Adenosine Al Receptor Mediated Neuroprotection of Shenmai Injection on Rat Cerebral Ischemia/Reperfusion Injury: an Experimental Study.
- Author:
Hua-rong LU
;
Sheng-wen SONG
;
Kun-yuan HAN
;
Hai-peng LIU
;
Shuang-dong CHEN
;
Jun-lu WANG
;
Qin-xue DAI
- Publication Type:Journal Article
- MeSH: Adenosine; Animals; Brain Ischemia; drug therapy; Drug Combinations; Drugs, Chinese Herbal; pharmacology; therapeutic use; Infarction, Middle Cerebral Artery; Mice; Neuroprotection; physiology; Neuroprotective Agents; pharmacology; therapeutic use; Rats; Rats, Sprague-Dawley; Receptor, Adenosine A1; metabolism; Reperfusion Injury; drug therapy; Xanthines
- From: Chinese Journal of Integrated Traditional and Western Medicine 2015;35(9):1109-1112
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe whether adenosine Al receptor (Al R) mediated neuroprotection of Shenmai Injection (SI) on rat cerebral ischemia/reperfusion (I/R) injury.
METHODSThe 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).
CONCLUSIONSSI'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