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Age‐related changes in mitochondrial antioxidant enzyme Trx2 and TXNIP –Trx2– ASK 1 signal pathways in the auditory cortex of a mimetic aging rat model: changes to Trx2 in the auditory cortex
Author(s) -
Sun HaiYing,
Hu YuJuan,
Zhao XueYan,
Zhong Yi,
Zeng LingLing,
Chen XuBo,
Yuan Jie,
Wu Jing,
Sun Yu,
Kong Wen,
Kong WeiJia
Publication year - 2015
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.13324
Subject(s) - txnip , thioredoxin , biology , oxidative stress , neuroscience , microbiology and biotechnology , endocrinology
Age‐associated degeneration in the central auditory system, which is defined as central presbycusis, can impair sound localization and speech perception. Research has shown that oxidative stress plays a central role in the pathological process of central presbycusis. Thioredoxin 2 (Trx2), one member of thioredoxin family, plays a key role in regulating the homeostasis of cellular reactive oxygen species and anti‐apoptosis. The purpose of this study was to explore the association between Trx2 and the phenotype of central presbycusis using a mimetic aging animal model induced by long‐term exposure to d ‐galactose ( d ‐Gal). We also explored changes in thioredoxin‐interacting protein ( TXNIP ), apoptosis signal regulating kinase 1 ( ASK 1) and phosphorylated ASK 1 (p‐ ASK 1) expression, as well as the Trx2– TXNIP /Trx2– ASK 1 binding complex in the auditory cortex of mimetic aging rats. Our results demonstrate that, compared with control groups, the levels of Trx2 and Trx2– ASK 1 binding complex were significantly reduced, whereas TXNIP , ASK 1 p‐ ASK 1 expression, and Trx2– TXNIP binding complex were significantly increased in the auditory cortex of the mimetic aging groups. Our results indicated that changes in Trx2 and the TXNIP –Trx2– ASK 1 signal pathway may participate in the pathogenesis of central presbycusis.