Anti‐inflammatory activity of Sageretia thea in LPS‐stimulated RAW264.7 cells

p38丝裂原活化蛋白激酶 化学 NF-κB 脂多糖 αBκ 分子生物学 磷酸化 信号转导 生物化学 生物 免疫学 MAPK/ERK通路
作者
Gwang Hun Park,Gwang Hun Park,Jin Boo Jeong
出处
期刊:The FASEB Journal [Wiley]
卷期号:33 (S1)
标识
DOI:10.1096/fasebj.2019.33.1_supplement.lb389
摘要

Sageretia thea ( S. thea ) has been reported to exert various pharmacological activities such as anti‐oxidation, anti‐cancer 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 S. 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‐1β and IL‐6 in LPS‐stimulated RAW264.7 cells. ST‐L and ST‐B blocked LPS‐induced degradation of IκB‐α and nuclear accumulation of p65, which resulted to the inhibition of NF‐κB 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‐κB 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. Support or Funding Information This work was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (NRF‐2016R1D1A3B03931713 and NRF‐2018R1A6A1A03024862), and by a grant from National Institute of Forest Science in 2019. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

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