eNAMPT mAb intravenously following exposure to intratracheal lipopolysaccharide (LPS) or to a traumatic blast (125 kPa) but prior to initiation of ventilator-induced lung injury (VILI) (4 h). Yucatan minipigs received intravenous eNAMPT mAb 2 h after initiation of septic shock and VILI (12 h). Each rat/porcine ARDS/VILI model was strongly associated with evidence of severe inflammatory lung injury with NFkB pathway activation and marked dysregulation of the Akt/mTORC2 signaling pathway. eNAMPT neutralization dramatically reduced inflammatory indices and the severity of lung injury in each rat/porcine ARDS/VILI model (~ 50% reduction) including reduction in serum lactate, and plasma levels of eNAMPT, IL-6, TNFα and Ang-2. The eNAMPT mAb further rectified NFkB pathway activation and preserved the Akt/mTORC2 signaling pathway. These results strongly support targeting the eNAMPT/TLR4 inflammatory pathway as a potential ARDS strategy to reduce inflammatory lung injury and ARDS mortality.

scholarly journals Naringenin Protects Rats against Ang-II Induced Cardiac Hypertrophy and Fibrosis by Downregulating TGF-β1/Smads Signaling Pathways

2021 ◽  
Author(s):  
Xiaowei Chen ◽  
Xi Zhao ◽  
Han Wang ◽  
Hengdao Liu
Keyword(s):  
Signaling Pathway ◽  
Cardiac Remodeling ◽  
Cardiac Fibroblasts ◽  
Biological Properties ◽  
Heart Weight ◽  
Cardiomyocyte Hypertrophy ◽  
In Vitro Experiments ◽  
Sprague Dawley ◽  
Tgf Β1

Abstract Background:Naringenin (Nrg), a flavone found in several plant foods with various biological properties, has been shown prevention of cardiac remodeling. However, themechanisms underlying this suppression of cardiac remodeling has not been known clearly.Methods: Male Sprague Dawley (SD) rats were AngII infused via osmotic minipumps for 4 weeks and were given Nrg by gavage (100mg/kg/day) at the same time. In vitro experiments used cardiomyocyte and cardiac fibroblasts(CF) treated with AngII or AngII plus Nrg.Cardiac remodeling was assessed using the echocardiography and histological analysis. And, the effect of Nrg on TGF-β1/Smadssignaling pathway was investigated.Results: Treatmentwith Nrg(100mg/kg/day) decreased the ratio of heart weight to tibia length and hypertrophy markers in rats given AngII infusion. In vitro experiments demonstrated that AngII-induced cardiomyocyte hypertrophy and proliferation of CFs were significantly inhibited by Nrg administration. Nrg inhibited activation of the TGF-β1/Smad2/3 signaling pathway stimulated by AngII. Conclusions: Nrgsupplementation prevented cardiac remodeling via down-regulating the TGF-β1/Smad2/3 signaling pathway both in cardiomyocyte and CFs, and attenuating cardiac remodeling in AngII-induced rats model.

scholarly journals Intraperitoneal injection of PDTC on the NF-kB signaling pathway and osteogenesis indexes of young adult rats with anterior palatal suture expansion model

PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0243108
Author(s):  
Yafang Li ◽  
Yiqiang Qiao ◽  
Huanhuan Wang ◽  
Zao Wang
Keyword(s):  
Young Adult ◽  
Signaling Pathway ◽  
Intraperitoneal Injection ◽  
Control Group ◽  
Sprague Dawley ◽  
Adult Rats ◽  
Morphogenetic Protein ◽  
Sprague Dawley Rats ◽  
The Difference ◽  
Expansion Model

In recent years, many studies have found that mechanical tension can activiate NF-kB signal pathway and NF-kB plays an important role in the process of osteogenesis. However, it is still unclear whether this process exists in the anterior palatal suture expansion. In this paper, we mainly studied the effect of intraperitoneal injection of PDTC on the NF-kB signaling pathway and osteogenesis index of the anterior palatal suture expansion model in young adult rats. The expansion model is grouped and established: 45 male 8-week-old Sprague-Dawley rats were randomly divided into three groups, an expansion only (EO) group, an expansion plus PDTC (PE) group, and a control group. The results revealed that PDTC inhibited the activity of NF-kB signaling pathway and promote one morphogenetic protein 2 (BMP-2), steocalatin (OCN) expression. Compared with the control group, the optical density (OD) value of BMP in the EO group and PE group rats increased significantly from the first day to the seventh day, and the difference was statistically significant (P<0.05). After 6.0Gy irradiation, PDTC administration group could slightly increase the total SOD level in the liver and serum of rats, and reduce the MDA level in the liver and serum, especially the effect of 60mg/kg and 90mg/kg was the most obvious.

scholarly journals The protective effects of liguzinediol on congestive heart failure induced by myocardial infarction and its relative mechanism

