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1.
Front Mol Biosci ; 8: 699929, 2021.
Article in English | MEDLINE | ID: mdl-34368228

ABSTRACT

SARS-CoV-2 infection has become an urgent public health concern worldwide, severely affecting our society and economy due to the long incubation time and high prevalence. People spare no effort on the rapid development of vaccine and treatment all over the world. Amongst the numerous ways of tackling this pandemic, some approaches using extracellular vesicles (EVs) are emerging. In this review, we summarize current prevalence and pathogenesis of COVID-19, involving the combination of SARS-CoV-2 and virus receptor ACE2, endothelial dysfunction and micro thrombosis, together with cytokine storm. We also discuss the ongoing EVs-based strategies for the treatment of COVID-19, including mesenchymal stem cell (MSC)-EVs, drug-EVs, vaccine-EVs, platelet-EVs, and others. This manuscript provides the foundation for the development of targeted drugs and vaccines for SARS-CoV-2 infections.

2.
Free Radic Res ; 42(1): 12-9, 2008 Jan.
Article in English | MEDLINE | ID: mdl-18324519

ABSTRACT

Polypeptide from Chlamys farreri (PCF), a novel marine active material isolated from gonochoric Chinese scallop C. farreri, has potential antioxidant activity and protective effect against ultraviolet (UV) irradiation. The aim was to investigate whether PCF protects HaCaT cells from apoptosis induced by UVA and explore related molecular mechanisms. The results showed that PCF significantly prevented UVA-induced apoptosis of HaCaT cells. PCF not only strongly reduced the intracellular reactive oxygen species (ROS) production, but also diminished expression of acid sphingomyelinase (ASMase) and phosphorylated JNK in HaCaT cells radiated by UVA in a dose-dependent manner. Pre-treatment with ROS scavenger NAC, ASMase inhibitor desipramine or JNK inhibitor SP600125 was found to effectively prohibit UVA-induced apoptosis and desipramine markedly blocked phosphorylation of JNK. So it is concluded that PCF obviously protects HaCaT cells from apoptosis induced by UVA and protective effects may attribute to decreasing intracellular ROS level and blocking ASMase/JNK apoptotic signalling pathway.


Subject(s)
Antioxidants/pharmacology , Apoptosis/drug effects , JNK Mitogen-Activated Protein Kinases/metabolism , Keratinocytes/drug effects , Pectinidae , Peptides/pharmacology , Reactive Oxygen Species/metabolism , Sphingomyelin Phosphodiesterase/metabolism , Ultraviolet Rays , Acetylcysteine/pharmacology , Animals , Anthracenes/pharmacology , Antioxidants/isolation & purification , Cell Line , Desipramine/pharmacology , Dose-Response Relationship, Drug , Enzyme Activation , Free Radical Scavengers/pharmacology , Humans , JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors , Keratinocytes/enzymology , Keratinocytes/metabolism , Keratinocytes/pathology , Keratinocytes/radiation effects , Pectinidae/chemistry , Peptides/isolation & purification , Phosphorylation , Protein Kinase Inhibitors/pharmacology , Signal Transduction/drug effects , Signal Transduction/radiation effects , Sphingomyelin Phosphodiesterase/antagonists & inhibitors
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