tetano
Editor, Senior Moderator
Int J Mol Sci. 2018 Mar 23;19(4). pii: E965. doi: 10.3390/ijms19040965.
[h=1]Oxymatrine Inhibits Influenza A Virus Replication and Inflammation via TLR4, p38 MAPK and NF-κB Pathways.[/h] Dai JP[SUP]1[/SUP], Wang QW[SUP]2[/SUP], Su Y[SUP]3[/SUP], Gu LM[SUP]4[/SUP], Deng HX[SUP]5[/SUP], Chen XX[SUP]6[/SUP], Li WZ[SUP]7[/SUP], Li KS[SUP]8[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Oxymatrine (OMT) is a strong immunosuppressive agent that has been used in the clinic for many years. In the present study, by using plaque inhibition, luciferase reporter plasmids, qRT-PCR, western blotting, and ELISA assays, we have investigated the effect and mechanism of OMT on influenza A virus (IAV) replication and IAV-induced inflammation in vitro and in vivo. The results showed that OMT had excellent anti-IAV activity on eight IAV strains in vitro. OMT could significantly decrease the promoter activity of TLR3, TLR4, TLR7, MyD88, and TRAF6 genes, inhibit IAV-induced activations of Akt, ERK1/2, p38 MAPK, and NF-κB pathways, and suppress the expressions of inflammatory cytokines and MMP-2/-9. Activators of TLR4, p38 MAPK and NF-κB pathways could significantly antagonize the anti-IAV activity of OMT in vitro, including IAV replication and IAV-induced cytopathogenic effect (CPE). Furthermore, OMT could reduce the loss of body weight, significantly increase the survival rate of IAV-infected mice, decrease the lung index, pulmonary inflammation and lung viral titter, and improve pulmonary histopathological changes. In conclusion, OMT possesses anti-IAV and anti-inflammatory activities, the mechanism of action may be linked to its ability to inhibit IAV-induced activations of TLR4, p38 MAPK, and NF-κB pathways.
[h=4]KEYWORDS:[/h] MAPK; NF-κB; Oxymatrine; TLR; influenza A virus
PMID: 29570670 DOI: 10.3390/ijms19040965
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[h=1]Oxymatrine Inhibits Influenza A Virus Replication and Inflammation via TLR4, p38 MAPK and NF-κB Pathways.[/h] Dai JP[SUP]1[/SUP], Wang QW[SUP]2[/SUP], Su Y[SUP]3[/SUP], Gu LM[SUP]4[/SUP], Deng HX[SUP]5[/SUP], Chen XX[SUP]6[/SUP], Li WZ[SUP]7[/SUP], Li KS[SUP]8[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Oxymatrine (OMT) is a strong immunosuppressive agent that has been used in the clinic for many years. In the present study, by using plaque inhibition, luciferase reporter plasmids, qRT-PCR, western blotting, and ELISA assays, we have investigated the effect and mechanism of OMT on influenza A virus (IAV) replication and IAV-induced inflammation in vitro and in vivo. The results showed that OMT had excellent anti-IAV activity on eight IAV strains in vitro. OMT could significantly decrease the promoter activity of TLR3, TLR4, TLR7, MyD88, and TRAF6 genes, inhibit IAV-induced activations of Akt, ERK1/2, p38 MAPK, and NF-κB pathways, and suppress the expressions of inflammatory cytokines and MMP-2/-9. Activators of TLR4, p38 MAPK and NF-κB pathways could significantly antagonize the anti-IAV activity of OMT in vitro, including IAV replication and IAV-induced cytopathogenic effect (CPE). Furthermore, OMT could reduce the loss of body weight, significantly increase the survival rate of IAV-infected mice, decrease the lung index, pulmonary inflammation and lung viral titter, and improve pulmonary histopathological changes. In conclusion, OMT possesses anti-IAV and anti-inflammatory activities, the mechanism of action may be linked to its ability to inhibit IAV-induced activations of TLR4, p38 MAPK, and NF-κB pathways.
[h=4]KEYWORDS:[/h] MAPK; NF-κB; Oxymatrine; TLR; influenza A virus
PMID: 29570670 DOI: 10.3390/ijms19040965
Free full text