2020 ◽  
Author(s):  
Qi Chen ◽  
Dini Zhang ◽  
Yunhui Bi ◽  
Weiwei Zhang ◽  
Yuhan Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Ventricular Remodeling ◽  
Myocardial Cell ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Cardiac Functions ◽  
Tgf Β1

Abstract Background : Heart failure (HF) is one of the most common causes of cardiovascular diseases in the world. Currently, the drugs used to treat HF in the clinic may cause serious side effects. Liguzinediol, 2, 5-dimethyl-3, 6-dimethyl-pyrazine, is a compound synthesized after the structural modification of ligustrazine (one active ingredient of Szechwan Lovage Rhizome ). We aimed to observe the effects of liguzinediol on preventing HF and explore the related mechanisms. Methods : The ligation of left anterior descending coronary artery was operated to established the myocardial infarction (MI) model in Sprague–Dawley rats. Cardiac functions were recorded by echocardiography and hemodynamics. The changes in the Renin-Angiotensin-Aldosterone System (RAAS), inflammation, and oxidative stress were detected by radioimmunoassay and Elisa kits. Western blot and real-time PCR were applied to determine the expressions of the TGF-β1/Smads pathway. Results : Firstly, liguzinediol enhanced the systolic and diastolic functions of the heart in MI rats. Liguzinediol improved ventricular remodeling by reducing myocardial cell necrosis, as well as reducing collagen deposition and myocardial fibrosis. Then, liguzinediol suppressed the activation of RAAS, inhibited the synthesis of pro-inflammation factors, and reduced oxidative stress. In the end, liguzinediol also down-regulated the expressions of the TGF-β1/Smads pathway. Conclusions : Liguzinediol could alleviate HF caused by MI in rats, and the protective effect was associated with the regulation of the TGF-β1/Smads pathway.

Developmental exposure to paraquat and maneb can impair cognition, learning and memory in Sprague-Dawley rats

2016 ◽  
Vol 12 (10) ◽  
pp. 3088-3097 ◽  
Author(s):  
Bai Li ◽  
Xi He ◽  
Yan Sun ◽  
Baixiang Li
Keyword(s):  
Cognitive Function ◽  
Signaling Pathway ◽  
Learning And Memory ◽  
Sprague Dawley ◽  
Developmental Exposure ◽  
Rat Offspring ◽  
Sprague Dawley Rats

PQ–MB may affect the behavior and cognitive function of rat offspring through the cAMP–PKA–CREB signaling pathway.

scholarly journals In vivo regulation of renal expression of (pro)renin receptor by a low-sodium diet

2012 ◽  
Vol 303 (12) ◽  
pp. F1652-F1657 ◽  
Author(s):  
Luis C. Matavelli ◽  
Jiqian Huang ◽  
Helmy M. Siragy
Keyword(s):  
Signaling Pathway ◽  
Urinary Sodium Excretion ◽  
Sprague Dawley ◽  
No Donor ◽  
Low Sodium Diet ◽  
Sprague Dawley Rats ◽  
Cgmp Analog ◽  
Synthase Inhibitor ◽  
Renal Expression

Effects of low salt (LS) on (pro)renin receptor (PRR) expression are not well established. We hypothesized that LS enhances renal PRR expression via the cGMP-protein kinase G (PKG) signaling pathway. Sprague-Dawley rats were fed a normal-salt (NS) or LS diet associated with intrarenal cortical administration of vehicle (V), the nitric oxide (NO) synthase inhibitor nitro-l-arginine methyl ester (l-NAME), the NO donor S-nitroso- N-acetyl-dl-penicillamine (SNAP), the cGMP analog 8-bromoguanosine (8-Br)-cGMP, the guanylyl cyclase inhibitor 1H-[1, 2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), or a PKG inhibitor (PKGi) for 6 days via osmotic minipump. We evaluated the effects of each treatment on renal interstitial fluid (RIF) levels of nitrate/nitrite and cGMP and renal PRR expression. There were no significant changes in blood pressure with any of the treatments. Urinary sodium excretion was significantly lower in rats given a LS diet. Compared with NS + V, RIF nitrate/nitrite and cGMP levels increased in LS + V rats. In NS groups, RIF nitrate/nitrite and cGMP levels did not change with l-NAME, ODQ, or PKGi and increased in response to SNAP. 8-Br-cGMP increased RIF cGMP but not RIF nitrate/nitrite. In LS groups, RIF nitrate/nitrite decreased with l-NAME and did not change with ODQ or PKGi whereas RIF cGMP decreased with l-NAME, ODQ, and PKGi. PRR mRNA and protein increased in LS + V. In NS rats, PRR mRNA and protein increased in response to 8-Br-GMP and were not affected by any of other treatments. In LS rats, PRR mRNA and protein decreased significantly in response to l-NAME, ODQ, and PKGi. We conclude that LS intake enhances renal expression of PRR via cGMP-PKG signaling pathway.

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