Inhibition of ERK1/2 by silymarin in mouse mesangial cells.
10.4196/kjpp.2017.21.1.117
- Author:
Cha Kyung YOUN
1
;
Sung Il CHO
;
Min Young LEE
;
Young Jin JEON
;
Seog Ki LEE
Author Information
1. Department of Premedical Sciences, Chosun University College of Medicine, Gwangju 61452, Korea.
- Publication Type:Original Article
- Keywords:
Cytokine;
ERK1/2;
iNOS;
Mesangial cells;
Nitric oxide
- MeSH:
Animals;
Blotting, Western;
Cytokines;
Interferons;
Interleukins;
Mesangial Cells*;
Mice*;
Milk Thistle;
Necrosis;
Nitric Oxide;
Nitric Oxide Synthase Type II;
Phosphorylation;
Silymarin*
- From:The Korean Journal of Physiology and Pharmacology
2017;21(1):117-124
- CountryRepublic of Korea
- Language:English
-
Abstract:
The present study aimed to show that pro-inflammatory cytokines [tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and interleukin (IL)-1β] synergistically induce the production of nitric oxide (NO) production in mouse mesangial cells, which play an important role in inflammatory glomerular injury. We also found that co-treatment with cytokines at low doses (TNF-α; 5 ng/ml, IFN-γ; 5 ng/ml, and IL-1β; 1.25 U/ml) synergistically induced NO production, whereas treatment with each cytokine alone did not increase NO production at doses up to 100 ng/ml or 50 U/ml. Silymarin, a polyphenolic flavonoid isolated from milk thistle (Silybum marianum), attenuates cytokine mixture (TNF-α, IFN-γ, and IL-1β)-induced NO production. Western blot and RT-PCR analyses showed that silymarin inhibits inducible nitric oxide synthase (iNOS) expression in a dose-dependent manner. Silymarin also inhibited extracellular signal-regulated protein kinase-1 and -2 (ERK1/2) phosphorylation. Collectively, we have demonstrated that silymarin inhibits NO production in mouse mesangial cells, and may act as a useful anti-inflammatory agent.
