4.5 Article

The ethanolic extract of Curcuma longa grown in Korea exhibits anti-neuroinflammatory effects by activating of nuclear transcription factor erythroid-2-related factor 2/heme oxygenase-1 signaling pathway

Journal

BMC COMPLEMENTARY MEDICINE AND THERAPIES
Volume 22, Issue 1, Pages -

Publisher

BMC
DOI: 10.1186/s12906-022-03825-5

Keywords

Curcuma longa; Anti-neuroinflammation; BV2 microglial cells; Nuclear factor kappa B; Mitogen-activated protein kinases; Heme oxigenase-1

Funding

  1. Rural Development Administration, Republic of Korea
  2. [PJ01497501]
  3. [PJ01586401]

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The 50% ethanolic extract of Curcuma longa (CLE) has been found to have anti-neuroinflammatory effects against LPS-induced microglial cells activation. CLE inhibits the production and expression of pro-inflammatory mediators by negative regulation of NF-kappa B and MAPK signaling pathways. These effects are mediated by the HO-1/Nrf2 signaling pathway.
Background: Curcuma longa has been used as spices, food preservative, coloring material, and traditional medicine. This plant also has long been used for a variety of diseases including dyslipidemia, stomach disorders, arthritis, and hepatic diseases. The aim of the present investigation was to examine the anti-neuroinflammatory effects of the 50% ethanolic extract of C. longa in lipopolysaccharide (LPS)-induced BV2 microglial cells. Methods: Griess reaction was employed to measure the production of nitric oxide (NO), and the levels of prostaglandin E2 (PGE(2)) and pro-inflammatory cytokines such as interleukin 1-beta (IL-1 beta), IL-6 and tumor necrosis factor-alpha (TNF-alpha) were determined by using profit ELISA kits. Western blotting was used to determine the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor kappa B (NF-kappa B), mitogen activated protein kinases (MAPKs), heme oxygenase-1 (HO-1) and nuclear factor erythroid-2-related factor 2 (Nrf2). Results: Pre-treatment with CLE inhibited the overproduction and overexpression of pro-inflammatory mediators including NO, PGE(2), iNOS, COX-2, and pro-inflammatory cytokines such as IL-1 beta, IL-6 and TNF-alpha in LPS-induced BV2 cells. In addition, CLE suppressed the activation of the NF-kappa B and three MAPK signaling pathways. Treatment with CLE induced HO-1 protein expression by activating Nrf2 pathway, and inhibiting the HO-1 expression reversed the anti-inflammatory effect of CLE. Conclusion: CLE showed anti-neuroinflammatory effects against LPS-induced microglial cells activation through the inhibition of production and expression of pro-inflammatory mediators by negative regulation of the NF-kappa B and MAPK signaling pathways. These anti-neuroinflammatory effects of CLE were mediated by HO-1/Nrf2 signaling pathway. Taken together, the present study suggests a potent effect of CLE to prevent neuroinflammatory diseases. It is necessary to perform additional efficacy evaluation through in vivo experiments.

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