6533b7d2fe1ef96bd125ed78
RESEARCH PRODUCT
Cryptochlorogenic acid attenuates LPS-induced inflammatory response and oxidative stress via upregulation of the Nrf2/HO-1 signaling pathway in RAW 264.7 macrophages.
Sun-dong ZhangXiang-yu QinYu-jie FuThomas EfferthXue-lian ZhaoChunjian ZhaoWei WangLiang YuHai-yan NiKou Pingsubject
0301 basic medicineLipopolysaccharidesAntioxidantMAP Kinase Signaling SystemNF-E2-Related Factor 2medicine.medical_treatmentImmunologyAnti-Inflammatory AgentsIκB kinasemedicine.disease_causeAntioxidants03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicinemedicineCaffeic acidImmunology and AllergyAnimalsPharmacologyInflammationRosmarinic acidMacrophagesNF-kappa BMembrane ProteinsNF-κBGlutathioneCell biologyI-kappa B KinaseOxidative Stress030104 developmental biologyRAW 264.7 Cellschemistry030220 oncology & carcinogenesisSignal transductionChlorogenic AcidInflammation MediatorsOxidative stressHeme Oxygenase-1Signal Transductiondescription
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.
year | journal | country | edition | language |
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2019-12-11 | International immunopharmacology |