Cornin ameliorates cerebral infarction in rats by antioxidant action and stabilization of mitochondrial function.
This study was conducted to investigate the efficacy of cornin, an iridoid glycoside, in an experimental cerebral ischemia induced by middle cerebral artery occlusion (MCAO) and reperfusion (I/R), and to elucidate the potential mechanism. Adult male Sprague-Dawley rats were subjected to MCAO for 1 h, then reperfusion for 23 h. Behavioral tests were used to evaluate the damage to central nervous system. The cerebral infarct volume and histopathological damage were assessed to evaluate the brain pathophysiological changes. Spectrophotometric assay methods were used to determine the activities of superoxide dismutase (SOD) and glutathione-peroxidase (GPx). Contents of malondialdehyde (MDA), the generation of reactive oxygen species (ROS) as well as respiratory control ratio and respiratory enzymes of the brain mitochondria were also determined. The results showed that cornin significantly decreased neurological deficit scores, and reduced cerebral infarct volume and degenerative neurons. Meanwhile, cornin significantly increased the brain ATP content, improved mitochondrial energy metabolism, inhibited the elevation of MDA content and ROS generation, and attenuated the decrease of SOD and GPx activities in brain mitochondria. These findings indicate that cornin has protective potential against cerebral ischemia injury and its protective effects may be due to amelioration of cerebral mitochondrial function and its antioxidant property.
Jiang
Wang-Lin
WL
Pharmacy Department, Binzhou Medical University, Yantai 264003, PR China.
Zhang
Shu-Ping
SP
Zhu
Hai-Bo
HB
Tian
Jing-Wei
JW
D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology; D002118:Calcium / Q000378:metabolism; D019069:Cell Respiration / Q000187:drug effects; D004579:Electron Transport / Q000187:drug effects; D005979:Glutathione Peroxidase / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D057889:Iridoid Glycosides; D039823:Iridoids / Q000627:therapeutic use*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008560:Membrane Fluidity / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D051336:Mitochondrial Membranes / Q000378:metabolism; D018696:Neuroprotective Agents / Q000627:therapeutic use; D010743:Phospholipids / Q000378:metabolism; D008517:Phytotherapy; D010936:Plant Extracts / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000188:drug therapy; D013482:Superoxide Dismutase / Q000378:metabolism; D032412:Verbena; D014867:Water / Q000378:metabolism
D057889:Iridoid Glycosides; D039823:Iridoids; D018696:Neuroprotective Agents; D010743:Phospholipids; D010936:Plant Extracts; D017382:Reactive Oxygen Species; D014867:Water; D008315:Malondialdehyde; C000511:cornin iridoid; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D002118:Calcium