环磷腺苷葡胺预处理对大鼠局灶性脑缺血海马iNOS含量的影响

Effects of MAC on iNOS expression after focal cerebral ischemia/reperfusion in rats

目的研究诱导型一氧化氮合酶(iNOS)在大鼠局灶性脑缺血再灌注损伤海马中的表达,观测环磷酸腺苷葡甲胺(MAC)在对其含量的影响,探讨MAC在脑缺血病理过程中的作用。方法线栓法建立大鼠局灶性脑缺血再灌注损伤模型,化学比色法检测脑组织诱导型一氧化氮合酶的活性。TTC染色观察再灌注48h缺血损伤面积。结果iNOS活性在正常组及假手术组脑组织内极低,在缺血再灌注组和治疗组活性显著升高(P<0.01),于再灌注48h达到高峰,在MAC预处理组显著低于缺血再灌注组(P<0.01),MAC预处理组TTC染色缺血损伤面积也显著低于缺血再灌注组(P<0.05)。结论iNOS在大鼠局灶性脑缺血再灌注中活性显著增高,MAC预处理能有效抑制iNOS激活,减轻缺血性损伤范围,在大鼠局灶性脑缺血再灌注中脑损伤中起到保护作用。

[Objective] To explore the adjustive effect of MAC on iNOS after focal ischemia/reperfution in rats; and reveal the mechanism of nourprotection by MAC. [Methods] The acute focal cererbral ischemia/reperfution modle was established with suture emboli as described by Nagasawa. The activiation of iNOS, from brian fissure, were detected by chemiseal colorimetric metrodtissures, another 24 rats were sacrified at 48 h after reperfution for TTC stain to detect the region of reperfutional harm. [Result] The activiation of iNOS was nearly undetected in normal group and sham group, and striking elevated in I/R and MAC groups （P 〈0.01）, furthermore it was significant weaker in MAC group than in MCAO/R group （P 〈0.01）, so as to TTC stain [Conclusions] The activation of iNOS in rats which were focal cererbral ischemia/reperfution operated was strikingly elevating, and MAC could inhibit this activation significandy, relieve the region of reperfutional harm.