title: Tanshinone IIA increases levels of NeuN, protein disulfide isomerase, and Na+/K+-ATPase and decreases evidence of microglial activation after cerebral ischemic injury.
abstract: This study was designed to clarify the neuroprotective effects of tanshinone IIA (TSA) following cerebral ischemic insult. Adult Sprague-Dawley rats were operated upon to achieve a middle cerebral artery occlusion to cause transient focal cerebral ischemia, which were then randomly divided into the sham-operated control group and cerebral ischemia/reperfusion (I/R) groups receiving a 2 h occlusion. The treatment groups received daily intraperitoneal injections of high or low doses of TSA, for 7 or 15 days. NeuN immunostaining revealed neuronal loss following I/R, which was partially prevented with subsequent TSA dosing. Protein disulfide isomerase and adenosine triphosphatase (Na(+)/K(+)-ATPase) levels were all depressed by means of I/R. TSA treatment markedly reversed the depression of all indices examined. The intensity of microglial activation, as evidenced with CD11b staining, was increased by means of cerebral artery occlusion, but this was partially reversed with subsequent TSA treatment. TSA may affect neuroprotection by way of minimizing deficits in energy metabolism and reduction of the extent of cell death within affected regions.
authors.affiliation: aNeurological Intensive Care Unit, Yuhuangding Hospital, Yantai bDepartment of Clinical Microbiology and Immunology, Xiang-ya School of Medicine cCenter of Experimental Medicine, The Third Xiang-ya Hospital dMedical Science Research Center, Xiangya Hospital, Central South University, Changsha, China.
authors.forename: Pu-Yuan
authors.initials: PY
authors.lastname: Wen
authors.forename: Jian
authors.initials: J
authors.lastname: Li
authors.forename: Bei-Ling
authors.initials: BL
authors.lastname: Lu
authors.forename: Jie
authors.initials: J
authors.lastname: Liu
authors.forename: Feng-Zhen
authors.initials: FZ
authors.lastname: Yang
authors.forename: Li
authors.initials: L
authors.lastname: Zhou
authors.forename: Hao
authors.initials: H
authors.lastname: Luo
authors.forename: Wen-Wen
authors.initials: WW
authors.lastname: Li
authors.forename: Jun
authors.initials: J
authors.lastname: Zhou
mesh_terms: D045784:Abietanes / Q000627:therapeutic use*; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D001921:Brain / Q000473:pathology; D039481:CD11b Antigen / Q000378:metabolism; D004195:Disease Models, Animal; D020244:Infarction, Middle Cerebral Artery / Q000150:complications / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D009422:Nervous System Diseases / Q000188:drug therapy / Q000209:etiology; D010751:Phosphopyruvate Hydratase / Q000378:metabolism*; D019704:Protein Disulfide-Isomerases / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*
chemical_list: D045784:Abietanes; D000894:Anti-Inflammatory Agents, Non-Steroidal; D039481:CD11b Antigen; C021751:tanshinone; D010751:Phosphopyruvate Hydratase; D019704:Protein Disulfide-Isomerases; D000254:Sodium-Potassium-Exchanging ATPase