Inhibition of ERK1/2 by silymarin in mouse mesangial cells
Inhibition of ERK1/2 by silymarin in mouse mesangial cells
- Cha Kyung Youn Sung Il Cho Min Young Lee Young Jin Jeon Seog Ki Lee
- 대한생리학회-대한약리학회
- The Korean Journal of Physiology & Pharmacology
- 제21권 제1호
- 등재여부 : KCI등재
- 2017.01
- 117 - 124 (8 pages)
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 (<i>Silybum marianum</i>), 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.