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Effect of hypobaric hypoxia on killing functions and secreting IL-6,TNF-α of peritoneal macrophages in mice / 中国免疫学杂志
Chinese Journal of Immunology ; (12): 344-348, 2018.
Artículo en Chino | WPRIM | ID: wpr-702731
ABSTRACT

Objective:

To explore the influence of high altitude hypoxia on the phagocytosis and killing functions of peritoneal macrophages in mice by establishing mouse model in high altitude hypoxic environment.

Methods:

①After exposure of mice to an altitude of 4 200 m,2 200 m and 400 m for 30 d respectively,flow cytometry was used to detect the phagocytosis and killing functions of peritoneal macrophages on staphylococcus aureus labeled with FITC.②The respiratory burst level of the cultured macrophage in mice was detected in 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) fluorescent probe method. ③The concentration of NO2- as a stable oxidative metabolite of NO in the supernatant of the cultured macrophages was measured with ELISA kits;④The release level of IL-6 and TNF-α in the cultured mice macrophage supernatant was also determined with ELISA kits.

Results:

After exposed under high altitude hypoxia for 30 d,compared with the control group (400 m),the phagocytosis,respiratory burst level and NO release in high altitude groups (4 200 m and 2 200 m) were all than those in the control group(400 m) (P<0.05).While the concentration of IL-6 and TNF-α in the Mφ cultured supernatant showed an obvious increase (P<0.05).

Conclusion:

Exposure under high altitude hypoxia (at altitude of 4 200 m and 2 200 m) for 30 d compromised the phagocytosis and oxygen dependent cytolyticactivity functions,and also raised the cytokines secretion level of IL-6 and TNF-α in Mφ,thereby affecting the innate immune response ability of Mφ in body.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Immunology Año: 2018 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Immunology Año: 2018 Tipo del documento: Artículo