Format

Send to

Choose Destination
Mol Med Rep. 2016 Sep;14(3):2368-72. doi: 10.3892/mmr.2016.5512. Epub 2016 Jul 13.

Emodin‑8‑O‑glucuronic acid, from the traditional Chinese medicine qinghuobaiduyin, affects the secretion of inflammatory cytokines in LPS‑stimulated raw 264.7 cells via HSP70.

Author information

1
PET/CT Center, Hunan Provincial Tumor Hospital, Changsha, Hunan 410013, P.R. China.
2
Department of Burns and Plastic Surgery, Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, P.R. China.

Abstract

Qinghuobaiduyin (QHBDY) is a traditional Chinese medicine, which has an opsonization effect on the immune system. However, which chemical compound in QHBDY underlies the therapeutic effect remains to be elucidated. The present study was designed to investigate the effect of emodin‑8‑O‑glucuronic acid, a chemical compound isolated from QHBDY, on the secretion of inflammatory cytokines in lipopolysaccharide (LPS)‑stimulated Raw 264.7 cells. The compound was isolated from QHBDY and identified as emodin‑8‑O‑glucuronic acid using liquid chromatography‑mass spectrometryn. The results obtained from an ELISA assay showed that emodin‑8‑O‑glucuronic acid inhibited the elevated expression levels of tumor necrosis factor‑α (TNF‑α), interleukin (IL)‑1β and IL‑10 in the LPS‑stimulated Raw 264.7 cells, which occurred in a dose‑dependent manner. In addition, emodin‑8‑O‑glucuronic acid induced the expression of heat shock protein 70 (HSP70) in the LPS‑stimulated Raw 264.7 cells, as demonstrated using western blot analysis. The effect of emodin‑8‑O‑glucuronic acid on the secretion of TNF‑α, IL‑1β and IL‑10 was attenuated by the knockdown of HSP70. In conclusion, the present study demonstrated that emodin‑8‑O‑glucuronic acid effectively suppressed LPS‑induced inflammatory cytokine secretion, and this effect was attained by the increased expression of HSP70.

PMID:
27430303
DOI:
10.3892/mmr.2016.5512
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Spandidos Publications
Loading ...
Support Center