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Molecules. 2017 Nov 21;22(11). pii: E2019. doi: 10.3390/molecules22112019.

The Protective Effects of Astaxanthin on the OVA-Induced Asthma Mice Model.

Author information

1
College of Pharmacy, Sunchon National University, 255 Jungangno, Suncheon 540-950, Korea. hyh7733@naver.com.
2
College of Pharmacy, Sunchon National University, 255 Jungangno, Suncheon 540-950, Korea. hong9217@naver.com.
3
College of Pharmacy, Sunchon National University, 255 Jungangno, Suncheon 540-950, Korea. motomoto1210@naver.com.
4
College of Pharmacy, Sunchon National University, 255 Jungangno, Suncheon 540-950, Korea. ksz1353@naver.com.
5
College of Pharmacy, Sunchon National University, 255 Jungangno, Suncheon 540-950, Korea. 6525140@hanmail.net.
6
Singapore Bioimaging Consortium, Agency for Science, Technology and Research, 11 Biopolis Way, No. 02-02 Helios, Singapore 138667, Singapore. joadon09@nate.com.
7
Suncheon Research Center for Natural Medicines, Suncheon 540-950, Korea. kang8404@nate.com.
8
College of Pharmacy, Sunchon National University, 255 Jungangno, Suncheon 540-950, Korea. sungtae@sunchon.ac.kr.

Abstract

Although astaxanthin has a variety of biological activities such as anti-oxidant effects, inhibitory effects on skin deterioration and anti-inflammatory effects, its effect on asthma has not been studied. In this paper, the inhibitory effect of astaxanthin on airway inflammation in a mouse model of ovalbumin (OVA)-induced asthma was investigated. We evaluated the number of total cells, Th1/2 mediated inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and airway hyperresponsiveness as well as histological structure. The level of total IgE, IgG1, IgG2a, OVA-specific IgG1, and OVA-specific IgG2a were also examined. The oral administration of 50 mg/mL astaxanthin inhibited the respiratory system resistance, elastance, newtonian resistance, tissue damping, and tissue elastance. Also, astaxanthin suppressed the total cell number, IL-4, and IL-5, and increased the IFN-γ in the BALF. In the sera, total IgE, IgG1, and OVA-specific IgG1 were reduced by astaxanthin exposure and IgG2a and OVA-specific IgG2a were enhanced via oral administration of astaxanthin. Infiltration of inflammatory cells in the lung, production of mucus, lung fibrosis, and expression of caspase-1 or caspase-3 were suppressed in OVA-induced asthmatic animal treated with astaxanthin. These results suggest that astaxanthin may have therapeutic potential for treating asthma via inhibiting Th2-mediated cytokine and enhancing Th1-mediated cytokine.

KEYWORDS:

airway hyperresponsiveness (AHR); astaxanthin; asthma; helper T cells (Th cells)

PMID:
29160801
PMCID:
PMC6150233
DOI:
10.3390/molecules22112019
[Indexed for MEDLINE]
Free PMC Article

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