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氢疗法通过抑制核因子κB信号通路促进放射性肺损伤中巨噬细胞向M2亚型极化。

Hydrogen therapy promotes macrophage polarization to the M2 subtype in radiation lung injury by inhibiting the NF-κB signalling pathway.

作者信息

Gao Xue, Niu Shiying, Li Lulu, Zhang Xiaoyue, Cao Xuetao, Zhang Xinhui, Pan Wentao, Sun Meili, Zhao Guoli, Zheng Xuezhen, Song Guohua, Zhang Yueying

机构信息

Department of Pathophysiology, School of Clinical and Basic Medicine, Shandong First Medical University, China.

Department of Pathology, The First Affiliated Hospital of Shandong First Medical University, China.

出版信息

Heliyon. 2024 May 11;10(10):e30902. doi: 10.1016/j.heliyon.2024.e30902. eCollection 2024 May 30.

DOI:10.1016/j.heliyon.2024.e30902
PMID:38826750
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11141264/
Abstract

BACKGROUND: Radiotherapy has become a standard treatment for chest tumors, but a common complication of radiotherapy is radiation lung injury. Currently, there is still a lack of effective treatment for radiation lung injury. METHODS: A mouse model of radioactive lung injury (RILI) was constructed and then treated with different cycles of hydrogen inhalation. Lung function tests were performed to detect changes in lung function.HE staining was used to detect pathological changes in lung tissue. Immunofluorescence staining was used to detect the polarization of macrophages in lung tissue. Immunohistochemistry was used to detect changes in cytokine expression in lung tissues. Western Blot was used to detect the expression of proteins related to the NF-κB signalling pathway. RESULTS: Lung function test results showed that lung function decreased in the model group and improved in the treatment group.HE staining showed that inflammatory response was evident in the model group and decreased in the treatment group. Immunohistochemistry results showed that the expression of pro-inflammatory factors was significantly higher in the model group, and the expression of pro-inflammatory factors was significantly higher in the treatment group. The expression of pro-inflammatory factors in the treatment group was significantly lower than that in the model group, and the expression of anti-inflammatory factors in the treatment group was higher than that in the model group. Immunofluorescence showed that the expression of M1 subtype macrophages was up-regulated in the model group and down-regulated in the treatment group. The expression of M2 subtype macrophages was up-regulated in the treatment group relative to the model group. Western Blot showed that P-NF-κB p65/NF-κB p65 was significantly increased in the model group, and P-NF-κB p65/NF-κB p65 was decreased in the treatment group. CONCLUSION: Hydrogen therapy promotes macrophage polarization from M1 to M2 subtypes by inhibiting the NF-κB signalling pathway, thereby attenuating the inflammatory response to radiation lung injury.

摘要

背景：放射治疗已成为胸部肿瘤的标准治疗方法，但放射性肺损伤是放射治疗的常见并发症。目前，对于放射性肺损伤仍缺乏有效的治疗方法。 方法：构建放射性肺损伤（RILI）小鼠模型，然后用不同周期的氢气吸入进行治疗。进行肺功能测试以检测肺功能变化。采用苏木精-伊红（HE）染色检测肺组织的病理变化。采用免疫荧光染色检测肺组织中巨噬细胞的极化情况。采用免疫组织化学检测肺组织中细胞因子表达的变化。采用蛋白质印迹法检测与核因子κB（NF-κB）信号通路相关蛋白的表达。 结果：肺功能测试结果显示，模型组肺功能下降，治疗组肺功能改善。HE染色显示，模型组炎症反应明显，治疗组炎症反应减轻。免疫组织化学结果显示，模型组促炎因子表达显著升高，治疗组促炎因子表达显著降低，且治疗组抗炎因子表达高于模型组。免疫荧光显示，模型组M1亚型巨噬细胞表达上调，治疗组下调。与模型组相比，治疗组M2亚型巨噬细胞表达上调。蛋白质印迹法显示，模型组磷酸化核因子κB p65/核因子κB p65显著升高，治疗组降低。 结论：氢气疗法通过抑制NF-κB信号通路促进巨噬细胞从M1亚型向M2亚型极化，从而减轻放射性肺损伤的炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/5fe85a8c916c/mmcfigs12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/1577a6769422/gr1a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/654f395ece18/gr2a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/f187bff9fc76/gr3a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/9ab3a4808f3f/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/ee268619b9f5/mmcfigs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/9f4a88f5e0da/mmcfigs2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/d86fabd55c80/mmcfigs3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/397aa15efb9c/mmcfigs4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/af6d2371aa80/mmcfigs5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/31c7284b3f49/mmcfigs6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/02439c4008ca/mmcfigs7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/e44107b9a29c/mmcfigs8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/a20303a66127/mmcfigs9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/7256d7d02f13/mmcfigs10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/56c802f11a15/mmcfigs11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/5fe85a8c916c/mmcfigs12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/1577a6769422/gr1a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/654f395ece18/gr2a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/f187bff9fc76/gr3a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/9ab3a4808f3f/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/ee268619b9f5/mmcfigs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/9f4a88f5e0da/mmcfigs2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/d86fabd55c80/mmcfigs3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/397aa15efb9c/mmcfigs4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/af6d2371aa80/mmcfigs5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/31c7284b3f49/mmcfigs6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/02439c4008ca/mmcfigs7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/e44107b9a29c/mmcfigs8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/a20303a66127/mmcfigs9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/7256d7d02f13/mmcfigs10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/56c802f11a15/mmcfigs11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af5/11141264/5fe85a8c916c/mmcfigs12.jpg

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[2]
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本文引用的文献

[1]
Hydrogen Regulates Ulcerative Colitis by Affecting the Intestinal Redox Environment.

J Inflamm Res. 2024-2-12

[2]
Exploring the polarization of M1 and M2 macrophages in the context of skin diseases.

Mol Biol Rep. 2024-2-1

[3]
Epithelial Responses in Radiation-Induced Lung Injury (RILI) Allow Chronic Inflammation and Fibrogenesis.

Radiat Res. 2023-5-1

[4]
Renin-angiotensin system inhibitors mitigate radiation pneumonitis by activating ACE2-angiotensin-(1-7) axis via NF-κB/MAPK pathway.

Sci Rep. 2023-5-23

[5]
Immunomodulatory role of azithromycin: Potential applications to radiation-induced lung injury.

Front Oncol. 2023-3-8

[6]
High Concentration Hydrogen Mitigates Sepsis-Induced Acute Lung Injury in Mice by Alleviating Mitochondrial Fission and Dysfunction.

J Pers Med. 2023-1-29

[7]
Effects of molecular hydrogen supplementation on fatigue and aerobic capacity in healthy adults: A systematic review and meta-analysis.

Front Nutr. 2023-2-2

[8]
Effects of hydrogen-rich saline in neuroinflammation and mitochondrial dysfunction in rat model of sepsis-associated encephalopathy.

J Transl Med. 2022-11-26

[9]
Abrocitinib Attenuates Microglia-Mediated Neuroinflammation after Traumatic Brain Injury via Inhibiting the JAK1/STAT1/NF-κB Pathway.

Cells. 2022-11-13

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Int J Radiat Biol. 2023

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