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#33672590   2021/02/20 To Up

Molecular and Biochemical Pathways of Catalpol in Alleviating Diabetes Mellitus and Its Complications.

Catalpol isolated from is a potent antioxidant and investigated against many disorders. This review appraises the key molecular pathways of catalpol against diabetes mellitus and its complications. Multiple search engines including Google Scholar, PubMed, and Science Direct were used to retrieve publications containing the keywords "Catalpol", "Type 1 diabetes mellitus", "Type 2 diabetes mellitus", and "diabetic complications". Catalpol promotes IRS-1/PI3K/AKT/GLUT2 activity and suppresses Phosphoenolpyruvate carboxykinase (PEPCK) and Glucose 6-phosphatase (G6Pase) expression in the liver. Catalpol induces myogenesis by increasing MyoD/MyoG/MHC expression and improves mitochondria function through the AMPK/PGC-1α/PPAR-γ and TFAM signaling in skeletal muscles. Catalpol downregulates the pro-inflammatory markers and upregulates the anti-inflammatory markers in adipose tissues. Catalpol exerts antioxidant properties through increasing superoxide dismutase (sod), catalase (cat), and glutathione peroxidase (gsh-px) activity in the pancreas and liver. Catalpol has been shown to have anti-oxidative, anti-inflammatory, anti-apoptosis, and anti-fibrosis properties that in turn bring beneficial effects in diabetic complications. Its nephroprotective effect is related to the modulation of the AGE/RAGE/NF-κB and TGF-β/smad2/3 pathways. Catalpol produces a neuroprotective effect by increasing the expression of protein Kinase-C (PKC) and Cav-1. Furthermore, catalpol exhibits a cardioprotective effect through the apelin/APJ and ROS/NF-κB/Neat1 pathway. Catalpol stimulates proliferation and differentiation of osteoblast cells in high glucose condition. Lastly, catalpol shows its potential in preventing neurodegeneration in the retina with NF-κB downregulation. Overall, catalpol exhibits numerous beneficial effects on diabetes mellitus and diabetic complications.
Subrat Kumar Bhattamisra, Hui Min Koh, Shin Yean Lim, Hira Choudhury, Manisha Pandey

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#33667414   2021/02/23 To Up

Modulation of APLNR Signaling Is Required during the Development and Maintenance of the Hematopoietic System.

Apelin receptor (APLNR/AGTRLl1/APJ) marks a transient cell population during the differentiation of hematopoietic stem and progenitor cells (HSPCs) from pluripotent stem cells, but its function during the production and maintenance of hematopoietic stem cells is not clear. We generated an Aplnr-tdTomato reporter mouse embryonic stem cell (mESC) line and showed that HSPCs are generated exclusively from mesodermal cells that express Aplnr-tdTomato. HSPC production from mESCs was impaired when Aplnr was deleted, implying that this pathway is required for their production. To address the role of APLNR signaling in HSPC maintenance, we added APELIN ligands to ex vivo AGM cultures. Activation of the APLNR pathway in this system impaired the generation of long-term reconstituting HSPCs and appeared to drive myeloid differentiation. Our data suggest that the APLNR signaling is required for the generation of cells that give rise to HSCs, but that its subsequent downregulation is required for their maintenance.
Melany Jackson, Antonella Fidanza, A Helen Taylor, Stanislav Rybtsov, Richard Axton, Maria Kydonaki, Stephen Meek, Tom Burdon, Alexander Medvinsky, Lesley M Forrester

2884 related Products with: Modulation of APLNR Signaling Is Required during the Development and Maintenance of the Hematopoietic System.

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#33663236   2021/03/05 To Up

In Vitro and In Vivo Evaluation of a Small-Molecule APJ (Apelin Receptor) Agonist, BMS-986224, as a Potential Treatment for Heart Failure.

