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. 2015 Jun;10(6):875–877. doi: 10.4103/1673-5374.158335

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Copyright: © Neural Regeneration Research

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Kavalactons might be neuroprotective via multiple pathways.

Kavalactone activates the p38, which in turn activates downstream kinase, and phosphorylation and degradation of IκB leads to translocation of NF-κB to the nucleus. One of the gene expression activated by NF-κB activation is COX-2. COX-2 converts arachidoinic acid into prostaglandins and up-regulation of many pro-inflamamtory cytokine follows. (2) Upon oxidative stress, the transcription factor Nrf2 was activated and released from keap1 (not shown in this diagram). ERK phosphorylation is upstream to the Nrf2 activation in neural cells treated with kavalacones. Nrf2 translocates to the nucleus and binds to the a cis-acting ARE to activate many downstream antioxidation genes, including HO-1, and protects the cells from oxidative stress and cell death. Inhibitory activity of kavalactone single compound on signaling molecule. Activation activity of kavalactone single compound on signaling molecule. Member of a signaling pathway promotes the activity of the next member. Member of a signaling pathway inihibits the activity of the next member.

IκB: Inhibitor of kappaB; NF-κB: nuclear factor-kappaB; COX-2: cyclooxygenase 2; Nrf2: NF-E2-related factor 2; ERK: extracellular regulated protein kinases; HO-1: heme oxygenase 1; iNOS: inducible nitric oxide synthase; NO: nitric oxide; ARE: antioxidant responsive element; DDK: dihydro-5,6-dehydrokavain; DK: dehydrokavain.

Inline graphic — Kavalactons might be neuroprotective via multiple pathways.

Kavalactone activates the p38, which in turn activates downstream kinase, and phosphorylation and degradation of IκB leads to translocation of NF-κB to the nucleus. One of the gene expression activated by NF-κB activation is COX-2. COX-2 converts arachidoinic acid into prostaglandins and up-regulation of many pro-inflamamtory cytokine follows. (2) Upon oxidative stress, the transcription factor Nrf2 was activated and released from keap1 (not shown in this diagram). ERK phosphorylation is upstream to the Nrf2 activation in neural cells treated with kavalacones. Nrf2 translocates to the nucleus and binds to the a cis-acting ARE to activate many downstream antioxidation genes, including HO-1, and protects the cells from oxidative stress and cell death. Inhibitory activity of kavalactone single compound on signaling molecule. Activation activity of kavalactone single compound on signaling molecule. Member of a signaling pathway promotes the activity of the next member. Member of a signaling pathway inihibits the activity of the next member.

IκB: Inhibitor of kappaB; NF-κB: nuclear factor-kappaB; COX-2: cyclooxygenase 2; Nrf2: NF-E2-related factor 2; ERK: extracellular regulated protein kinases; HO-1: heme oxygenase 1; iNOS: inducible nitric oxide synthase; NO: nitric oxide; ARE: antioxidant responsive element; DDK: dihydro-5,6-dehydrokavain; DK: dehydrokavain.