Neuroprotective effects of scutellarin against hypoxic-ischemic-induced cerebral injury via augmentation of antioxidant defense capacity.
An increasing number of studies has indicated that hypoxic-ischemic-induced cerebral injury is partly mediated via oxidative stress. Recent researches have focused on searching for drug and herbal manipulations to protect against hypoxic-ischemic-induced oxidative cell damage. Scutellarin is a flavonoid derived from the Erigeron breviscapus (vant.) and has been reported to exhibit neuroprotective properties. However, its precise mechanism, particularly its antioxidation mechanism, remains elusive. In the present study, we investigated the neuroprotective effects of scutellarin on middle cerebral artery occlusion (MCAO)-induced brain damage in rats, and oxygen-glucose deprivation (OGD)-induced toxicity in primary culture of rat cortical neurons. In vivo, intraperitoneal injections of scutellarin (20 and 60 mg/kg) improved the neurological score and diminished the percentage of brain infarct volume. At the same time, scutellarin significantly increased superoxide dismutase (SOD), catalase (CAT) activities and glutathione (GSH) level in ischemic brain tissues, enhancing endogenous antioxidant activity. Moreover, pretreatment of scutellarin (25, 50 and 100 μM) protected neurons against lethal stimuli, decreased the percentage of apoptotic cells and inhibited reactive oxygen species (ROS) generation in OGD-induced primary cortical neurons in vitro. These results suggest that the preventive and therapeutic potential of scutellarin in cerebral injury patients is, at least in part, ascribed to augmentation of cellular antioxidant defense capacity.
Key Laboratory of Traditional Chinese Medicine Pharmacology Tianjin, People's Republic of China.
Hong
H
Guo
Li-Min
LM
Hu
Shao-Xia
SX
Wang
Yu-Lin
YL
Wang
Fang
F
Shi
Hui
H
Li
Yang
Y
Liu
Li-Yuan
LY
Kang
Xiu-Mei
XM
Gao
D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D047310:Apigenin / Q000737:chemistry / Q000494:pharmacology*; D020520:Brain Infarction / Q000188:drug therapy / Q000378:metabolism; D002540:Cerebral Cortex / Q000166:cytology; D004365:Drugs, Chinese Herbal / Q000737:chemistry / Q000494:pharmacology; D005965:Glucuronates / Q000737:chemistry / Q000494:pharmacology*; D020925:Hypoxia-Ischemia, Brain / Q000188:drug therapy* / Q000378:metabolism*; D020244:Infarction, Middle Cerebral Artery / Q000188:drug therapy / Q000378:metabolism; D008297:Male; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D018696:Neuroprotective Agents / Q000737:chemistry / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects*; D061251:Primary Cell Culture; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism
D000975:Antioxidants; D004365:Drugs, Chinese Herbal; D005965:Glucuronates; D018696:Neuroprotective Agents; D017382:Reactive Oxygen Species; C484876:scutellarin; D047310:Apigenin