Open AccessIntravitreal Injection of Hydrogen Peroxide Induces Acute Retinal Degeneration, Apoptosis, and Oxidative Stress in Mice
Author(s) -
Bing Huang,
JiZhao Liang,
Zhaodong Xi,
Shaowan Chen,
Tsz Kin Ng,
Haoyu Chen
Publication year - 2018
Publication title -
oxidative medicine and cellular longevity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.494
H-Index - 93
eISSN - 1942-0900
pISSN - 1942-0994
DOI - 10.1155/2018/5489476
Subject(s) - outer nuclear layer , retina , retinal , ganglion cell layer , oxidative stress , inner nuclear layer , retinal degeneration , apoptosis , retinal ganglion cell , biology , retinal pigment epithelium , microbiology and biotechnology , chemistry , pathology , medicine , biochemistry , neuroscience
Purpose Oxidative stress is a common pathological condition for multiple retinal diseases. Hydrogen peroxide (H 2 O 2 ) has been applied as an oxidative stress inducer for the in vitro studies. Here, we report the in vivo effect of H 2 O 2 exposure to the mouse retina and its underlying mechanism.Methods The H 2 O 2 or saline solution was intravitreally injected into the eyes of female C57BL/6J mice for two consecutive days. The retinal structure was evaluated by in vivo imaging using spectral domain optical coherence tomography (OCT) and validated by histological assessment as well as retinal marker expression. In addition, retinal stress, cell apoptosis, and antioxidant enzyme expression were also determined.Results Retinal and outer nuclear layer thickness thinning was observed at days 7 and 14 by OCT imaging with the treatment of 10 μ g H 2 O 2 , which was confirmed by the histopathological analysis. The expressions of photoreceptor ( Rho , Rora , Rorb , and Rcvrn ), bipolar cell ( Chat and Calb2 ), and retinal pigment epithelial ( Rpe65 ) markers were reduced in the H 2 O 2 -treated group, whereas the expression of retinal ganglion cell marker ( Tubb3 ) was increased. TUNEL-positive cells were obviously found in the outer nuclear layer and inner nuclear layer of H 2 O 2 -treated mice but sparely found in the ganglion cell layer. Coherently, apoptotic gene expressions ( Casp3 , Casp9 , Bax , and Parp8 ) were significantly increased in the retina with increasing dosages of H 2 O 2 , while Bcl2 expression was mildly decreased. In addition, the expressions of Gfap and antioxidant enzyme genes ( Txn2 , Sod2 , and Gpx4 ) were significantly upregulated in the retina after the H 2 O 2 treatment, compared to the vehicle control group.Conclusions This study revealed that intravitreal injection of H 2 O 2 induces acute retinal damage by increasing oxidative stress and cell apoptosis in the retina. This acute retinal degeneration mouse model could provide a platform for drug screening against oxidative stress and retinal diseases.