Purchase this article with an account.
Qian Wang, Jian Qi, Ranran Hu, Ying Chen, Aize Kijlstra, Peizeng Yang; Effect of Berberine on Proinflammatory Cytokine Production by ARPE-19 Cells following Stimulation with Tumor Necrosis Factor-α. Invest. Ophthalmol. Vis. Sci. 2012;53(4):2395-2402. doi: 10.1167/iovs.11-8982.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Berberine (BBR) is a well-known drug used in traditional medicine and has been shown to possess anti-inflammatory properties. Whether it can affect the production of inflammatory cytokines by RPE cells is not yet clear and was therefore the subject of our study.
ARPE-19 cells were cultured with TNF-α in the presence or absence of BBR to different time points. Concentrations of IL-6, IL-8, and monocyte chemoattractant protein-1 (MCP-1) in the supernatant were measured by using an ELISA. The mRNA expression of these cytokines was measured by real-time PCR. Phosphorylation of p38 mitogen-activated protein kinase (MAPK), extracellular signal–regulated kinase (ERK1/2), and c-Jun N-terminal kinase (JNK) was measured by Western blot assay. The signal transduction mechanisms involved in cytokine production were evaluated using various inhibitors for p38, ERK1/2, and JNK.
TNF-α significantly increased the expression of IL-6, IL-8, and MCP-1 in ARPE-19 cells at both the protein and mRNA levels. It promoted the phosphorylation of p38, ERK1/2, and JNK. Inhibitory experiments showed that IL-6 was modulated by p38, whereas IL-8 and MCP-1 were modulated by p38, ERK1/2, and JNK signal pathways. BBR inhibited the expression of IL-6, IL-8, and MCP-1 remarkably at both protein and mRNA levels and down-regulated the phosphorylation of p38, ERK1/2, and JNK upon stimulation with TNF-α.
The present results suggested that BBR significantly inhibits the expression of inflammatory cytokines in ARPE-19 cells and that the inhibitory effect is mediated by down-regulation of the p38, ERK1/2, and JNK pathways.
This PDF is available to Subscribers Only