PMID- 36086967 OWN - NLM STAT- MEDLINE DCOM- 20220913 LR - 20220913 IS - 1578-1267 (Electronic) IS - 0301-0546 (Linking) VI - 50 IP - 5 DP - 2022 TI - Zeaxanthin attenuates OVA-induced allergic asthma in mice by regulating the p38 MAPK/beta-catenin signaling pathway. PG - 75-83 LID - 10.15586/aei.v50i5.664 [doi] AB - BACKGROUND: Asthma is a heterogeneous and complex chronic airway disease with a high incidence rate, characterized by chronic airway inflammation. Although the anti-inflammatory effect of zeaxanthin has been demonstrated in various disease models, its explicit role in allergic asthma remains elusive. METHODS: An allergic asthma model was established by ovalbumin (OVA) stimulation in BALB/c nude mice. The pathological examination, collagen deposition and expression of alpha-smooth muscle actin (alpha-SMA) in lung tissues were determined by hematoxylin and eosin (H&E), MASSON and immunofluorescence staining, respectively. Besides, the effect of zeaxanthin on inflammation and oxidative stress was assessed by the enzyme-linked immunosorbent assay (ELISA) and spectrophotometry measure. Moreover, the underlying mechanism was analyzed by detecting the expression of phosphorylated p38 (p-p38), p38, beta-catenin, p-c-Jun N-terminal kinase (p-JNK) and JNK with western blot assays. RESULTS: The distinct infiltration of inflammatory cells was observed in the OVA-induced asthma mice model with significantly increased concentrations of immunoglobulin E (IgE), interleukin-4 (IL-4), IL-5, IL-13 and eotaxin (p<0.001), which were prominently reversed by zeaxanthin treatment (p<0.001). In addition, zeaxanthin treatment decreased the OVA-induced collagen deposition and alpha-SMA expression. A similar inhibitory effect of zeaxanthin on the oxidative stress was also observed in the OVA-induced asthma mice model, as evidenced by the prominent decrease of malondialdehyde (MDA) concentration and the remarkable increase of superoxide dismutase (SOD), glutathione S transferase (GST) and Glutathione (GSH) concentrations (p<0.001). Moreover, zeaxanthin introduction markedly reduced the relative expressions of p-p38/p38, beta-catenin and p-JNK/JNK in the OVA-induced asthma mice model (p<0.001), indicating that zeaxanthin suppressed the p38 mitogen-activated protein kinase (p38 MAPK)/beta-catenin signaling pathway in the OVA-induced asthma mice model. CONCLUSIONS: Zeaxanthin attenuated OVA-induced allergic asthma in mice via modulating the p38 MAPK/beta-catenin signaling pathway. FAU - Jin, Xiaosheng AU - Jin X AD - Department of Respiration, Tongde Hospital of Zhejiang Province, Hangzhou, China. FAU - Jin, Weijing AU - Jin W AD - Department of Neonatology, Hangzhou Children's Hospital, Hangzhou, China; jinweijing0506@163.com. FAU - Li, Guoping AU - Li G AD - Department of Respiration, Tongde Hospital of Zhejiang Province, Hangzhou, China. FAU - Zheng, Jisheng AU - Zheng J AD - Department of Respiration, Tongde Hospital of Zhejiang Province, Hangzhou, China. LA - eng PT - Journal Article DEP - 20220901 PL - Singapore TA - Allergol Immunopathol (Madr) JT - Allergologia et immunopathologia JID - 0370073 RN - 0 (Zeaxanthins) RN - 0 (beta Catenin) RN - 9006-59-1 (Ovalbumin) RN - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases) SB - IM MH - Animals MH - *Asthma/etiology MH - Disease Models, Animal MH - Inflammation/complications MH - Mice MH - Mice, Inbred BALB C MH - Mice, Nude MH - Ovalbumin/adverse effects MH - Signal Transduction MH - Zeaxanthins/adverse effects MH - *beta Catenin/metabolism MH - p38 Mitogen-Activated Protein Kinases/metabolism OTO - NOTNLM OT - Asthma OT - ovalbumin OT - p38 MAPK OT - zeaxanthin OT - beta-catenin COIS- The authors state that there are no conflict of interest to disclose. EDAT- 2022/09/11 06:00 MHDA- 2022/09/14 06:00 CRDT- 2022/09/10 06:03 PHST- 2022/05/07 00:00 [received] PHST- 2022/06/02 00:00 [accepted] PHST- 2022/09/10 06:03 [entrez] PHST- 2022/09/11 06:00 [pubmed] PHST- 2022/09/14 06:00 [medline] AID - 10.15586/aei.v50i5.664 [doi] PST - epublish SO - Allergol Immunopathol (Madr). 2022 Sep 1;50(5):75-83. doi: 10.15586/aei.v50i5.664. eCollection 2022.