
Mechanisms underlying attenuation of apoptosis of cortical neurons in the hypoxic brain by flavonoids from the stems and leaves of Scutellaria baicalensis Georgi
Author(s) -
Guowang Miao,
Heng Zhao,
Ke Guo,
Jianjun Cheng,
Shufeng Zhang,
Xiaofeng Zhang,
Zhenling Cai,
Hong Miao,
Yunxiao Shang
Publication year - 2014
Publication title -
neural regeneration research/neural regeneration research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.93
H-Index - 38
eISSN - 1876-7958
pISSN - 1673-5374
DOI - 10.4103/1673-5374.141784
Subject(s) - scutellaria baicalensis , malondialdehyde , potassium cyanide , superoxide dismutase , pharmacology , glutathione peroxidase , chemistry , biochemistry , reactive oxygen species , apoptosis , glutathione , oxidative stress , cyanide , medicine , pathology , enzyme , traditional chinese medicine , inorganic chemistry , alternative medicine
Flavonoids from the stems and leaves of Scutellaria baicalensis Georgi, an antioxidant, markedly improve memory impairments and neuronal injuries. In the present study, primary cortical neurons of rats were exposed to potassium cyanide to establish a model of in vitro neural cell apoptosis. Inhibition of apoptosis by flavonoids from the stems and leaves of Scutellaria baicalensis Georgi at concentrations of 18.98, 37.36, and 75.92 μg/mL was detected using this model. These flavonoids dramatically increased cell survival, inhibited cell apoptosis and excessive production of malondialdehyde, and increased the activities of superoxide dismutase, glutathione peroxidase, and Na(+)-K(+)-ATPase in primary cortical neurons exposed to potassium cyanide. The flavonoids from the stems and leaves of Scutellaria baicalensis Georgi were originally found to have a polyhydric structure and to protect against cerebral hypoxia in in vitro and in vivo models, including hypoxia induced by potassium cyanide or cerebral ischemia. The present study suggests that flavonoids from the stems and leaves of Scutellaria baicalensis Georgi exert neuroprotective effects via modulation of oxidative stress, such as malondialdehyde, superoxide dismutase, glutathione peroxidase and Na(+)-K(+)-ATPase disorders induced by potassium cyanide.