scholarly journals The Inhibition of H1N1 Influenza Virus-Induced Apoptosis by Surface Decoration of Selenium Nanoparticles with β-Thujaplicin through Reactive Oxygen Species-Mediated AKT and p53 Signaling Pathways

ACS Omega ◽  
2020 ◽  
Vol 5 (47) ◽  
pp. 30633-30642
Author(s):  
Changbing Wang ◽  
Haiyang Chen ◽  
Danyang Chen ◽  
Mingqi Zhao ◽  
Zhengfang Lin ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Influenza Virus ◽  
Signaling Pathways ◽  
H1n1 Influenza ◽  
Selenium Nanoparticles ◽  
Oxygen Species ◽  
H1n1 Influenza Virus ◽  
P53 Signaling ◽  
Surface Decoration ◽  
Induced Apoptosis

Inhibition of H1N1 influenza virus-induced apoptosis by selenium nanoparticles functionalized with arbidol through ROS-mediated signaling pathways

2019 ◽  
Vol 7 (27) ◽  
pp. 4252-4262 ◽  
Author(s):  
Yinghua Li ◽  
Zhengfang Lin ◽  
Guifang Gong ◽  
Min Guo ◽  
Tiantian Xu ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Signaling Pathways ◽  
Clinical Application ◽  
Antiviral Agent ◽  
H1n1 Influenza ◽  
Selenium Nanoparticles ◽  
Drug Resistant ◽  
H1n1 Influenza Virus ◽  
Induced Apoptosis

As an effective antiviral agent, the clinical application of arbidol is limited by the appearance of drug-resistant viruses.

scholarly journals The Inhibition of H1N1 influenza virus-induced apoptosis by functionalized Selenium nanoparticles with β-Thujaplicin through ROS-mediated P53 and AKT signaling pathways

2020 ◽  
Author(s):  
Changbing Wang ◽  
Mingqi Zhao ◽  
Zhengfang Lin ◽  
Min Guo ◽  
Tiantian Xu ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Signaling Pathways ◽  
Mdck Cells ◽  
Biological Activities ◽  
Chromatin Condensation ◽  
H1n1 Influenza ◽  
Selenium Nanoparticles ◽  
H1n1 Influenza Virus ◽  
Biomedical Intervention ◽  
Mechanistic Investigation

Abstract β-Thujaplicin possess a variety of biological activities. The use of modified biological nanoparticles (NPs) to develop novel anti-influenza drugs has increased in recent years. Selenium nanoparticles (SeNPs) with antiviral has attracted increasing attention for biomedical intervention. Functionalized SeNPs by β-Thujaplicin (Se@TP) surface modified with superior antiviral were synthesized in this study. β-Thujaplicin decoration of SeNPs obviously inhibited H1N1 infection and were less toxicity. Se@TP could inhibit H1N1 from infecting Madin Darby Canine Kidney (MDCK) cells and block chromatin condensation and DNA fragmentation. Se@TP obviously prevented MDCK cells from generating reactive oxygen species (ROS). Furthermore, Se@TP prevent lung injury in H1N1 infected mice through eosin staining and hematoxylin in vivo . Additionally, when treated with Se@TP, the DNA damage of lung tissues reduced substantially by TUNEL-DAPI test. Mechanistic investigation revealed that Se@TP inhibited H1N1 influenza virus from infecting MDCK cells through induction of apoptosis via suppression AKT and p53 signaling pathways through Immunohistochemical assay. Our results suggest that β-Thujaplicin modified SeNPs as carriers is an efficient way to achieve antiviral pharmaceutical candidate for H1N1 influenza.

scholarly journals Inhibition of H1N1 influenza virus by selenium nanoparticles loaded with zanamivir through p38 and JNK signaling pathways

RSC Advances ◽  
2017 ◽  
Vol 7 (56) ◽  
pp. 35290-35296 ◽  
Author(s):  
Zhengfang Lin ◽  
Yinghua Li ◽  
Min Guo ◽  
Misi Xiao ◽  
Changbing Wang ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Signaling Pathways ◽  
Clinical Application ◽  
Influenza Virus Infection ◽  
Aqueous Solubility ◽  
H1n1 Influenza ◽  
Solubility Limit ◽  
H1n1 Influenza Virus ◽  
Jnk Signaling

Zanamivir is an effective drug for influenza virus infection, but strong molecular polarity and aqueous solubility limit its clinical application.

