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Hydrogen-rich saline attenuates eosinophil activation in a guinea pig model of allergic rhinitis via reducing oxidative stress.
J Inflamm (Lond) 2017; 14:1JI

Abstract

BACKGROUND

It is well considered that reactive oxygen species (ROS) plays a prominent causative role in the development of allergic rhinitis (AR), and eosinophils cells as important allergic inflammatory cells contribute to elevating oxidative stress. Hydrogen, emerging as a novel antioxidant, has been proven effective in selectively reducing ROS in animals models of oxidative damage. We herein aim to verify protective effects of hydrogen on eosinophils cells in guinea pigs models of AR.

METHODS

Thirty two guinea pigs were random divided into four groups, and AR model was established through ovalbumin sensitization. The guinea pigs were injected with hydrogen-rich saline (Normal-HRS and AR-HRS group) or normal saline (control and AR group). The frequencies of sneezing and scratching were recorded. The IgE level, blood eosinophil count and eosinophil cationic protein (ECP) level in serum were measured. The serum malondialdehyde (MDA) and superoxide dismutase (SOD) assays were also measured to evaluate oxidative stress. The expression levels of eotaxin mRNA and protein in the nasal mucosa were also determined by real-time RT-PCR, Western blot and immunofluorescence.

RESULTS

HRS reduced the ROS and MDA levels and increased SOD level in guinea pigs of AR-HRS group accompanied with decreased frequency of sneezing and scratches. Meanwhile, there was a decline of the number of eosinophils cells in blood and of thelevel of ECP in serum in the AR-HRS group. HRS also significantly decreased the expression of eotaxin in nasal mucosa.

CONCLUSION

HRS may play a protective role in attenuating allergic inflammation, and suppressing the increase and activation of eosinophils in AR possibly through antioxidation effect of hydrogen.

Authors+Show Affiliations

Department of Otolaryngology, Tongji Hospital, Tongji University, 389 Xincun road, Putuo District, Shanghai, 200065 China.Department of Otolaryngology, Tongji Hospital, Tongji University, 389 Xincun road, Putuo District, Shanghai, 200065 China.Department of Otolaryngology, Tongji Hospital, Tongji University, 389 Xincun road, Putuo District, Shanghai, 200065 China.Department of Otolaryngology, Tongji Hospital, Tongji University, 389 Xincun road, Putuo District, Shanghai, 200065 China.Department of Otolaryngology, Tongji Hospital, Tongji University, 389 Xincun road, Putuo District, Shanghai, 200065 China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28100959

Citation

Yu, Shaoqing, et al. "Hydrogen-rich Saline Attenuates Eosinophil Activation in a Guinea Pig Model of Allergic Rhinitis Via Reducing Oxidative Stress." Journal of Inflammation (London, England), vol. 14, 2017, p. 1.
Yu S, Zhao C, Che N, et al. Hydrogen-rich saline attenuates eosinophil activation in a guinea pig model of allergic rhinitis via reducing oxidative stress. J Inflamm (Lond). 2017;14:1.
Yu, S., Zhao, C., Che, N., Jing, L., & Ge, R. (2017). Hydrogen-rich saline attenuates eosinophil activation in a guinea pig model of allergic rhinitis via reducing oxidative stress. Journal of Inflammation (London, England), 14, p. 1. doi:10.1186/s12950-016-0148-x.
Yu S, et al. Hydrogen-rich Saline Attenuates Eosinophil Activation in a Guinea Pig Model of Allergic Rhinitis Via Reducing Oxidative Stress. J Inflamm (Lond). 2017;14:1. PubMed PMID: 28100959.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hydrogen-rich saline attenuates eosinophil activation in a guinea pig model of allergic rhinitis via reducing oxidative stress. AU - Yu,Shaoqing, AU - Zhao,Chuanliang, AU - Che,Na, AU - Jing,Lin, AU - Ge,Rongming, Y1 - 2017/01/13/ PY - 2016/11/03/received PY - 2016/12/09/accepted PY - 2017/1/20/entrez PY - 2017/1/20/pubmed PY - 2017/1/20/medline KW - Allergic rhinitis KW - Eosinophil KW - Eosinophil cationic protein KW - Eotaxin KW - Guinea pig KW - Hydrogen-rich saline KW - Reactive oxygen species SP - 1 EP - 1 JF - Journal of inflammation (London, England) JO - J Inflamm (Lond) VL - 14 N2 - BACKGROUND: It is well considered that reactive oxygen species (ROS) plays a prominent causative role in the development of allergic rhinitis (AR), and eosinophils cells as important allergic inflammatory cells contribute to elevating oxidative stress. Hydrogen, emerging as a novel antioxidant, has been proven effective in selectively reducing ROS in animals models of oxidative damage. We herein aim to verify protective effects of hydrogen on eosinophils cells in guinea pigs models of AR. METHODS: Thirty two guinea pigs were random divided into four groups, and AR model was established through ovalbumin sensitization. The guinea pigs were injected with hydrogen-rich saline (Normal-HRS and AR-HRS group) or normal saline (control and AR group). The frequencies of sneezing and scratching were recorded. The IgE level, blood eosinophil count and eosinophil cationic protein (ECP) level in serum were measured. The serum malondialdehyde (MDA) and superoxide dismutase (SOD) assays were also measured to evaluate oxidative stress. The expression levels of eotaxin mRNA and protein in the nasal mucosa were also determined by real-time RT-PCR, Western blot and immunofluorescence. RESULTS: HRS reduced the ROS and MDA levels and increased SOD level in guinea pigs of AR-HRS group accompanied with decreased frequency of sneezing and scratches. Meanwhile, there was a decline of the number of eosinophils cells in blood and of thelevel of ECP in serum in the AR-HRS group. HRS also significantly decreased the expression of eotaxin in nasal mucosa. CONCLUSION: HRS may play a protective role in attenuating allergic inflammation, and suppressing the increase and activation of eosinophils in AR possibly through antioxidation effect of hydrogen. SN - 1476-9255 UR - https://www.unboundmedicine.com/medline/citation/28100959/Hydrogen_rich_saline_attenuates_eosinophil_activation_in_a_guinea_pig_model_of_allergic_rhinitis_via_reducing_oxidative_stress_ L2 - https://journal-inflammation.biomedcentral.com/articles/10.1186/s12950-016-0148-x DB - PRIME DP - Unbound Medicine ER -