Longdan Xiegan Tang attenuates liver injury and hepatic insulin resistance by regulating the angiotensin-converting enzyme 2/Ang (1-7)/Mas axis-mediated anti-inflammatory pathway in rats

2021 ◽  
pp. 114072
Author(s):  
Chengliang Wang ◽  
Liying Ren ◽  
Shankang Chen ◽  
Huihui Zheng ◽  
Yifan Yang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Injury ◽  
Angiotensin Converting Enzyme ◽  
Hepatic Insulin Resistance ◽  
Converting Enzyme ◽  
Inflammatory Pathway ◽  
Angiotensin Converting Enzyme 2 ◽  
Anti Inflammatory

scholarly journals Ginsenoside Rc Ameliorates Endothelial Insulin Resistance via Upregulation of Angiotensin-Converting Enzyme 2

2021 ◽  
Vol 12 ◽  
Author(s):  
Yaozhen Wang ◽  
Wenwen Fu ◽  
Yan Xue ◽  
Zeyuan Lu ◽  
Yuangeng Li ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Endothelial Dysfunction ◽  
Angiotensin Converting Enzyme ◽  
Vascular Complications ◽  
Health Concern ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Anti Inflammatory ◽  
Ginsenoside Rc

Type 2 diabetes mellitus (T2DM) is a major health concern which may cause cardiovascular complications. Insulin resistance (IR), regarded as a hallmark of T2DM, is characterized by endothelial dysfunction. Ginsenoside Rc is one of the main protopanaxadiol-type saponins with relatively less research on it. Despite researches confirming the potent anti-inflammatory and antioxidant activities of ginsenoside Rc, the potential benefits of ginsenoside Rc against vascular complications have not been explored. In the present study, we investigated the effects of ginsenoside Rc on endothelial IR and endothelial dysfunction with its underlying mechanisms using high glucose- (HG-) cultured human umbilical vein endothelial cells (HUVECs) in vitro and a type 2 diabetic model of db/db mice in vivo. The results showed that ginsenoside Rc corrected the imbalance of vasomotor factors, reduced the production of Ang (angiotensin) II, and activated angiotensin-converting enzyme 2 (ACE2)/Ang-(1–7)/Mas axis in HG-treated HUVECs. Besides, ginsenoside Rc improved the impaired insulin signaling pathway and repressed oxidative stress and inflammatory pathways which constitute key factors leading to IR. Interestingly, the effects of ginsenoside Rc on HG-induced HUVECs were abolished by the selective ACE2 inhibitor MLN-4760. Furthermore, ginsenoside Rc exhibited anti-inflammatory as well as antioxidant properties and ameliorated endothelial dysfunction via upregulation of ACE2 in db/db mice, which were confirmed by the application of MLN-4760. In conclusion, our findings reveal a novel action of ginsenoside Rc and demonstrate that ginsenoside Rc ameliorated endothelial IR and endothelial dysfunction, at least in part, via upregulation of ACE2 and holds promise for the treatment of diabetic vascular complications.

scholarly journals COVID-19 and Liver injury: hepatology perspectives

2020 ◽  
Vol 2 (3) ◽  
pp. 01-04
Author(s):  
Irami Filho
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Severe Acute Respiratory Syndrome ◽  
Angiotensin Converting Enzyme ◽  
Liver Damage ◽  
Clinical Manifestations ◽  
Protein S ◽  
Clinical Syndrome ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2

SARS-CoV-2, a severe acute respiratory syndrome caused by Coronavirus 2, discovered in 2019 in China, is responsible for the current pandemic declared by the WHO since March 2020. The clinical syndrome caused by Covid-19 has a broad spectrum of severity. The most common clinical manifestations are fever, dry cough, dyspnea, fatigue, and anosmia. The virus binds to receptors for angiotensin-converting enzyme 2 (ECA2) and serine protease TMPRSS2 for protein S initiation, which are expressed not only in the lungs but also in the liver, colonic, esophageal and biliary epithelial cells. In this context, the liver is a potential target for COVID-19 infection. Liver damage occurs during the course and treatment of viral infection in patients with or without previous liver disease. Therefore, the characteristics of liver injury associated with COVID-19 were reviewed based on research related, in the context of the pandemic.

