腺苷A_1受体激动剂CHA对缺血后脑组织β－EP含量的影响

The Effect of Adenosine on Concentration of β-EP in Cerebral Ischemic Gerbils

用放射免疫法测定沙土鼠半球缺血模型脑组织中β－ＥＰ（β－ｅｎｄｏｒｐｈｉｎ）含量，观察缺血后β－ＥＰ含量的变化及腺苷Ａ１受体激动剂ＣＨＡ（ｃｙｃｌｏｈｅｘｙｌａｄｅｎｏｓｉｎｅ）对缺血后β－ＥＰ含量变化的影响。结果显示：沙土鼠缺血８ｈ后β－ＥＰ含量明显增加，且与卒中症状呈正相关，与脑比重呈负相关。ＣＨＡ可以改善卒中症状，减轻脑水肿，抑制缺血后β－ＥＰ的升高。提示缺血后中枢β－ＦＰ增加会加重缺血性损伤，腺苷对内源性阿片肽系统具有抑制作用，腺苷抑制β－ＥＰ的升高可能是其抗缺血性脑损伤的又一机理。

The concentration of beta-endorphin(β-EP)was determined in gerbil cerebral cortex at 8h after unilateral ligation of left common carotid artery(LCCA)by radioimmunoassay.The effect of cyclohexyl adenosine(CHA)on the concentration of β-EP was observed. The relationship between the content of β-EP and the ischemic cerebral edema and the stroke index were studied. It was found that the concentration of β-EP was significantly increased in the cerebral cortex of ligated side in control animals(0. 7281 ±0. 2666pg/g wet wt,n=19,P<0. 01 )as compared with sham-opareted animals(0. 4417±0. 0753 pg/g wet wt,n=10)and significantly decreased in CHA-treated animals(0. 5738±0. 1362 pg/g wet wt,n=16,P<0. 05)as compared with the control ones, There was a significant positive correlation between the concentration of β-EP and stroke index(r=0. 4948,P<0. 01 ) and a significant negative correlation between the concentration of β-EP and specific gravity at the ligated side(r=-0. 6014,P<0. 01). The results indicate that the neuroprotective effect of CHA on cerebral ischemia may be related to the decrease of β-EP concentration.