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. 2022 Dec 7;23(24):15471. doi: 10.3390/ijms232415471

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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The proposed mechanism of astaxanthin-mediated protective effects on gastric ulcer. H. pylori infection, chronic alcohol consumption, and ingestion of nonsteroidal anti-inflammatory drugs can cause gastric ulcer development. Astaxanthin exerts anti-ulcer activity by its anti-oxidant and anti-inflammatory effects. For antioxidant activity, astaxanthin enhances the activity of anti-oxidant enzymes such as glutathione (GSH) peroxidase, superoxide dismutase (SOD), and catalase. These enzymes reduce the levels of reactive oxygens species (ROS) which increase the levels of lipid peroxides and 8-hydroxy-2′-deoxyguanosin. ROS activate nuclear factor-κB (NF-κB) to induce expression of inflammatory cytokines including interleukin (IL)-8. These cytokines result in dysregulated acid secretion, mucosal damage, and neutrophil recruitment in gastric mucosal tissues. Astaxanthin inhibits these ROS-mediated alterations and mucosal damage. In addition, astaxanthin activates peroxisome proliferator-activated receptor-γ (PPAR-γ) to induce expression of SOD2 and catalase that reduces ROS in gastric epithelial cells. In immune cells, astaxanthin shows antimicrobial activity by shifting pro-inflammatory T helper type 1 (Th1) response towards anti-inflammatory Th2 response. It stimulates mitogen-induced lympho-proliferation and increases T and B cell subpopulation. Thus, astaxanthin shows inhibitory effect on gastric ulcer development. Inhibit, ; increase, . Red arrows represent the effects of astaxanthin.

Inline graphic — The proposed mechanism of astaxanthin-mediated protective effects on gastric ulcer. H. pylori infection, chronic alcohol consumption, and ingestion of nonsteroidal anti-inflammatory drugs can cause gastric ulcer development. Astaxanthin exerts anti-ulcer activity by its anti-oxidant and anti-inflammatory effects. For antioxidant activity, astaxanthin enhances the activity of anti-oxidant enzymes such as glutathione (GSH) peroxidase, superoxide dismutase (SOD), and catalase. These enzymes reduce the levels of reactive oxygens species (ROS) which increase the levels of lipid peroxides and 8-hydroxy-2′-deoxyguanosin. ROS activate nuclear factor-κB (NF-κB) to induce expression of inflammatory cytokines including interleukin (IL)-8. These cytokines result in dysregulated acid secretion, mucosal damage, and neutrophil recruitment in gastric mucosal tissues. Astaxanthin inhibits these ROS-mediated alterations and mucosal damage. In addition, astaxanthin activates peroxisome proliferator-activated receptor-γ (PPAR-γ) to induce expression of SOD2 and catalase that reduces ROS in gastric epithelial cells. In immune cells, astaxanthin shows antimicrobial activity by shifting pro-inflammatory T helper type 1 (Th1) response towards anti-inflammatory Th2 response. It stimulates mitogen-induced lympho-proliferation and increases T and B cell subpopulation. Thus, astaxanthin shows inhibitory effect on gastric ulcer development. Inhibit, ; increase, . Red arrows represent the effects of astaxanthin.