scholarly journals Nonsteroidal anti-inflammatory drugs and ibuprofen for COVID-19: a systematic review

2020 ◽  
Vol 22 (12) ◽  
pp. 31-36
Author(s):  
Marina V. Leonova ◽  
Keyword(s):  
Systematic Review ◽  
Angiotensin Converting Enzyme ◽  
Observational Studies ◽  
World Health ◽  
Supporting Evidence ◽  
Converting Enzyme ◽  
Nsaid Treatment ◽  
Angiotensin Converting Enzyme 2 ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

COVID-19 pandemic is currently the most pressing public health problem worldwide. Despite growing knowledge about the nature of SARS-CoV-2-assosiated severe acute respiratory syndrome, the treatment options are still poorly defined. The safety of nonsteroidal anti-inflammatory drugs (NSAIDs), in particular ibuprofen, has been questioned without any supporting evidence. This has contributed to a number of observational studies evaluating the effect of ibuprofen on COVID-19 disease outcomes. A search of publications was carried out and a systematic review of 9 studies was presented, pharmacodynamic effects of ibuprofen were considered in terms of the effect on angiotensin-converting enzyme 2 and cyclooxygenase. The studies data have shown no direct interaction between ibuprofen and SARS-CoV-2, no evidence that ibuprofen affects the up-regulation of angiotensin-converting enzyme 2 as a COVID-19 receptor in human studies. Observational studies have not found evidence that ibuprofen, when used chronically before COVID-19 or when acutely used to relieve symp-toms of COVID-19, contributes to infection or increases the risk of adverse outcomes (mortality, risk of hospitalization, risk of mechanical ventilation). Subse-quently, international regulatory authorities (World Health Organization, European Medical Agency, FDA) concluded that there is no link between the more severe course of COVID-19 and NSAID treatment; paracetamol and other NSAIDs (ibuprofen) are recommended to treat the symptoms of COVID-19; patients on chronic NSAID treatment are warned not to discontinue it, as their condition may worsen.

Thermodynamics of the interaction between the spike protein of severe acute respiratory syndrome- coronavirus-2 and the receptor of human angiotensin converting enzyme 2. Effects of possible ligands

2020 ◽  
Author(s):  
Cristina Garcia-Iriepa ◽  
Cecilia Hognon ◽  
Antonio Francés-Monerris ◽  
Isabel Iriepa ◽  
Tom Miclot ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Molecular Mechanisms ◽  
Molecular Design ◽  
Binding Free Energy ◽  
Transmembrane Protein ◽  
Spike Protein ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Rational Molecular Design ◽  
Rational Evaluation

<div><p>Since the end of 2019, the coronavirus SARS-CoV-2 has caused more than 180,000 deaths all over the world, still lacking a medical treatment despite the concerns of the whole scientific community. Human Angiotensin-Converting Enzyme 2 (ACE2) was recently recognized as the transmembrane protein serving as SARS-CoV-2 entry point into cells, thus constituting the first biomolecular event leading to COVID-19 disease. Here, by means of a state-of-the-art computational approach, we propose a rational evaluation of the molecular mechanisms behind the formation of the complex and of the effects of possible ligands. Moreover, binding free energy between ACE2 and the active Receptor Binding Domain (RBD) of the SARS-CoV-2 spike protein is evaluated quantitatively, assessing the molecular mechanisms at the basis of the recognition and the ligand-induced decreased affinity. These results boost the knowledge on the molecular grounds of the SARS-CoV-2 infection and allow to suggest rationales useful for the subsequent rational molecular design to treat severe COVID-19 cases.</p></div>

Sign in / Sign up

Export Citation Format

Share Document