Cryptochlorogenic acid attenuates LPS-induced inflammatory response and oxidative stress via upregulation of the Nrf2/HO-1 signaling pathway in RAW 264.7 macrophages

  • Int Immunopharmacol. 2020 Jun:83:106436. doi: 10.1016/j.intimp.2020.106436.
Xue-Lian Zhao  1 ,  Liang Yu  1 ,  Sun-Dong Zhang  1 ,  Kou Ping  1 ,  Hai-Yan Ni  1 ,  Xiang-Yu Qin  1 ,  Chun-Jian Zhao  1 ,  Wei Wang  1 ,  Thomas Efferth  2 ,  Yu-Jie Fu  3
Affiliations
  • 1. College of Chemistry, Chemical Engineering and Resource Utilization, Northeast Forestry University, Harbin 150040, China; Key Laboratory of Forest Plant Ecology, Ministry of Education, Northeast Forestry University, Harbin 150040, China.
  • 2. Institute of Pharmacy and Biochemistry, Johannes Gutenberg University, 55128 Mainz, Germany.
  • 3. College of Chemistry, Chemical Engineering and Resource Utilization, Northeast Forestry University, Harbin 150040, China; Key Laboratory of Forest Plant Ecology, Ministry of Education, Northeast Forestry University, Harbin 150040, China; College of Forestry, Beijing Forestry University, Beijing 100083, China; Beijing Advanced Innovation Center for Tree Breeding by Molecular Design, Beijing Forestry University, Beijing 100083, China. Electronic address: [email protected].
PMID: 32234671 DOI: 10.1016/j.intimp.2020.106436
Abstract

Phenolic acids are found in natural Plants, such as caffeic acid, rosmarinic acid, and chlorogenic acid. They have long been used as pharmacological actives, owing to their anti-inflammatory and antioxidant activities. Cryptochlorogenic acid (CCGA) is a special isomer of chlorogenic acid; the pharmacological effects and related molecular mechanisms of CCGA have been poorly reported. In the present study, the antioxidant and anti-inflammatory effects of CCGA in RAW 264.7 macrophages and the underlying mechanisms were investigated. The results revealed that CCGA dose-dependently inhibited LPS-induced production of NO, TNF-α, and IL-6 and blocked iNOS, COX-2, TNF-α, and IL-6 expressions. CCGA also significantly increased the GSH/GSSG ratio and SOD activity and reduced the MDA level. Moreover, CCGA suppressed the nuclear translocation of NF-κB by hindering the phosphorylation of IκB kinase (IKK) and degrading IκB. It also downregulated the phosphorylation of MAPKs. Our results indicated that CCGA significantly inhibited NF-κB activation by controlling the expression of pro-inflammatory factors and promoting the nuclear transfer of Nrf2. In conclusion, CCGA could attenuate LPS-induced inflammatory symptoms by modulating NF-κB/MAPK signaling cascades and inhibit LPS-induced oxidative stress via Nrf2 nuclear translocation.

Keywords
Anti-inflammatory; Antioxidant; Cryptochlorogenic acid; MAPK; NF-κB; Nrf2.
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