.; Zhao, X.; Ma, B.; Xu, Z.; Li, C. Astaxanthin Offers Antioxidant Protection in LPS-Induced Dendritic Cells for Inflammatory Control. Mar. Drugs 2021, 19, 534. doi.org/ 10.3390/md19100534 Academic Editors: Donatella Degl’Innocenti and Marzia Vasarri Received: 31 August 2021 Accepted: 21 September 2021 Published: 23 SeptemberAbstract: Astaxanthin, originating from marine organisms, is CLK review usually a organic bioactive compound with potent antioxidant activity. Here, we evaluated the antioxidant ability of astaxanthin on dendritic cells (DCs), a key target of immune regulation, for inflammatory manage within a sepsis model. Our final results showed that astaxanthin suppressed nitric oxide (NO) production, reactive oxygen species (ROS) production, and lipid peroxidation activities in LPS-induced DCs and LPS-challenged mice. Moreover, the reduced glutathione (GSH) levels and the GSH/GSSG ratio have been increased, suggesting that astaxanthin elevated the amount of cellular reductive status. Meanwhile, the activities of antioxidant enzymes, like glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD), were considerably upregulated. Astaxanthin also inhibited the LPS-induced secretions of IL-1, IL-17, and TGF- cytokines. Ultimately, we located that the expressions of heme oxygenase 1 (HO-1) and nuclear factor erythroid 2-related factor 2 (Nrf2) have been considerably upregulated by astaxanthin in LPSinduced DCs, suggesting that the HO-1/Nrf2 pathway plays a important function within the suppression of oxidative stress. These benefits suggested that astaxanthin possesses strong antioxidant qualities in DC-related inflammatory responses, which is expected to have potential as a process of sepsis remedy. Key phrases: astaxanthin; oxidative anxiety; sepsis; dendritic cells; inflammationPublisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.1. Introduction Sepsis is definitely an organic dysfunction caused by a disordered host response to infection by viruses, fungi, and bacteria [1], which remains a significant trigger of morbidity and mortality worldwide, with enhanced burden in low- and middle-resource settings [5]. In the United states, the treatment of sepsis accounted for more than USD 20 billion (five.2 ) in total hospital expenses in 2011 [6]. An CCR5 Storage & Stability extrapolation from high-income nation data suggests that on a yearly basis, you can find an estimated 31.five million sepsis and 19.four million extreme sepsis cases, with a possible five.three million deaths globally [7]. Even though greater than 100 clinical therapeutic trials have already been performed, no therapy solutions for sepsis are currently authorized by the US Food and Drug Administration (FDA) [8]. Right after infection, the components from the pathogen, including lipopolysaccharide (LPS), a key element of the bacterial cell wall, are recognized by macrophages, dendritic cells (DCs), along with other immune cells, and then the overloaded inflammatory immune response is activated in early septic sufferers [9]. Historically, direct anti-hyperinflammatory strategiesCopyright: 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access post distributed under the terms and situations from the Inventive Commons Attribution (CC BY) license ( creativecommons.org/licenses/by/ four.0/).Mar. Drugs 2021, 19, 534. doi.org/10.3390/mdmdpi/journal/marinedrugsMar. Drugs 2021, 19,2 ofthat attempt to block cytokines, for example interleukin-1 (IL-1) and tumor necrosis aspect (TNF), have been
