PMID- 36578522 OWN - NLM STAT- MEDLINE DCOM- 20221230 LR - 20230103 IS - 1942-0994 (Electronic) IS - 1942-0900 (Print) IS - 1942-0994 (Linking) VI - 2022 DP - 2022 TI - Honokiol Ameliorates DSS-Induced Mouse Colitis by Inhibiting Inflammation and Oxidative Stress and Improving the Intestinal Barrier. PG - 1755608 LID - 10.1155/2022/1755608 [doi] LID - 1755608 AB - Ulcerative colitis (UC) is a multifactor intestinal disease with increased morbidity. Recently, pleiotropic drugs with exact biosafety have been urgently needed. Honokiol (HKL) is the major bioactive component of traditional Chinese medicine "Houpu," with almost no toxic effects and approved anti-inflammation, antioxidant, antispasmodic, etc. effects. This study examined the therapeutic effect of HKL in dextran sulfate sodium- (DSS-) induced experimental colitis. In vivo, C57BL/6 mice received 3% DSS for seven days to generate UC, and HKL was pretreated for five days and given during the whole DSS-induced period. In vitro, RAW264.7 macrophages were stimulated with lipopolysaccharide (LPS) to induce inflammation, and mouse colon epithelial cells (MCEC) were treated with HKL or pretreated with HKL and then stimulated with LPS-induced macrophage supernate to investigate the barrier enhancement roles. HKL significantly ameliorated disease activity index (DAI), colon length, and histopathological scores in DSS-induced colitis. The inflammatory mediators of interleukin 1beta (IL-1beta), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX2) were decreased, and the tight conjunction proteins were increased in the HKL-treated group both in vivo and in vitro. Above all, HKL can relieve experimental UC through anti-inflammation, antioxidant, and epithelial barrier enhancement roles. These effects were associated with peroxisome proliferator-activated receptor gamma (PPARgamma)/nuclear factor-kappaB (NF-kappaB) p65, sirtuin3 (SIRT3)/adenosine 5'-monophosphate- (AMP-) activated protein kinase (AMPK), and nuclear factor erythroid 2-related factor 2 (NRF2)/heme oxygenase 1 (HO1) signaling pathways. In conclusion, after further clinical studies, HKL may be a promising drug for UC. CI - Copyright (c) 2022 Lu Wang and Junping Wang. FAU - Wang, Lu AU - Wang L AUID- ORCID: 0000-0003-4945-5332 AD - Department of Gastroenterology, Second Hospital of Shanxi Medical University, Taiyuan, China. AD - The Fifth Clinical Medical College of Shanxi Medical University, Taiyuan, Shanxi, China. FAU - Wang, Junping AU - Wang J AUID- ORCID: 0000-0002-9360-4131 AD - The Fifth Clinical Medical College of Shanxi Medical University, Taiyuan, Shanxi, China. AD - Department of Gastroenterology, Fifth Hospital of Shanxi Medical University, Taiyuan, Shanxi, China. LA - eng PT - Journal Article DEP - 20221219 PL - United States TA - Oxid Med Cell Longev JT - Oxidative medicine and cellular longevity JID - 101479826 RN - 11513CCO0N (honokiol) RN - 0 (Lipopolysaccharides) RN - 0 (Antioxidants) RN - 0 (NF-kappa B) RN - 0 (Anti-Inflammatory Agents) RN - 0 (Interleukin-6) RN - 9042-14-2 (Dextran Sulfate) SB - IM MH - Animals MH - Mice MH - Lipopolysaccharides/adverse effects MH - Antioxidants/metabolism MH - Mice, Inbred C57BL MH - *Colitis/chemically induced/drug therapy/pathology MH - Inflammation/pathology MH - *Colitis, Ulcerative/chemically induced MH - Colon MH - NF-kappa B/metabolism MH - Anti-Inflammatory Agents/adverse effects MH - Interleukin-6/metabolism MH - Oxidative Stress MH - Dextran Sulfate/toxicity MH - Disease Models, Animal PMC - PMC9792244 COIS- The authors have declared that no conflict of interest exists. EDAT- 2022/12/30 06:00 MHDA- 2022/12/31 06:00 PMCR- 2022/12/19 CRDT- 2022/12/29 02:25 PHST- 2022/08/12 00:00 [received] PHST- 2022/11/18 00:00 [revised] PHST- 2022/11/25 00:00 [accepted] PHST- 2022/12/29 02:25 [entrez] PHST- 2022/12/30 06:00 [pubmed] PHST- 2022/12/31 06:00 [medline] PHST- 2022/12/19 00:00 [pmc-release] AID - 10.1155/2022/1755608 [doi] PST - epublish SO - Oxid Med Cell Longev. 2022 Dec 19;2022:1755608. doi: 10.1155/2022/1755608. eCollection 2022.