Abstract:
BACKGROUND:Our study aimed to screen and explore the expression of inflammatory factors in keloid patients and to investigate how hyperbaric oxygen (HBO) therapy affects the expression levels of interleukin-12p40 (IL-12p40), macrophage inflammatory protein-1β (MIP-1β), platelet-derived growth factor-BB (PDGF-BB), and interleukin-1 receptor antagonist (IL-1Ra). OBJECTIVE:30 patients were randomly selected and divided into the following 3 groups: keloid samples from keloid patients treated with HBO therapy (A), keloid samples from keloid patients treated without HBO therapy (B), and normal control skin samples derived from individuals who had no clear scarring (C). Each group included 10 samples. METHODS:Inflammatory factors in the keloid tissues were measured with the MILLIPLEX multiplexed Luminex system. Hematoxylin and eosin staining, immunohistochemical staining, and Western blotting were used to observe the morphological differences in different tissues and the expression levels. RESULTS:The expression levels of inflammatory mediators, including IL-12p40, MIP-1β, PDGF-BB, and IL-1Ra, in keloid tissues were significantly different from those in samples of normal skin. Hematoxylin and eosin staining showed significantly greater inflammatory infiltration in keloid tissue. Significantly different expression levels were observed in group A, B, and C. CONCLUSION:Significantly altered levels of inflammatory factors in the samples from keloid patients were observed, suggesting that formation of a keloid is potentially related to inflammatory responses. HBO therapy could significantly affect the expression levels of IL-12p40, MIP-1β, PDGF-BB, and IL-1Ra, indicating that the effects of HBO therapy are associated with the attenuation of inflammatory responses.
journal_name
Medicine (Baltimore)journal_title
Medicineauthors
Hao Y,Dong X,Zhang M,Liu H,Zhu L,Wang Ydoi
10.1097/MD.0000000000019857subject
Has Abstractpub_date
2020-04-01 00:00:00pages
e19857issue
16eissn
0025-7974issn
1536-5964pii
00005792-202004170-00094journal_volume
99pub_type
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