Premium
Hydrogen treatment reduces tendon adhesion and inflammatory response
Author(s) -
Meng Jia,
Yu Pan,
Tong Jian,
Sun Wenshuang,
Jiang Hui,
Wang Yicun,
Xue Kaiwen,
Xie Farong,
Qian Hong,
Liu Naicheng,
Zhao Jianning,
Bao Nirong
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27441
Subject(s) - malondialdehyde , superoxide dismutase , glutathione , chemistry , tendon , saline , western blot , antioxidant , adhesion , andrology , oxidative stress , biochemistry , medicine , surgery , enzyme , organic chemistry , gene
A rat model of tendon repair was established to investigate the effects of hydrogen water on tendon adhesion reduction. Thirty‐six Sprague Dawley rats were randomly divided into a normal saline (NS) group and a hydrogen water (HS) group according to the processing reagents after a tendon repairing operation. Pre‐ and postoperative superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH) in subjects’ serum were observed. Skin fibroblasts were grouped into an NS group, H 2 O 2 group, H 2 group, and H 2 O 2 H 2 group. Expressions of Nrf2, CATA, and γ‐GCS were also tested by Western blot analysis. 8‐OHdG, GSH, MDA, and SOD of the cells were analyzed by the enzyme‐linked immunosorbent assay method. The postoperative SOD activity and GSH contents were significantly reduced ( P < 0.05), whereas the postoperative MDA level was significantly increased ( P < 0.05). Similarly, the postoperative HS group showed significantly higher SOD activity and GSH contents ( P < 0.05) but lower MDA ( P < 0.05) compared with the postoperative NS group. MDA and 8‐OHdG were significantly decreased in hydrogen‐rich medium, while SOD and GSH were increased. The expression of Nrf2, CATA, and γ‐GCS in antioxidant system were reduced after H 2 O 2 processing, which were restored after the application of hydrogen‐rich medium. Hydrogen water can reduce tendon adhesion after tendon repairing and prohibit excessive inflammatory response, which could be associated with the activation of the Nrf2 pathway.