New heart failure therapies that safely augment cardiac contractility and output are needed. Previous apelin peptide studies have highlighted the potential for APJ (apelin receptor) agonism to enhance cardiac function in heart failure. However, apelin's short half-life limits its therapeutic utility. Here, we describe the preclinical characterization of a novel, orally bioavailable APJ agonist, BMS-986224.
Peter Gargalovic, Pancras Wong, Joelle Onorato, Heather Finlay, Tao Wang, Mujing Yan, Earl Crain, Stéphane St-Onge, Madeleine Héroux, Michel Bouvier, Carrie Xu, Xue-Qing Chen, Claudia Generaux, Michael Lawrence, Ruth Wexler, David Gordon

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#33660355   2021/03/04 To Up

Supplement therapy with apelin for improving the TSH level and lipid disorders in PTU-induced hypothyroid rats.

Hyperlipidemia is a common metabolic disorder in the general population, which may arise in hypothyroidism. Apelin is an endogenous ligand which acts as an adiponectin, and is involved in energy storage and metabolism. This study evaluated the effects of apelin administration per se or in combination with T4 on the serum level of thyroid-stimulating hormone, body weight and lipid profile, along with the serum level of apelin, and its mRNA expression in heart, in 6-propyl-2-thiouracil (PTU)-induced hypothyroid rats. Male Wistar rats were assigned to five different groups: Control, H (hypothyroid), H+A, H+T, and H+A+T. All groups except the control one received PTU (0.05%) in the drinking water for six weeks. In addition to PTU, the H+A, H+T, and H+A+T groups, received apelin (200 μg/kg/day, i.p.), L-thyroxin (T4) (20 μg/kg/day, via gavage tube), and apelin+T4 during the last 14 days of the trial, respectively. A combined application of T4 and apelin in the H+A+T group effectively diminished mean TSH level, LDL-C/HDL-C ratio and atherogenic index (AI) in these animals when compared to these values for the H group. co-administration of Apelin with T4 may offer valuable therapeutic benefits, specifically lowering blood plasma TSH, and lipid disorder and atherosclerosis biomarkers, in PTU-induced hypothyroid rats. This article is protected by copyright. All rights reserved.
Mohammad Badavi, Martin Grootveld, Fereshteh Jafari, Mahin Dianat, Farzaneh Faraji Shahrivar

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#33657655   2021/03/03 To Up

Evodiamine alleviates lipopolysaccharide-induced pulmonary inflammation and fibrosis by activating apelin pathway.

Inflammation can cause a series of inflammatory lung disease, which seriously endangers human health. Pulmonary fibrosis is a kind of inflammatory disease with end-stage lung pathological changes. It has complicated and unknown pathogenesis and is still lack of effective therapeutic drugs. LPS-induced inflammation is a common feature of many infectious inflammations such as pneumonia, bacteremia, glomerulonephritis, etc. Evodiamine, one of the main components of Evodia rutaecarpa, is an alkaloid with excellent antiinflammatory effects. In this study, we evaluated the protective capacities of evodiamine on LPS-induced inflammatory damages in vitro and in vivo. MTT method, flow cytometry, immunofluorescence, and other methods were used for in vitro study to determine the protective capacities of evodiamine. The results suggest that evodiamine can protect murine macrophages from the LPS-nigericin-induced damages by (a) inhibiting cellular apoptosis, (b) inhibiting inflammatory cytokines releasing, and (c) activating the apelin pathway. We also used the exogenous apelin-13 peptide co-cultured with LPS-nigericin in RAW264.7 cells and found that apelin-13 contributes to protecting the effects of evodiamine. In vivo, the ELISA method and immunohistochemistry were used to examine inflammatory cytokines, apelin, and histological changes. BALB/c mice were exposed to LPS and subsequent administration of evodiamine (p.o.)for some time, the results of the alveolar lavage fluid and the tissue slices showed that evodiamine treatment alleviated the pulmonary inflammation and fibrosis, stimulated apelin expression and inhibited the inflammatory cytokines. These results provide a basis for the protective effect and mechanism of evodiamine in LPS-induced inflammation and suggest that it might be potential therapeutics in human pulmonary infections.
Cui Ye, Nan Zhang, Qian Zhao, Xin Xie, Xiang Li, Hong-Ping Zhu, Cheng Peng, Wei Huang, Bo Han

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#33645481   2021/02/28 To Up

A Review on Novel Ligand Targeted Delivery for Cardiovascular Disorder.