scholarly journals Inhibitory activity of selenium nanoparticles functionalized with oseltamivir on H1N1 influenza virus

2017 ◽  
Vol Volume 12 ◽  
pp. 5733-5743 ◽  
Author(s):  
Yinghua Li ◽  
Zhengfang Lin ◽  
Min Guo ◽  
Yu Xia ◽  
Mingqi Zhao ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Inhibitory Activity ◽  
H1n1 Influenza ◽  
Selenium Nanoparticles ◽  
H1n1 Influenza Virus

Silver Nanoparticle Based Codelivery of Oseltamivir to Inhibit the Activity of the H1N1 Influenza Virus through ROS-Mediated Signaling Pathways

2016 ◽  
Vol 8 (37) ◽  
pp. 24385-24393 ◽  
Author(s):  
Yinghua Li ◽  
Zhengfang Lin ◽  
Mingqi Zhao ◽  
Tiantian Xu ◽  
Changbing Wang ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Signaling Pathways ◽  
Silver Nanoparticle ◽  
H1n1 Influenza ◽  
H1n1 Influenza Virus

ASK1 Is Activated by Treatment with Arsenic Trioxide through Accumulation of Reactive Oxygen Species and May Suppress Apoptosis through NF-kappaB in Leukemia Cells.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4394-4394 ◽  
Author(s):  
Ayako Arai ◽  
Weihua Yan ◽  
Hidenori Ichijo ◽  
Osamu Miura
Keyword(s):  
Reactive Oxygen Species ◽  
Signaling Pathways ◽  
Dominant Negative ◽  
The Other ◽  
Leukemia Cells ◽  
Oxygen Species ◽  
Low Concentrations ◽  
High Concentrations ◽  
Nf Kappab ◽  
Induced Apoptosis

Abstract Arsenic trioxide (ATO), a remarkably effective reagent for treatment of relapsed acute promyelocytic leukemia (APL), is reported to induce differentiation of APL cells at low concentrations and apoptosis at high concentrations. Induction of granulocytic differentiation is considered to be a specific effect of ATO on APL cells. By contrast, ATO commonly induces apoptosis of various tumor cells of hematological malignancies, including chronic myeloid leukemia cells expressing the BCR/ABL fusion kinase, as well as those of solid tumors. It was reported that ATO treatment induced intracellular accumulation of reactive oxygen species (ROS) by inhibiting glutathione peroxidase activity. Accumulated ROS induced a decline in cellular mitochondrial membrane potential, followed by cytochrome c release, caspase 3 activation, and apoptosis of cells. On the other hand, it is well known that adequate dose of ROS is indispensable for proliferation and survival of a variety of cells, including hematopoietic cells. Thus, various intracellular signaling pathways are strictly regulated and activated downstream of ROS to promote or suppress apoptosis, and the signaling pathways activated by ROS accumulation induced by ATO need to be defined to understand the mechanisms for ATO-induced apoptosis. Apoptosis signal-regulating kinase 1 (ASK1) is a ubiquitously expressed mitogen-activated protein kinase kinase kinase that activates the JNK and p38 signaling pathways and is involved in regulation of apoptosis. Here we find that ATO treatment of NB4 and K562 leukemia cells induces activation of ASK1. ATO induced accumulation of ROS, and the ASK1 activation was suppressed by cotreatment with an antioxidant, N-acetyl-l-cysteine. Although the Rho family GTPases Rac and cdc42 were activated by ATO, overexpression of their dominant-negative mutants did not suppress ATO-induced ASK1 activation. ASK1 activation was induced most significantly at low concentrations of ATO, where G2/M arrest but not apoptosis was induced. On the other hand, ASK1 activation induced by ATO was barely detectable at high concentrations, where apoptosis was induced significantly. By contrast, JNK and p38 were activated in dose-dependent manners by ATO. Murine embryonic fibroblasts (MEFs) derived from ASK1-deficient mice were more prone to ATO-induced apoptosis than control MEFs. Moreover, ASK1 was activated by ATO in a more sustained manner in ATO-resistant leukemia cell lines than in sensitive cell lines. Finally, a dominant-negative ASK1 mutant reduced ATO-induced NF-kappaB activation in leukemia cells. Together, the results indicate that ASK1 is activated by ATO through ROS generation independent of activation of Rac and cdc42 and may play a negative role in induction of apoptosis, possibly through activation of NF-kappaB.

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