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Sageretia thea Inhibits Inflammation through Suppression of NF- κ B and MAPK and Activation of Nrf2/HO-1 Signaling Pathways in RAW264.7 Cells.

  • Kim, Ha Na1
  • Park, Gwang Hun2
  • Park, Su Bin1
  • Kim, Jeong Dong1
  • Eo, Hyun Ji2
  • Son, Ho-Jun2
  • Song, Jeong Ho2
  • Jeong, Jin Boo1, 3
  • 1 * Department of Medicinal Plant Resources, National Institute of Forest Science, Yongju 36040, Republic of Korea. , (North Korea)
  • 2 ‡ Agricultural Science and Technology Research Institute, Andong National University, Andong 36729, Republic of Korea. , (North Korea)
  • 3 † Forest Medicinal Resources Research Center, National Institute of Forest Science, Yongju 36040, Republic of Korea. , (North Korea)
Published Article
The American journal of Chinese medicine
Publication Date
Jan 01, 2019
DOI: 10.1142/S0192415X19500198
PMID: 30834779


Sageretia thea (S. thea) commonly known as Chinese sweet plum or Chinese bird plum has been used for treating hepatitis and fevers in Korea and China. S. thea has been reported to exert anti-oxidant, anticancer and anti-human immunodeficiency virus activity. However, there is little study on the anti-inflammatory activity of S. thea. Thus, we evaluated the anti-inflammatory effect of extracts of leaves (ST-L) and branches (ST-B) from Sageretia thea in LPS-stimulated RAW264.7 cells. ST-L and ST-B significantly inhibited the production of the pro-inflammatory mediators such as NO, iNOS, COX-2, IL-1 β and IL-6 in LPS-stimulated RAW264.7 cells. ST-L and ST-B blocked LPS-induced degradation of I κ B- α and nuclear accumulation of p65, which resulted in the inhibition of NF- κ B activation in RAW264.7 cells. ST-L and ST-B also attenuated the phosphorylation of ERK1/2, p38 and JNK in LPS-stimulated RAW264.7 cells. In addition, ST-L and ST-B increased HO-1 expression in RAW264.7 cells, and the inhibition of HO-1 by ZnPP reduced the inhibitory effect of ST-L and ST-B against LPS-induced NO production in RAW264.7 cells. Inhibition of p38 activation and ROS elimination attenuated HO-1 expression by ST-L and ST-B, and ROS elimination inhibited p38 activation induced by ST-L and ST-B. ST-L and ST-B dramatically induced nuclear accumulation of Nrf2, but this was significantly reversed by the inhibition of p38 activation and ROS elimination. Collectively, our results suggest that ST-L and ST-B exerts potential anti-inflammatory activity by suppressing NF- κ B and MAPK signaling activation, and activating HO-1 expression through the nuclear accumulation of Nrf2 via ROS-dependent p38 activation. These findings suggest that ST-L and ST-B may have great potential for the development of anti-inflammatory drug to treat acute and chronic inflammatory disorders.

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