PMID- 30578839
OWN - NLM
STAT- MEDLINE
DCOM- 20191224
LR  - 20191224
IS  - 1872-9754 (Electronic)
IS  - 0197-0186 (Linking)
VI  - 124
DP  - 2019 Mar
TI  - NADPH oxidase inhibitor apocynin decreases mitochondrial dysfunction and 
      apoptosis in the ventral cochlear nucleus of D-galactose-induced aging model in 
      rats.
PG  - 31-40
LID - S0197-0186(18)30577-1 [pii]
LID - 10.1016/j.neuint.2018.12.008 [doi]
AB  - Presbycusis has become a common sensory deficit in humans. Oxidative damage to 
      mitochondrial DNA and mitochondrial dysfunction is strongly associated with the 
      aging of the auditory system. A previous study established a mimetic rat model of 
      aging using D-galactose (D-gal) and first reported that NADPH oxidase-dependent 
      mitochondrial oxidative damage and apoptosis in the ventral cochlear nucleus 
      (VCN) might contribute to D-gal-induced central presbycusis. In this study, we 
      investigated the effects of apocynin, an NADPH oxidase inhibitor, on 
      mitochondrial dysfunction and mitochondria-dependent apoptosis in the VCN of 
      D-gal-induced aging model in rats. Our data showed that apocynin decreased NADPH 
      oxidase activity, H(2)O(2) levels, mitochondrial DNA common deletion, and 
      8-hydroxy-2-deoxyguanosine (8-OHdG) expression and increased total superoxide 
      dismutase (T-SOD) and glutathione peroxidase (GSH-Px) activity in the VCN of 
      D-gal-induced aging model in rats. Moreover, apocynin also decreased the protein 
      levels of phospho-p47(phox) (p-p47(phox)), tumor necrosis factor alpha (TNFalpha), 
      and uncoupling protein 2 (UCP2) in the VCN of D-gal-induced aging model in rats. 
      Meanwhile, apocynin alleviated mitochondrial ultrastructure damage and enhanced 
      ATP production and mitochondrial membrane potential (MMP) levels in the VCN of 
      D-gal-induced aging model in rats. Furthermore, apocynin inhibited cytochrome c 
      (Cyt c) translocation from mitochondria to the cytoplasm and suppressed caspase 
      3-dependent apoptosis in the VCN of D-gal-induced aging model in rats. 
      Consequently, our findings suggest that neuronal survival promoted by an NADPH 
      oxidase inhibitor is a potentially effective method to enhance the resistance of 
      neurons to central presbycusis.
CI  - Copyright (c) 2018. Published by Elsevier Ltd.
FAU - Du, Zheng-De
AU  - Du ZD
AD  - Department of Otorhinolaryngology, Beijing Friendship Hospital, Capital Medical 
      University, 95 Yongan Road, Xicheng District, Beijing, 100050, China.
FAU - Yu, Shukui
AU  - Yu S
AD  - Department of Otorhinolaryngology, Beijing Friendship Hospital, Capital Medical 
      University, 95 Yongan Road, Xicheng District, Beijing, 100050, China.
FAU - Qi, Yue
AU  - Qi Y
AD  - Department of Otorhinolaryngology, Beijing Friendship Hospital, Capital Medical 
      University, 95 Yongan Road, Xicheng District, Beijing, 100050, China.
FAU - Qu, Teng-Fei
AU  - Qu TF
AD  - Department of Otorhinolaryngology, Beijing Friendship Hospital, Capital Medical 
      University, 95 Yongan Road, Xicheng District, Beijing, 100050, China.
FAU - He, Lu
AU  - He L
AD  - Department of Otorhinolaryngology, Beijing Friendship Hospital, Capital Medical 
      University, 95 Yongan Road, Xicheng District, Beijing, 100050, China.
FAU - Wei, Wei
AU  - Wei W
AD  - Department of Otology, Shengjing Hospital, China Medical University, 36 Sanhao 
      Street, Heping District, Shenyang, 110004, China.
FAU - Liu, Ke
AU  - Liu K
AD  - Department of Otorhinolaryngology, Beijing Friendship Hospital, Capital Medical 
      University, 95 Yongan Road, Xicheng District, Beijing, 100050, China. Electronic 
      address: liuke@ccmu.edu.cn.
FAU - Gong, Shu-Sheng
AU  - Gong SS
AD  - Department of Otorhinolaryngology, Beijing Friendship Hospital, Capital Medical 
      University, 95 Yongan Road, Xicheng District, Beijing, 100050, China. Electronic 
      address: gongss1962@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20181220
PL  - England
TA  - Neurochem Int
JT  - Neurochemistry international
JID - 8006959
RN  - 0 (Acetophenones)
RN  - 0 (Enzyme Inhibitors)
RN  - B6J7B9UDTR (acetovanillone)
RN  - EC 1.6.3.- (NADPH Oxidases)
RN  - X2RN3Q8DNE (Galactose)
SB  - IM
MH  - Acetophenones/*pharmacology
MH  - Aging/*drug effects/metabolism
MH  - Animals
MH  - Apoptosis/drug effects/physiology
MH  - Cochlear Nucleus/*drug effects/metabolism
MH  - Enzyme Inhibitors/pharmacology
MH  - Galactose/*toxicity
MH  - Male
MH  - Maze Learning/drug effects/physiology
MH  - Mitochondria/*drug effects/metabolism
MH  - NADPH Oxidases/*antagonists & inhibitors/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
OTO - NOTNLM
OT  - Apocynin
OT  - Apoptosis
OT  - Central presbycusis
OT  - D-galactose
OT  - Mitochondrial dysfunction
OT  - NADPH oxidase
EDAT- 2018/12/24 06:00
MHDA- 2019/12/25 06:00
CRDT- 2018/12/23 06:00
PHST- 2018/10/25 00:00 [received]
PHST- 2018/12/01 00:00 [revised]
PHST- 2018/12/17 00:00 [accepted]
PHST- 2018/12/24 06:00 [pubmed]
PHST- 2019/12/25 06:00 [medline]
PHST- 2018/12/23 06:00 [entrez]
AID - S0197-0186(18)30577-1 [pii]
AID - 10.1016/j.neuint.2018.12.008 [doi]
PST - ppublish
SO  - Neurochem Int. 2019 Mar;124:31-40. doi: 10.1016/j.neuint.2018.12.008. Epub 2018 
      Dec 20.