Emodin Inhibits Lipopolysaccharide-Induced Inflammation by Activating Autophagy in RAW 264.7 Cells*

Yan-jie TU; Bo TAN; Lei JIANG; Zhong-hua WU; Hong-ji YU; Xiao-qian LI; Ai-dong YANG

doi:10.1007/s11655-020-3477-9

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Emodin Inhibits Lipopolysaccharide-Induced Inflammation by Activating Autophagy in RAW 264.7 Cells*

Original Article | Updated：2021-09-01

- Emodin Inhibits Lipopolysaccharide-Induced Inflammation by Activating Autophagy in RAW 264.7 Cells*
- Chinese Journal of Integrative Medicine Vol. 27, Issue 5, Pages: 345-352(2021)
- Affiliations：
  
  1.Research Centre on Application of Classical Prescriptions, Basic Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai (201203), China
  2.Department of Febrile Disease, Basic Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai (201203), China
  3.Clinical Pharmacokinetic Laboratory, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai (201203), China
- Author bio：
  
  Prof. YANG Ai-dong, E-mail: aidongy@126.com
- Funds：
- DOI：10.1007/s11655-020-3477-9
  CLC：
- Published：01 May 2021，
  
  Published Online：25 August 2020，
  
  Accepted：31 December 2019
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Yan-jie TU, Bo TAN, Lei JIANG, et al. Emodin Inhibits Lipopolysaccharide-Induced Inflammation by Activating Autophagy in RAW 264.7 Cells*. [J]. Chinese Journal of Integrative Medicine 27(5):345-352(2021)
DOI：

Yan-jie TU, Bo TAN, Lei JIANG, et al. Emodin Inhibits Lipopolysaccharide-Induced Inflammation by Activating Autophagy in RAW 264.7 Cells*. [J]. Chinese Journal of Integrative Medicine 27(5):345-352(2021) DOI： 10.1007/s11655-020-3477-9.

摘要

Abstract

Objective:

To investigate the effects of emodin on inflammation and autophagy in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages and reveal its underlying mechanism.

Methods:

3-(4

5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay was conducted to find the appropriate dose for emodin. RAW264.7 cells pretreated with different concentrations (0–50 μmol/L) of emodin or vehicle for 2 h prior to exposure to LPS for 16 h. Cell morphology was examined and propidium iodide staining was used to examine cell cycle. Expressions of inflammation-related proteins [nuclear factor-kappaB (NF-κB) and I-kappaB (IκB)α] and autophagy-related proteins [light chain (LC) 3

P62/sequestosome 1

mammalian target of rapamycin (mTOR)

and p-mTOR] were examined using Western blot analysis. Expression of inflammation-related cytokines including tumor necrosis factor (TNF)-α

interleukin (IL)-1β and IL-6 were detected by enzyme-linked immunosorbent assay. Autophagy was examined with LC3B fluorescence intensity and aggregation. The effect of emodin on autophagy was conducted with an autophagy inhibitor

3-methyladenine (3-MA).

Results:

The expression of NF-κB in LPS-induced cells was significantly increased (

0.01) and simultaneously IκBα decreased compared with the normal cell (

0.05). The expressions of TNF-α

IL-1β

and IL-6 proteins in the LPS-induced RAW264.7 cells were significantly higher than in the normal cell (

0.05 or

0.01). LPS increased the percentage of cells in the G0/G1 phase

which was recovered by emodin at different doses (12.5

and 50μmol/L

0.05 or

0.01). The mediumdose (25 μml/L) emodin decreased the expressions of NF-κB

P62 and p-mTOR (

0.01) and increased IκBα expression

LC3B Ⅱ/Ⅰ ratio as well as LC3B fluorescence intensity (

0.05 or

0.01). Meanwhile

the enhanced autophagic effects of emodin

such as the increment of LC3BⅡ/ ratio and the decrement of P62 expression

were suppressed by autophagy inhibitor 3-MA.

Conclusion:

Emodin could inhibit inflammation of mice RAW264.7 macrophages induced by LPS

possibly through activating autophagy.

关键词

Keywords

emodinlipopolysaccharideinflammationautophagy

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