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Peroxiredoxin 1/2 protects brain against H 2 O 2 ‐induced apoptosis after subarachnoid hemorrhage
Author(s) -
Lu Yue,
Zhang Xiang-Sheng,
Zhou Xiao-Ming,
Gao Yong-Yue,
Chen Chun-Lei,
Liu Jing-Peng,
Ye Zhen-Nan,
Zhang Zi-Huan,
Wu Ling-Yun,
Li Wei,
Hang Chun-Hua
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.201801150r
Subject(s) - apoptosis , oxidative stress , subarachnoid hemorrhage , in vivo , western blot , peroxiredoxin , ask1 , medicine , chemistry , biology , pathology , endocrinology , biochemistry , peroxidase , microbiology and biotechnology , gene , cell cycle , cyclin dependent kinase 2 , enzyme
Recent studies suggest that peroxiredoxin1/2 (Prx1/2) may be involved in the pathophysiology of post‐ischemic inflammatory responses in the brain. In this study, we assessed the distribution and function of Prx1/2 in mice after experimental subarachnoid hemorrhage (SAH). We investigated the distribution of Prx1/2 in the brains of mice both in vivo and in vitro using immunofluorescence staining. The expression of Prx1/2 after SAH was determined by Western blot. Adenanthin was used to inhibit Prx1/2 function, and Prx1/2 overexpression was achieved by injecting adeno‐associated virus. Oxidative stress and neuronal apoptosis were assessed both in vivo and in vitro . The neurologic function, inflammatory response, and related cellular signals were analyzed. The results showed that Prx1 was mainly expressed in astrocytes, and Prx2 was abundant in neurons. The expression of Prx1/2 was elevated after SAH, and their expression levels peaked before proinflammatory cytokines. Inhibiting Prx1/2 promoted neuronal apoptosis by increasing the hydrogen peroxide (H 2 O 2 ) levels via the apoptosis signal‐regulating kinase 1/p38 pathway. By contrast, overexpression of Prx1/2 attenuated oxidative stress and neuronal apoptosis after SAH. Thus, early expression of Prx1/2 may protect the brain from oxidative damage after SAH and may provide a novel target for treating SAH.—Lu, Y., Zhang, X.‐S., Zhou, X.‐M., Gao, Y.‐Y., Chen, C.‐L., Liu, J.‐P., Ye, Z.‐N., Zhang, Z.‐H., Wu, L.‐Y., Li, W., Hang, C.‐H. Peroxiredoxin 1/2 protects brain against H 2 O 2 ‐induced apoptosis after subarachnoid hemorrhage. FASEB J. 33, 3051–3062 (2019). www.fasebj.org