Suppressive Effect of Tetrahydrocurcumin on Pseudomonas aeruginosa Lipopolysaccharide-Induced Inflammation by Suppressing JAK/STAT and Nrf2/HO-1 Pathways in Microglial Cells.

Autor: Lin HW; Department of Optometry, Asia University, Taichung 41354, Taiwan.; Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, Taiwan., Chen TC; Institute of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan., Yeh JH; Institute of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan., Tsou SC; Department of Nutrition, Chung Shan Medical University, Taichung 40201, Taiwan., Wang I; Rehabilitation Sciences & Technology, University of Wisconsin-Milwaukee, Milwaukee, WI, USA., Shen TJ; Department of Microbiology and Immunology, School of Medicine, Chung-Shan Medical University, Taichung 40201, Taiwan., Chuang CJ; Emergency Department, Kaohsiung Municipal United Hospital, Kaohsiung 80457, Taiwan., Chang YY; Department of Microbiology and Immunology, School of Medicine, Chung-Shan Medical University, Taichung 40201, Taiwan.; Clinical Laboratory, Chung Shan Medical University Hospital, Taichung 40201, Taiwan.
Jazyk: angličtina
Zdroj: Oxidative medicine and cellular longevity [Oxid Med Cell Longev] 2022 Mar 11; Vol. 2022, pp. 4978556. Date of Electronic Publication: 2022 Mar 11 (Print Publication: 2022).
DOI: 10.1155/2022/4978556
Abstrakt: Brain inflammation, a pathological feature of neurodegenerative disorders, exhibits elevated microglial activity and increased levels of inflammatory factors. The present study was aimed at assessing the anti-inflammatory response of tetrahydrocurcumin (THC), the primary hydrogenated metabolite of curcumin, which was applied to treat Pseudomonas aeruginosa ( P.a. ) lipopolysaccharide- (LPS-) stimulated BV2 microglial cells. THC reduced P.a. LPS-induced mortality and the production of inflammatory mediators IL-6, TNF- α , MIP-2, IP-10, and nitrite. A further investigation revealed that THC decreased these inflammatory cytokines synergistically with JAK/STAT signaling inhibitors. THC also increased Nrf2/HO-1 signaling transduction which inhibits iNOS/COX-2/pNF κ B cascades. Additionally, the presence of the HO-1 inhibitor Snpp increased the levels of IP-10, IL-6, and nitrite while THC treatment reduced those inflammatory factors in P.a. LPS-stimulated BV2 cells. In summary, we demonstrated that THC exhibits anti-inflammatory activities in P.a. LPS-induced inflammation in brain microglial cells by inhibiting STAT1/3-dependent NF- κ B activation and inducing Nrf2-mediated HO-1 expression.
Competing Interests: The authors reported no proprietary or commercial interest in any product mentioned or concept discussed in this article.
(Copyright © 2022 Hui-Wen Lin et al.)
Databáze: MEDLINE