title: [Adenosine Al Receptor Mediated Neuroprotection of Shenmai Injection on Rat Cerebral Ischemia/Reperfusion Injury: an Experimental Study].
abstract: OBJECTIVE
  To observe whether adenosine Al receptor (Al R) mediated neuroprotection of Shenmai Injection (SI) on rat cerebral ischemia/reperfusion (I/R) injury.
  
  
  METHODS
  The focal cerebral I/R model was established by middle cerebral artery occlusion (MCAO). Totally 60 successfully modeled rats was divided into 5 groups according to randomized block principle, i.e., the model group, the SI group, the SI + AlR antagonist (1,3-dipropyl-8-cyclopentylxanthine, DPCPX) group, the AlR antagonist control group, and the dimethyl sulfoxide (DMSO) control group, 12 in each group. Besides, a sham-operation group was set up (n =12). SI at 15 mL/kg was peritoneally injected to mice in the SI group immediately after cerebral I/R. Equal volume of normal saline was injected to mice in the model group and the sham-operation group. DPCPX at 1 mg/mL was peritoneally injected to mice in the Al R antagonist control group 30 min before peritoneal injecting SI. DPCPX at 1 mg/kg and DMSO at 1 mL/kg were peritoneally injected to mice in the AlR antagonist control group and the DMSO control group 30 min immediately before cerebral I/R. Rats' neurobehavioral scores were assessed after 24 h reperfusion. The volume of cerebral infarction and Bcl-2 protein expression of cerebral infarction penumbra were also detected. Results Compared with the sham-operation group, neurobehavioral scores, the volume of cerebral infarction, and Bcl-2 protein expression increased (all P <0. 05). Compared with the model group, neurobehavioral scores and the volume of cerebral infarction obviously decreased, but Bcl-2 protein expression increased in the SI group (all P <0. 05). Compared with the SI group, neurobehavioral scores increased, the volume of cerebral infarction was obviously enlarged, and Bcl-2 protein expression was obviously reduced in the A1R antagonist control group (all P <0. 05).
  
  
  CONCLUSIONS
  SI's neurobehavioral scores could be partially reversed in the Al R antagonist control group, the volume of cerebral infarction and Bcl-2 protein expression improved. AlR might possibly meditate neuroprotection of SI on MACO mire
authors.forename: Hua-rong
authors.initials: HR
authors.lastname: Lu
authors.forename: Sheng-wen
authors.initials: SW
authors.lastname: Song
authors.forename: Kun-yuan
authors.initials: KY
authors.lastname: Han
authors.forename: Hai-peng
authors.initials: HP
authors.lastname: Liu
authors.forename: Shuang-dong
authors.initials: SD
authors.lastname: Chen
authors.forename: Jun-lu
authors.initials: JL
authors.lastname: Wang
authors.forename: Qin-xue
authors.initials: QX
authors.lastname: Dai
mesh_terms: D000241:Adenosine; D000818:Animals; D002545:Brain Ischemia / Q000188:drug therapy*; D004338:Drug Combinations; D004365:Drugs, Chinese Herbal / Q000494:pharmacology* / Q000627:therapeutic use; D020244:Infarction, Middle Cerebral Artery; D051379:Mice; D000066829:Neuroprotection / Q000502:physiology*; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D043682:Receptor, Adenosine A1 / Q000378:metabolism*; D015427:Reperfusion Injury / Q000188:drug therapy*; D014970:Xanthines
chemical_list: D004338:Drug Combinations; D004365:Drugs, Chinese Herbal; D018696:Neuroprotective Agents; D043682:Receptor, Adenosine A1; D014970:Xanthines; C009252:fructus schizandrae, radix ginseng, radix ophiopogonis drug combination; C051360:1,3-dipropyl-8-cyclopentylxanthine; D000241:Adenosine