The anti-inflammatory effect of paeoniflorin on cerebral infarction induced by ischemia-reperfusion injury in Sprague-Dawley rats.
Paeoniflorin, a component in Paeonia lactiflora Pall, inhibits nuclear factor-kappaB expression in chronic hypoperfusion rat and has anti-inflammatory properties. Therefore, the aim of the present study was to investigate the effect of paeoniflorin on cerebral infarct, and the involvement of anti-inflammation. We established an animal model of cerebral infarct by occluding both the common carotid arteries and the right middle cerebral artery for 90 min, followed by reperfusion of 24 hours. The ratios of cerebral infarction area to total brain area, and neuro-deficit score were used as an index to observe the effects of paeoniflorin on cerebral infarct. ED1 (mouse anti rat CD68), interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), intercellular adhesion molecular-1 (ICAM-1), myeloperoxidase (MPO) immunostaining and apoptotic cells in the cerebral infarction region also were studied. The results indicated that both pre-treatment and post-treatment with paeoniflorin reduced the ratio of cerebral infarction area; pre-treatment with paeoniflorin also reduced the neurological deficit score. The counts of ED1, IL-1beta, TNF-alpha, ICAM-1 of microvessels and MPO immunoreactive cells and apoptotic cells were increased in the cerebral infarction region; however, these increases were reduced by Paeoniflorin pre-treatment. In conclusion, Paeoniflorin reduced cerebral infarct and neurological deficit in ischemia-reperfusion injured rats, suggesting that paeoniflorin may have a similar effect in humans and might be a suitable treatment for stroke. Paeoniflorin reduced cerebral infarct, at least in part, involves the anti-inflammatory properties.
Tang
Nou-Ying
NY
China Medical University, Taichung, Taiwan.
Liu
Chung-Hsiang
CH
Hsieh
Ching-Tou
CT
Hsieh
Ching-Liang
CL
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D017209:Apoptosis / Q000187:drug effects; D001565:Benzoates / Q000494:pharmacology / Q000627:therapeutic use*; D001921:Brain / Q000187:drug effects; D001952:Bridged-Ring Compounds / Q000494:pharmacology / Q000627:therapeutic use*; D002544:Cerebral Infarction / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology; D004195:Disease Models, Animal; D005960:Glucosides / Q000494:pharmacology / Q000627:therapeutic use*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D039821:Monoterpenes; D009422:Nervous System Diseases / Q000517:prevention & control*; D029596:Paeonia / Q000737:chemistry*; D009195:Peroxidase / Q000378:metabolism; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000150:complications / Q000188:drug therapy*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D000097382:CD68 Molecule; D006027:Glycosides
D000893:Anti-Inflammatory Agents; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D001565:Benzoates; D001952:Bridged-Ring Compounds; D005960:Glucosides; D018799:Intercellular Adhesion Molecule-1; D053583:Interleukin-1beta; D039821:Monoterpenes; D009195:Peroxidase; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C015423:peoniflorin; D006027:Glycosides