tetano
Editor, Senior Moderator
Biomed Pharmacother. 2018 Jun;102:1161-1175. doi: 10.1016/j.biopha.2018.03.161. Epub 2018 Apr 6.
[h=1]Antiviral effects of Ma Huang Tang against H1N1 influenza virus infection in vitro and in an ICR pneumonia mouse model.[/h] Wei W[SUP]1[/SUP], Wan H[SUP]1[/SUP], Peng X[SUP]1[/SUP], Zhou H[SUP]1[/SUP], Lu Y[SUP]2[/SUP], He Y[SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Ma Huang Tang (MHT), a classical Chinese herbal decoction which has been used in clinic for thousands of years, was very effective in treating the upper respiratory tract infection. But its activity against influenza virus A, the anti-inflammatory effect and the underlying mechanisms have been poorly investigated in previous researches. In this study, the antiviral efficacy of MHT directly inhibiting influenza virus A was investigated in vitro in MDCK cells. In an ICR pneumonia mouse model infected with influenza virus A PR/8/34, MHT (8, 4 and 2 g/kg) were oral administrated for 7 days after viral challenge, to evaluate the effect of MHT on ameliorating viral pneumonia and decipher the underlying mechanisms. The in vitro results showed that MHT possessed antiviral activity with low toxicity. The in vivo assays showed that MHT (8 and 4 g/kg) significantly attenuated lung histopathological changes, decreased lung index, interleukin (IL)-4,5, tumor necrosis factor alpha (TNF-α), CD3[SUP]+[/SUP], CD8[SUP]+[/SUP] T cell levels, increased IL-2, gamma interferon (IFN-γ), CD4[SUP]+[/SUP] T cell levels and CD4[SUP]+[/SUP]/CD8[SUP]+[/SUP] ratio, inhibited toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and tumor necrosis factor receptor associated factor 6 (TRAF6) protein levels. All these results demonstrate that MHT can strikingly ameliorate influenza virus A pneumonia in mice, which is associated with the regulating effect of MHT in the imbalance of body's immune function and the MyD88-dependent signaling pathway of TLR4.
[h=4]KEYWORDS:[/h] Inflammation response; Influenza virus; Ma Huang Tang; MyD88; TLR4; TRAF6
PMID: 29710534 DOI: 10.1016/j.biopha.2018.03.161
[h=1]Antiviral effects of Ma Huang Tang against H1N1 influenza virus infection in vitro and in an ICR pneumonia mouse model.[/h] Wei W[SUP]1[/SUP], Wan H[SUP]1[/SUP], Peng X[SUP]1[/SUP], Zhou H[SUP]1[/SUP], Lu Y[SUP]2[/SUP], He Y[SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Ma Huang Tang (MHT), a classical Chinese herbal decoction which has been used in clinic for thousands of years, was very effective in treating the upper respiratory tract infection. But its activity against influenza virus A, the anti-inflammatory effect and the underlying mechanisms have been poorly investigated in previous researches. In this study, the antiviral efficacy of MHT directly inhibiting influenza virus A was investigated in vitro in MDCK cells. In an ICR pneumonia mouse model infected with influenza virus A PR/8/34, MHT (8, 4 and 2 g/kg) were oral administrated for 7 days after viral challenge, to evaluate the effect of MHT on ameliorating viral pneumonia and decipher the underlying mechanisms. The in vitro results showed that MHT possessed antiviral activity with low toxicity. The in vivo assays showed that MHT (8 and 4 g/kg) significantly attenuated lung histopathological changes, decreased lung index, interleukin (IL)-4,5, tumor necrosis factor alpha (TNF-α), CD3[SUP]+[/SUP], CD8[SUP]+[/SUP] T cell levels, increased IL-2, gamma interferon (IFN-γ), CD4[SUP]+[/SUP] T cell levels and CD4[SUP]+[/SUP]/CD8[SUP]+[/SUP] ratio, inhibited toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and tumor necrosis factor receptor associated factor 6 (TRAF6) protein levels. All these results demonstrate that MHT can strikingly ameliorate influenza virus A pneumonia in mice, which is associated with the regulating effect of MHT in the imbalance of body's immune function and the MyD88-dependent signaling pathway of TLR4.
[h=4]KEYWORDS:[/h] Inflammation response; Influenza virus; Ma Huang Tang; MyD88; TLR4; TRAF6
PMID: 29710534 DOI: 10.1016/j.biopha.2018.03.161