Inhibition of COX‑2 and PGE2 in LPS‑stimulated RAW264.7 cells by lonimacranthoide VI, a chlorogenic acid ester saponin

Guan,Fuqin; Wang,Haiting; Shan,Yu; Chen,Yu; Wang,Ming; Wang,Qizhi; Yin,Min; Zhao,Youyi; Feng,Xu; Zhang,Jianhua

doi:10.3892/br.2014.314

September-October 2014 Volume 2 Issue 5

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September-October 2014 Volume 2 Issue 5

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Article

Inhibition of COX‑2 and PGE2 in LPS‑stimulated RAW264.7 cells by lonimacranthoide VI, a chlorogenic acid ester saponin

Authors:
- Fuqin Guan
- Haiting Wang
- Yu Shan
- Yu Chen
- Ming Wang
- Qizhi Wang
- Min Yin
- Youyi Zhao
- Xu Feng
- Jianhua Zhang
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Affiliations: Jiangsu Key Laboratory for Bioresources of Saline Soils, Institute of Botany, Jiangsu Province and Chinese Academy of Sciences/Nanjing Botanical Garden Memorial Sun Yat-Sen, Nanjing, Jiangsu 210014, P.R. China, College of Life Science, Nanjing Agricultural University, Nanjing 210095, P.R. China
Pages: 760-764
|
Published online on: July 11, 2014

https://doi.org/10.3892/br.2014.314
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Abstract

Lonimacranthoide VI, first isolated from the flower buds of Lonicera macranthoides in our previous study, is a rare chlorogenic acid ester acylated at C‑23 of hederagenin. In the present study, the anti‑inflammatory effects of lonimacranthoide VI were studied. Lipopolysaccharides (LPS) induced an inflammatory response through the production of prostaglandin E2 (PGE2), and these levels were reduced when lonimacranthoide VI was pre‑administered. Additionally, the mechanism of the anti‑inflammatory effects of lonimacranthoide VI was investigated by measuring cyclooxygenase (COX) activity and mRNA expression. The results showed that lonimacranthoide VI inhibited mRNA expression and in vitro activity of COX‑2 in a dose‑dependent manner, whereas only the higher lonimacranthoide VI concentration possibly reduced COX‑1 expression and in vitro activity. Taken together, these results indicate that lonimacranthoide VI is an important anti‑inflammatory constituent of Lonicera macranthoides and that the anti‑inflammatory effect is attributed to the inhibition of PGE2 production through COX activity and mRNA expression.

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