Cardiovascular disease covers the various disorders like ischemic heart disease, hyperlipidemia, atherosclerosis, myocardial infarction, and hypertension etc. There are many synthetic drugs are available for the treatment of cardiovascular therapy, but they have several drawbacks like high dosing, toxicity, elevated blood potassium levels, low blood pressure, and gastrointestinal issues etc. To overcome these side effects of synthetic drugs by targeting the drug to the specific cardiac tissue is the best novel method in the cardiovascular therapy. The highest targeting efficacy of Ligand-based therapy with proper mechanisms and improved expandability provides a novel therapeutic strategy in the cardiovascular disease. Ligand therapy is cost-effective compared to cell-based therapy. The surface area of protein has much larger than the orally bioavailable drug. So, the targeting of various less active drug molecules to the particular ligand can be possible. The efficacy of ligands to induce cardiomyocytes proliferation has been ratified and point out the fact that ligand-based approaches are effective for cardiac transformation. Ligands interact with proteins in target cells, which are influenced through the chemical signals. These various receptors possess selective binding of biased ligands and also energizing the intracellular signaling pathway. The ligands can directly stabilize the active receptor conformations by a non-standard connective site. The key function of ligands is functional selectivity, which enhances the therapeutic efficacy and minimizes the side effects of drugs through the interpretation of signal transduction pathways. This review covers the role and effectiveness of novel ligands in the cardiovascular disorders.
Shweta Jaiswal, P S Rajnikanth, Sunita Thakur, Payal Deepak, Sneha Anand

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#33643639   2021/02/16 To Up

Plasma apelin level in acute myocardial infarction and its relation with prognosis: A prospective study.

Apelin is a novel adipocytokine with a significant role in ischemia/reperfusion injury that is synthesized and secreted in myocardial cells and coronary endothelium. There is debate on its value for the diagnosis and prognosis of myocardial infarction. We aimed to investigate plasma apelin level in patients with acute ST segment elevation (STEMI) and non-ST segment elevation (NSTEMI) myocardial infarction and its relationship with left ventricular function and prognostic parameters.
Ozge Guzelburc, Refik Demirtunc, Servet Altay, Tugba Kemaloglu Oz, Gulsah Tayyareci

2570 related Products with: Plasma apelin level in acute myocardial infarction and its relation with prognosis: A prospective study.

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#33640616   2021/02/20 To Up

Neuroprotective gain of Apelin/APJ system.

Apelin is an endogenous ligand of G protein-coupled receptor APJ. In recent years, many studies have shown that the apelin/APJ system has neuroprotective properties, such as anti-inflammatory, anti-oxidative stress, anti-apoptosis, and regulating autophagy, blocking excitatory toxicity. Apelin/APJ system has been proven to play a role in various neurological diseases and may be a promising therapeutic target for nervous system diseases. In this paper, the neuroprotective properties of the apelin/APJ system and its role in neurologic disorders are reviewed. Further understanding of the pathophysiological effect and mechanism of the apelin/APJ system in the nervous system will help develop new therapeutic interventions for various neurological diseases.
Jia-Xiu Zhou, Nian-Nian Shuai, Bo Wang, Xin Jin, Xin Kuang, Shao-Wen Tian

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#33640615   2021/02/18 To Up

Apelin-13 attenuates spatial memory impairment by anti-oxidative, anti-apoptosis, and anti-inflammatory mechanism against ethanol neurotoxicity in the neonatal rat hippocampus.

