Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 4 de 4
Filter
1.
Article in Chinese | WPRIM | ID: wpr-878989

ABSTRACT

In this paper, Asarum polysaccharides(AP) were extracted, and its composition was analyzed to study the activity against H1 N1 influenza virus in vitro and its intervention effect on mice with kidney Yang deficiency syndrome. AP was prepared by the strategy of water extraction and alcohol precipitation, the content was determined, and its monosaccharide composition was analyzed. The cell Real-time monitoring system and Reed-Muench model were adopted to evaluate the antiviral activity of AP in vitro. And the mouse model of kidney Yang deficiency syndrome was established in vivo to compare the efficacy of Mahuang Xixin Fuzi Decoction(MXF) and AP. MXF group and AP group were treated with clinical equivalent doses of 1.8 g·kg~(-1)·d~(-1) and 0.077 g·kg~(-1)·d~(-1) respectively, once a day for 6 consecutive days. Real-time PCR was used to detect the relative expression of M gene of H1 N1 influenza virus and cytokines in lung tissue. The content of AP in Asarum was 25.22%, and the protein content was 0.8%. And the monosaccharide composition was identified as L-rhamnose, D-arabinose, D-xylose, D-glucose, D-galactose and D-mannose. TI values of Tamiflu, MXF and AP were 30.00, 8.06 and 10.33, respectively. Three different doses of AP could significantly reduce the concentration of virus in supernatant. Compared with the model mice, lung indexes of MXF group and AP group decreased significantly(P<0.05), and the relative expression of M gene decreased significantly(P<0.05). The relative expressions of IL-10 and IFN-γ were up-regulated to varying degrees, while the relative gene expressions of IL-1β, IL-6 and MCP-1 were down-regulated to different degrees. In addition, AP could significantly enhance the expression of TNF-α(P<0.01). AP had a good anti-influenza virus activity in vitro, and could protect mice with kidney Yang deficiency syndrome by reducing the viral load in lung tissue, decreasing inflammation damage in lung tissue, and regulating the expression of inflammatory cytokines. Compared with the prescription of MXF, AP had a better antiviral activity.


Subject(s)
Animals , Antiviral Agents/therapeutic use , Asarum , Cytokines/genetics , Drugs, Chinese Herbal , Influenza A Virus, H1N1 Subtype , Influenza, Human/genetics , Lung , Mice , Polysaccharides
2.
Chinese Medical Journal ; (24): 2429-2436, 2020.
Article in English | WPRIM | ID: wpr-877825

ABSTRACT

BACKGROUND@#Endothelial cells play a key role in the cytokine storm caused by influenza A virus. MicroRNA-155 (miR-155) is an important regulator in inflammation. Its role in the inflammatory response to influenza A infection, however, has yet to be elucidated. In this study, we explored the role as well as the underlying mechanism of miR-155 in the cytokine production in influenza A-infected endothelial cells.@*METHODS@#Human pulmonary microvascular endothelial cells (HPMECs) were infected with the influenza A virus strain H1N1. The efficiency of H1N1 infection was confirmed by immunofluorescence. The expression levels of proinflammatory cytokines and miR-155 were determined using real-time polymerase chain reaction. A dual-luciferase reporter assay characterized the interaction between miR-155 and sphingosine-1-phosphate receptor 1 (S1PR1). Changes in the target protein levels were determined using Western blot analysis.@*RESULTS@#MiR-155 was elevated in response to the H1N1 infection in HPMECs (24 h post-infection vs. 0 h post-infection, 3.875 ± 0.062 vs. 1.043 ± 0.013, P = 0.001). Over-expression of miR-155 enhanced inflammatory cytokine production (miR-155 mimic vs. negative control, all P < 0.05 in regard of cytokine levels) and activation of nuclear factor kappa B in infected HPMECs (miR-155 mimic vs. negative control, P = 0.004), and down-regulation of miR-155 had the opposite effect. In addition, S1PR1 was a direct target of miR-155 in the HPMECs. Inhibition of miR-155 enhanced the expression of the S1PR1 protein. Down-regulation of S1PR1 decreased the inhibitory effect of the miR-155 blockade on H1N1-induced cytokine production and nuclear factor kappa B activation in HPMECs.@*CONCLUSION@#MiR-155 maybe modulate influenza A-induced inflammatory response by targeting S1PR1.


Subject(s)
Down-Regulation , Endothelial Cells , Humans , Influenza A Virus, H1N1 Subtype/genetics , Influenza A virus , Influenza, Human/genetics , MicroRNAs/genetics , Sphingosine-1-Phosphate Receptors
3.
Weekly Epidemiological Monitor. 2017; 10 (11): 1
in English | IMEMR | ID: emr-187399

ABSTRACT

In view of the need to enhance the functions of Influenza Laboratories in the Region, an assessment of the existing capacity and gaps have been conducted in the Eastern Mediterranean Region recently. Currently, 16 National Influenza Centres [NICs] in 15 Member States of the Region and Influenza Laboratories in seven countries, namely -Djibouti, Libya, Palestine, Saudi Arabia, Somalia, UAE and Yemen have been included in this assessment


Subject(s)
Humans , Orthomyxoviridae/pathogenicity , Influenza, Human/genetics , Respiratory Syncytial Viruses/growth & development , Influenza, Human
4.
Journal of Infection and Public Health. 2009; 2 (2): 74-80
in English | IMEMR | ID: emr-91759

ABSTRACT

In December 2006, three human specimens were received that were suspected positive for influenza A[H5N1]. The specimens were tested using real time PCR. And the presence of A[H5N1] virus was confirmed in 2 patients [16F and 26M], The NA sequence from A[H5N1] positive specimens collected before and after antiviral therapy revealed a mutation [N294S] [N295S according to N1 numbering], previously associated with resistance to oseltamivir. When tested with NA inhibition assays, the two N294S viruses from Egypt exhibited from 57 to 138-fold reduction in susceptibility to oseltamivir, depending on the assay. To our knowledge, this is the first time oseltamivir resistance has been detected in A[H5N1] infecting a human prior to treatment


Subject(s)
Influenza, Human/genetics , Oseltamivir , Drug Resistance , Mutation , Polymerase Chain Reaction , Neuraminidase , Public Health , Pneumonia , Respiratory Distress Syndrome
SELECTION OF CITATIONS
SEARCH DETAIL