2. Academic Validation
  3. Esculentoside B inhibits inflammatory response through JNK and downstream NF-κB signaling pathway in LPS-triggered murine macrophage RAW 264.7 cells

Esculentoside B inhibits inflammatory response through JNK and downstream NF-κB signaling pathway in LPS-triggered murine macrophage RAW 264.7 cells

  • Int Immunopharmacol. 2019 Mar:68:156-163. doi: 10.1016/j.intimp.2019.01.003.
Fukushi Abekura 1,  Junyoung Park 1,  Choong-Hwan Kwak 2,  Sun-Hyung Ha 1,  Seung-Hak Cho 3,  Young-Chae Chang 4,  Ki-Tae Ha 5,  Hyeun-Wook Chang 6,  Young-Choon Lee 7,  Tae-Wook Chung 8,  Cheorl-Ho Kim 9
Affiliations

Affiliations

  • 1 Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo 2066, Jangan-Gu, Suwon, Gyunggi-Do 16419, Republic of Korea.
  • 2 Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo 2066, Jangan-Gu, Suwon, Gyunggi-Do 16419, Republic of Korea; Division of Applied Medicine, School of Korean Medicine, Pusan National University, Yangsan City, Gyeongsangnam-Do, Republic of Korea.
  • 3 Division of Enteric Diseases, Center for Infectious Diseases Research, Korea National Institute of Health, Heungdeok-gu, Cheongju 363-951, Republic of Korea.
  • 4 Research Institute of Biomedical Engineering and Department of Medicine, Catholic University of Daegu School of Medicine, Daegu, Republic of Korea. Electronic address: ycchang@cu.ac.kr.
  • 5 Division of Applied Medicine, School of Korean Medicine, Pusan National University, Yangsan City, Gyeongsangnam-Do, Republic of Korea. Electronic address: haggis@pnu.ac.kr.
  • 6 College of Pharmacy, Yeungnam University, Gyeongsan 701-947, Republic of Korea.
  • 7 Faculty of Medicinal Biotechnology, Dong-A University, Saha-Gu, Busan, Republic of Korea. Electronic address: yclee@dau.ac.kr.
  • 8 Division of Applied Medicine, School of Korean Medicine, Pusan National University, Yangsan City, Gyeongsangnam-Do, Republic of Korea.
  • 9 Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo 2066, Jangan-Gu, Suwon, Gyunggi-Do 16419, Republic of Korea. Electronic address: chkimbio@skku.edu.
PMID: 30639961 DOI: 10.1016/j.intimp.2019.01.003
Abstract

Natural compound esculentoside B (EsB), (2S,4aR,6aR,6aS,6bR,8aR,9R,10R,11S,12aR,14bS)-11-hydroxy-9-(hydroxymethyl)-2 methoxycarbonyl-2,6a,6b,9,12a-pentamethyl-10-[(2S,3R,4S,5R)-3,4,5-trihydroxyoxan-2-yl]oxy-1,3,4,5,6,6a,7,8,8a,10,11,12,13,14b-tetradecahydropicene-4a-carboxylic acid with molecular weight of 664.833, isolated from roots of Phytolacca acinosa Roxb has been widely used as a constituent of traditional Chinese medicine (TCM). However, the anti-inflammatory capacity of EsB has not been reported yet. Therefore, the objective of this study was to investigate anti-inflammatory activities of EsB in LPS-treated macrophage RAW 264.7 cells. EsB could inhibit nitric oxide (NO) production. EsB also suppressed gene and protein expression levels of inducible isoform of NO Synthase (NOS) and cyclooxygenase-2 in a dose-dependent manner. In addition, EsB decreased gene expression and protein secretion levels of pro-inflammatory cytokines such as IL-1β, TNF-α, and IL-6. EsB remarkably suppressed nuclear translocation of nuclear factor kappa-B (NF-κB) from cytosolic space. Phosphorylation of IκB was also inhibited by EsB. Moreover, EsB specifically down-regulated phospho-c-Jun N-terminal kinase (p-JNK), but not p-p38 or phospho-extracellular signal-regulated kinase 1/2 (p-ERK1/2). Taken together, these results suggest that EsB has inhibitory effect on inflammatory response by inactivating NF-κB and p-JNK. It could be used as a new modulatory drug for effective treatment of inflammation-related diseases.

Keywords

Esculentoside B; Inflammation; JNK pathway; LPS; RAW264.7 cells.

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