Journal
BIOMEDICINE & PHARMACOTHERAPY
Volume 109, Issue -, Pages 555-562Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2018.10.112
Keywords
Gambogic acid; Inflammation; Nrf2; NF-kappa B; MAPKs
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Gambogic acid (GA), a natural product with a xanthone structure, was previously demonstrated to exert anti-inflammatory effects. The aim of this study was to evaluate the anti-inflammatory activity of GA on LPS-stimulated mouse macrophage RAW264.7 and its anti-inflammatory mechanism. Pretreatment with GA inhibited LPS-induced production of nitric oxide (NO) and prostaglandin E2 (PGE2) through reducing the expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). GA also decreased the expressions of proinflammatory cytokines, including TNF-alpha, IL-6 and IL-beta. The activation of nuclear factor-kappa B (NF-kappa B) and the Mitogen activated phosphokinases (MAPKs) regulates pro-inflammatory factors. Further experiments demonstrated that the nuclear translocation of NF-kappa B, a promoting regulator in inflammation, was blocked via inhibiting the phosphorylation event of I kappa B alpha by GA. Meanwhile, the Mitogen activated phosphokinase (MAPK) signaling pathways were also suppressed. However, activation of nuclear factor erythroid 2-related factor (Nrf2) can inhibit inflammation. GA could activate the nucleus translocation of Nrf2 and up-regulated the expression of heme oxygenase-1 (HO-1). Taken together, GA exhibited its anti-inflammatory activities through Nrf2 activation and NF-kappa B depression, thus could be a candidate for the prevention and treatment of diseases that involve excessive inflammation.
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