Hydrogen therapy promotes macrophage polarization to the M2 subtype by inhibiting the NF-κB signaling pathway
10.13491/j.issn.1004-714X.2024.01.006
- VernacularTitle:氢气疗法通过抑制NF-κB通路促进巨噬细胞向M2亚型极化
- Author:
Xue GAO
1
,
2
;
Shiying NIU
1
,
3
;
Guohua SONG
2
;
Lulu LI
2
;
Xiaoyue ZHANG
4
;
Wentao PAN
2
;
Xuetao CAO
1
,
2
;
Xinhui ZHANG
1
,
2
;
Meili SUN
5
;
Guoli ZHAO
6
;
Yueying ZHANG
1
,
2
Author Information
1. Department of Pathology, The First Affiliated Hospital of Shandong First Medical University, Jinan 250117 China
2. Department of Pathophysiology, School of Clinical and Basic Medicine, Shandong First Medical University, Jinan 250117 China.
3. Department of Pathology, Linfen Central Hospital, Shanxi Province, Linfen 041000 China.
4. Department of Pathology, The First Affiliated Hospital of Shandong First Medical University, Jinan 250117 China.
5. Department of Oncology, Affiliated Central Hospital of Shandong First Medical University, Jinan 250117 China.
6. Department of Pathology, Liaocheng Infectious Disease Hospital, Liaocheng 252000 China.
- Publication Type:OriginalArticles
- Keywords:
Hydrogen;
Radiation-induced lung injury;
Macrophage polarization;
Pathological mechanism
- From:
Chinese Journal of Radiological Health
2024;33(1):33-39
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of hydrogen therapy in reducing radiation-induced lung injury and the specific mechanism. Methods Forty C57BL/6 mice were randomly divided into four groups: normal control group, model group, hydrogen therapy group I, and hydrogen therapy group II. A mouse model of radiation-induced lung injury was established. The pathological changes in the lung tissue of the mice were examined with HE staining. Immunofluorescence staining was used to detect the expression of surface markers of M1 and M2 macrophages to observe macrophage polarization. The expression of interleukin (IL)-6, tumor necrosis factor-α (TNF-α), and IL-10 in the lung tissue was measured by immunohistochemistry. The expression of nuclear factor-kappa B (NF-κB) p65 and phosphorylated NF-κB (P-NF-κB) p65 was measured by Western blot. Results HE staining showed that compared with the control group, the model group exhibited alveolar septal swelling and thickening, vascular dilatation and congestion, and inflammatory cell infiltration in the lung tissue; the hydrogen groups had significantly reduced pathological damage and inflammatory response than the model group, with more improvements in hydrogen group II than in hydrogen group I. Immunohistochemical results showed that compared with those in the control group, the levels of the inflammatory cytokines IL-6 and TNF-α were significantly increased in the model group; the hydrogen groups showed significantly decreased IL-6 and TNF-α levels and a significantly increased level of the anti-inflammatory factor IL-10 than the model group, which were more marked in hydrogen group II than in hydrogen group I. Immunofluorescence results showed that compared with the control group, the expression of the surface marker of M1 macrophages in the model group was significantly upregulated; the hydrogen groups showed significantly downregulated M1 marker and significantly upregulated M2 marker, and hydrogen group II showed significantly increased M2 marker compared with hydrogen group I. Western blot results showed that compared with that in the control group, the ratio of P-NF-κB p65/NF-κB p65 in the model group was significantly increased; the P-NF-κB p65/NF-κB p65 ratio was significantly reduced in the hydrogen groups than in the model group, and was significantly lower in hydrogen group II than in hydrogen group I. Conclusion Hydrogen inhalation therapy may reduce the inflammatory response of radiation-induced lung injury by inhibiting the NF-κB signaling pathway to promote the polarization of the macrophage M1 subtype to the M2 subtype.
