2. Academic Validation
  3. Downregulation of NO and PGE2 in LPS-stimulated BV2 microglial cells by trans-isoferulic acid via suppression of PI3K/Akt-dependent NF-κB and activation of Nrf2-mediated HO-1

Downregulation of NO and PGE2 in LPS-stimulated BV2 microglial cells by trans-isoferulic acid via suppression of PI3K/Akt-dependent NF-κB and activation of Nrf2-mediated HO-1

  • Int Immunopharmacol. 2014 Jan;18(1):203-11. doi: 10.1016/j.intimp.2013.11.020.
Matharage Gayani Dilshara 1,  Kyoung-Tae Lee 2,  Rajapaksha Gedara Prasad Tharanga Jayasooriya 1,  Chang-Hee Kang 1,  Sang Rul Park 1,  Yung Hyun Choi 3,  Il-Whan Choi 4,  Jin-Won Hyun 5,  Weon-Young Chang 5,  Yeon-Su Kim 6,  Hak-Ju Lee 2,  Gi-Young Kim 7
Affiliations

Affiliations

  • 1 Laboratory of Immunobiology, Department of Marine Life Sciences, Jeju National University, Ara-1 Dong, Jeju 690-756, Republic of Korea.
  • 2 Division of Wood Chemistry & Microbiology, Department of Forest Products, Korea Forest Research Institute, 57 Hoegiro, Dongdaemun-gu, Seoul 130-712, Republic of Korea.
  • 3 Department of Biochemistry, College of Oriental Medicine, Dong-Eui University, Busan 614-050, Republic of Korea.
  • 4 Department of Microbiology, College of Medicine, Inje University, Busan 614-735, Republic of Korea.
  • 5 School of Medicine, Jeju National University, Jeju 690-756, Republic of Korea.
  • 6 Management Strategy Team, Korea Forestry Promotion Institute, Mapo-gu, Seoul 121-914, Republic of Korea.
  • 7 Laboratory of Immunobiology, Department of Marine Life Sciences, Jeju National University, Ara-1 Dong, Jeju 690-756, Republic of Korea. Electronic address: immunkim@jejunu.ac.kr.
PMID: 24291391 DOI: 10.1016/j.intimp.2013.11.020
Abstract

Little is known about whether trans-isoferulic acid (TIA) regulates the production of lipopolysaccharide (LPS)-induced proinflammatory mediators. Therefore, we examined the effect of TIA isolated from Clematis mandshurica on LPS-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production in BV2 microglial cells. We found that TIA inhibited the production of LPS-induced NO and PGE2 without accompanying cytotoxicity in BV2 microglial cells. TIA also downregulated the expression levels of specific regulatory genes such as inducible NO Synthase (iNOS) and cyclooxygenase-2 (COX-2) by suppressing LPS-induced NF-κB activity via dephosphorylation of PI3K/Akt. In addition, we demonstrated that a specific NF-κB Inhibitor PDTC and a selective PI3K/Akt Inhibitor, LY294002 effectively attenuated the expression of LPS-stimulated iNOS and COX-2 mRNA, while LY294002 suppressed LPS-induced NF-κB activity, suggesting that TIA attenuates the expression of these proinflammatory genes by suppressing PI3K/Akt-mediated NF-κB activity. Our results showed that TIA suppressed NO and PGE2 production through the induction of nuclear factor erythroid 2-related factor 2 (Nrf2)-dependent heme oxygenase-1 (HO-1). Taken together, our data indicate that TIA suppresses the production of proinflammatory mediators such as NO and PGE2, as well as their regulatory genes, in LPS-stimulated BV2 microglial cells, by inhibiting PI3K/Akt-dependent NF-κB activity and enhancing Nrf2-mediated HO-1 expression.

Keywords

Heme oxgenase-1; Nitric oxide; Nuclear factor erythroid 2-related factor 2; Nuclear factor-κB; Prostaglandin E(2); Trans-isoferulic acid.

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