异亚丙基莽草酸抗大鼠脑缺血再灌注损伤的炎症机制初探

 目的研究异亚丙基莽草酸(ISA)对大脑中动脉缺血再灌注大鼠的影响及初步作用机制。方法栓线法建立大鼠大脑中动脉缺血再灌注模型,缺血3h,再灌注21h后以TTC染色法测定脑梗死范围,比色法测定脑组织匀浆中髓过氧化物酶(MPO)活性,ELISA法测定匀浆中IL-1β,IL-8,TNF-α含量。结果ISA 200,100 mg·kg^-1可明显减少模型大鼠的脑梗死范围,降低脑组织匀浆MPO活性以及IL-1β,IL-8,TNF-α的水平。结论ISA对局灶性脑缺血再灌注损伤具有明显的阻抑作用,其作用机制与抗炎症反应有关。

Effects of 3,4-oxo-isopropylidene shikimic acid(ISA) on the inflammatory reaction in rats subjected to middle cerebral artery ischemia and reperfusion and its probable mechanism

OBJECTIVE To study the effects of 3,4-oxo-isopropylidene shikimia acid(ISA) on the inflammatory reaction after cerebral ischemia and reperfusion in tMCAO(transient middle cerebral artery occlusion) rats, and its probable mechanism.METHODS The rats were subjected to MCAO for 3 h. After 21 h of reperfusion, TTC staining of brains was made to determine the size of cerebral infarction. The contents of IL-8,TNF-α, IL-1β and MPO in brain tissue were assayed. RESULTS After tMCAO, the vehicle group manifested the size of cerebral infarction as well as the content of TNF-α,IL-1β,IL-8 and MPO raised vs ISA group, ASA group and sham group. Above indicators were decreased significantly(P< 0.05 or 0.01 )in ISA 200,100 mg·kg^-1 and ASA 50 mg·kg^-1. CONCLUSION ISA can relieve the inflammatory reaction, namely leukocytic infiltrate and expression of inflammatory cytokine in brain tissue after cerebral ischemia and reperfusion, which may be an important mechanism for its resisting ischemic and reperfusion injury.