tetano
Editor, Senior Moderator
J Pharm Pharmacol. 2016 Feb 21. doi: 10.1111/jphp.12529. [Epub ahead of print]
[h=1]Red ginseng and vitamin C increase immune cell activity and decrease lung inflammation induced by influenza A virus/H1N1 infection.[/h] Kim H[SUP]1,[/SUP][SUP]2[/SUP], Jang M[SUP]1[/SUP], Kim Y[SUP]1[/SUP], Choi J[SUP]1[/SUP], Jeon J[SUP]1[/SUP], Kim J[SUP]3[/SUP], Hwang YI[SUP]1[/SUP], Kang JS[SUP]1,[/SUP][SUP]2[/SUP], Lee WJ[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] [h=4]OBJECTIVES:[/h] Because red ginseng and vitamin C have immunomodulatory function and anti-viral effect, we investigated whether red ginseng and vitamin C synergistically regulate immune cell function and suppress viral infection.
[h=4]METHODS:[/h] Red ginseng and vitamin C were treated to human peripheral blood mononuclear cells (PBMCs) or sarcoma-associated herpesvirus (KSHV)-infected BCBL-1, and administrated to Gulo(-/-) mice, which are incapable of synthesizing vitamin C, with or without influenza A virus/H1N1 infection.
[h=4]KEY FINDINGS:[/h] Red ginseng and vitamin C increased the expression of CD25 and CD69 of PBMCs and natural killer (NK) cells. Co-treatment of them decreased cell viability and lytic gene expression in BCBL-1. In Gulo(-/-) mice, red ginseng and vitamin C increased the expression of NKp46, a natural cytotoxic receptor of NK cells and interferon (IFN)-γ production. Influenza infection decreased the survival rate, and increased inflammation and viral plaque accumulation in the lungs of vitamin C-depleted Gulo(-/-) mice, which were remarkably reduced by red ginseng and vitamin C supplementation.
[h=4]CONCLUSIONS:[/h] Administration of red ginseng and vitamin C enhanced the activation of immune cells like T and NK cells, and repressed the progress of viral lytic cycle. It also reduced lung inflammation caused by viral infection, which consequently increased the survival rate.
? 2016 Royal Pharmaceutical Society, Journal of Pharmacy and Pharmacology.
[h=4]KEYWORDS:[/h] H1N1; influenza A virus; red ginseng; vitamin C
PMID: 26898166 [PubMed - as supplied by publisher]
[h=1]Red ginseng and vitamin C increase immune cell activity and decrease lung inflammation induced by influenza A virus/H1N1 infection.[/h] Kim H[SUP]1,[/SUP][SUP]2[/SUP], Jang M[SUP]1[/SUP], Kim Y[SUP]1[/SUP], Choi J[SUP]1[/SUP], Jeon J[SUP]1[/SUP], Kim J[SUP]3[/SUP], Hwang YI[SUP]1[/SUP], Kang JS[SUP]1,[/SUP][SUP]2[/SUP], Lee WJ[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] [h=4]OBJECTIVES:[/h] Because red ginseng and vitamin C have immunomodulatory function and anti-viral effect, we investigated whether red ginseng and vitamin C synergistically regulate immune cell function and suppress viral infection.
[h=4]METHODS:[/h] Red ginseng and vitamin C were treated to human peripheral blood mononuclear cells (PBMCs) or sarcoma-associated herpesvirus (KSHV)-infected BCBL-1, and administrated to Gulo(-/-) mice, which are incapable of synthesizing vitamin C, with or without influenza A virus/H1N1 infection.
[h=4]KEY FINDINGS:[/h] Red ginseng and vitamin C increased the expression of CD25 and CD69 of PBMCs and natural killer (NK) cells. Co-treatment of them decreased cell viability and lytic gene expression in BCBL-1. In Gulo(-/-) mice, red ginseng and vitamin C increased the expression of NKp46, a natural cytotoxic receptor of NK cells and interferon (IFN)-γ production. Influenza infection decreased the survival rate, and increased inflammation and viral plaque accumulation in the lungs of vitamin C-depleted Gulo(-/-) mice, which were remarkably reduced by red ginseng and vitamin C supplementation.
[h=4]CONCLUSIONS:[/h] Administration of red ginseng and vitamin C enhanced the activation of immune cells like T and NK cells, and repressed the progress of viral lytic cycle. It also reduced lung inflammation caused by viral infection, which consequently increased the survival rate.
? 2016 Royal Pharmaceutical Society, Journal of Pharmacy and Pharmacology.
[h=4]KEYWORDS:[/h] H1N1; influenza A virus; red ginseng; vitamin C
PMID: 26898166 [PubMed - as supplied by publisher]