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Inflammation. 2016 Feb;39(1):375-384. doi: 10.1007/s10753-015-0259-1.

Anti-Inflammatory Activity of Tanshinone IIA in LPS-Stimulated RAW264.7 Macrophages via miRNAs and TLR4-NF-κB Pathway.

Fan G1,2, Jiang X1,2, Wu X1,2, Fordjour PA1,2, Miao L1,2, Zhang H1,2, Zhu Y1,2, Gao X3,4.

Author information

1
State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, #312 Anshanxi Road, Nankai District, Tianjin, 300193, China.
2
Ministry of Education Key Laboratory of Pharmacology of Traditional Chinese Medical Formulae, Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, China.
3
State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, #312 Anshanxi Road, Nankai District, Tianjin, 300193, China. gaoxiumei@tjutcm.edu.cn.
4
Ministry of Education Key Laboratory of Pharmacology of Traditional Chinese Medical Formulae, Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, China. gaoxiumei@tjutcm.edu.cn.

Abstract

Inflammation is a physiological response to infection or injury and involves the innate and adaptive immune system. Tanshinone IIA (Tan IIA) is a well-known flavonoid that elicits an important therapeutic effect by inhibiting inflammatory response. In this study, we examined whether Tan IIA exerts anti-inflammatory activity and investigated the possible mechanisms, including Toll-like receptor 4 (TLR4)-MyD88-nuclear factor kappa B (NF-κB) signaling pathway and microRNA expression in lipopolysaccharide (LPS)-induced RAW264.7 cells. Tan IIA could attenuate the inflammatory reaction via decreasing cytokine, chemokine, and acute-phase protein production, including GM-CSF, sICAM-1, cxcl-1, MIP-1α, and tumor necrosis factor alpha (TNF-α), analyzed by Proteome profile array in LPS-induced RAW264.7 cells. Concurrently, the messenger RNA (mRNA) expressions of IL-1β, TNF-α, and COX-2 were also significantly reduced by Tan IIA. Additionally, Tan IIA decreased LPS-induced NF-κB activation and downregulated TLR4 and MyD88 protein expression levels. We also observed reduced microRNA-155, miR-147, miR-184, miR-29b, and miR-34c expression levels, while LPS-induced microRNA-105, miR-145a, miR-194, miR-383, miR-132, and miR-451a expression levels were upregulated using microRNA (miRNA) qPCR array. Our results indicate that Tan IIA could exert an anti-inflammatory effect on LPS-induced RAW264.7 cells by decreasing TLR4-MyD88-NF-κB signaling pathway and regulating a series of cytokine production and miRNA expression.

KEYWORDS:

TLR4–NF-κB pathway; inflammatory mediators; microRNA; tanshinone IIA

PMID:
26639663
DOI:
10.1007/s10753-015-0259-1
[Indexed for MEDLINE]

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