Metformin Protects Neurons against Oxygen-Glucose Deprivation/Reoxygenation -Induced Injury by Down-Regulating MAD2B
Author(s) -
Xianfang Meng,
Guangpin Chu,
Zhihua Yang,
Ping Qiu,
Yue Hu,
Xiaohe Chen,
Wenpeng Peng,
Chen Ye,
Fang-Fang He,
Chun Zhang
Publication year - 2016
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000452562
Subject(s) - neuroprotection , metformin , viability assay , reactive oxygen species , pharmacology , neurotoxicity , lactate dehydrogenase , biology , apoptosis , microbiology and biotechnology , chemistry , endocrinology , medicine , biochemistry , insulin , toxicity , enzyme
Metformin, the common medication for type II diabetes, has protective effects on cerebral ischemia. However, the molecular mechanisms are far from clear. Mitotic arrest deficient 2-like protein 2 (MAD2B), an inhibitor of the anaphase-promoting complex (APC), is widely expressed in hippocampal and cortical neurons and plays an important role in mediating high glucose-induced neurotoxicity. The present study investigated whether metformin modifies the expression of MAD2B and to exert its neuroprotective effects in primary cultured cortical neurons during oxygen-glucose deprivation/reoxygenation (OGD/R), a widely used in vitro model of ischemia/reperfusion.
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