It has been shown that alcohol consumption by pregnant women can have detrimental effects on the developing fetus and lead to fetal alcohol spectrum disorders (FASD). Exposure to alcohol in rat pups during this period causes long-term changes in the structure of the animal's hippocampus, leading to impaired hippocampal-related brain functions such as navigation tasks and spatial memory. Apelin-13, a principal neuropeptide with inhibitory effects on neuroinflammation and brain oxidative stress production, has beneficial properties on memory impairment and neuronal injury. The protective effects of apelin-13 have been evaluated on ethanol-related neurotoxicity in the hippocampus of rat pups. Rat pups from 2 until 10 postnatal day, similar to the third trimester of pregnancy in humans, were intubated total daily dose of ethanol (5/27 g/kg/day). Immediately after intubation, 25 and 50 μg/ kg of apelin-13 was injected subcutaneously. By using Morris water maze task, the hippocampus- dependent memory and spatial learning were evaluated 36 days after birth. Then, Immunohistochemical staining was done to determine the levels of GFAP and caspase-3. ELISA assay was also performed to measure both TNF-α and antioxidant enzymes levels. The current study demonstrates that administration of apelin-13 attenuates spatial memory impairment significantly (P < 0.001). After ethanol neurotoxicity, apelin-13 could also increase the catalase level (P < 0.001), activity of total superoxide dismutase as well as glutathione concentration noticeably (P < 0.05). Other impacts of it could be mentioned as attenuating TNF-α production and also preventing lipid peroxidation (P < 0.001). In addition, the results showed that the level of GFAP as a neuroinflammation factor and the number of active caspase-3 positive cells can be decreased by apelin-13 (P < 0.01). Regarding the protective effects of apelin-13 against ethanol-induced neurotoxicity, it is a promising therapeutic choice for FASD; but more studies are needed.
Fahimeh Mohseni, Behzad Garmabi, Mehdi Khaksari

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#33635165   2021/02/26 To Up

Gαi-biased apelin analogue protects against isoproterenol-induced myocardial dysfunction in rats.

Apelin-receptor (APJ) activation by apelin-13 (APLN-13) engages both Gαi proteins and β-arrestins, stimulating distinct intracellular pathways and triggering physiological responses like enhanced cardiac contractility. Substituting the C-terminal phenylalanine of APLN-13 with α-methyl-L-phenylalanine ((L-α-Me)Phe) or Benzoyl-L-phenylalanine (Bpa) generates biased analogues inducing APJ functional selectivity toward Gαi proteins. Using these original analogues, we proposed to investigate how the canonical Gαi signaling of APJ regulates the cardiac function, and to assess their therapeutic impact in a rat model of isoproterenol-induced myocardial dysfunction. In vivo and ex vivo infusions of either Bpa or (L-α-Me)Phe analogues failed to enhance rats left ventricular (LV) contractility compared to APLN-13. Inhibition of Gαi with pertussis-toxin injection optimized the cardiotropic effect of APLN-13 and revealed the inotropic impact of Bpa. Moreover, both APLN-13 and Bpa efficiently limited the forskolin-induced and PKA-dependent phosphorylation of phospholamban at the Ser16 in neonatal rat ventricular myocytes. However, only Bpa, significantly reduced the inotropic effect of forskolin infusion in isolated-perfused heart, highlighting its efficient bias toward Gαi. Compared to APLN-13, Bpa also markedly improved isoproterenol-induced myocardial systolic and diastolic dysfunctions. Bpa prevented cardiac weight increase, normalized both ANP and BNP mRNA expressions, and decreased LV fibrosis in isoproterenol-treated rats. Our results show that APJ-driven Gαi/adenylyl cyclase signaling is functional in cardiomyocytes and acts as negative feedback of the APLN-APJ-dependent inotropic response. Biased APJ signaling toward Gαi over the β-arrestin pathway offer a promising strategy in the treatment of cardiovascular diseases related to myocardial hypertrophy and high catecholamine levels.
David Coquerel, Eugénie Delile, Lauralyne Dumont, Frédéric Chagnon, Alexandre Murza, Xavier Sainsily, Dany Salvail, Philippe Sarret, Eric Marsault, Mannix Auger-Messier, Olivier Lesur

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