中文摘要：

目的：探讨缝隙连接在缺血后处理保护大鼠脑缺血再灌注损伤中的作用及其可能的机制。方法：60只雄性SD大鼠随机分为假手术（sham）组、缺血再灌注（ischmia／reperfusion，I／R）组、缺血后处理（ischemicpost—conditioning，IP0）组、甘珀酸（carbenox010ne，CBX）干预缺血再灌注（I／R＋CBX）组和甘珀酸干预缺血后处理（IPO＋CBX）组。采用线栓法建立大鼠大脑中动脉栓塞模型；Longgs法进行神经功能评分；TTC染色法和HE染色法分别检测大鼠脑梗死体积和脑组织形态学变化；WesternBlot法检测脑组织中缝隙连接蛋白43（Cx43）、蛋白激酶C（PKC）蛋白的表达。结果：与sham组相比，I／R组神经功能评分显著增高，脑梗死体积增大，细胞排列紊乱、胞核固缩等组织形态学改变显著；IP0可使I／R组损伤减轻；CBX可以进一步增强IPO对I／R损伤的保护作用。WesternBlot结果显示，I／R组较sham组Cx43表达增多，PKC表达降低；IPO组较I／R组Cx43表达降低（P〈0．01），PKC表达增高（P〈O．01），同时，IPO＋CBX组较IPO组也有类似的改变。结论：IPO可通过抑制缝隙连接而减轻I／R损伤，其机制可能与影响PKC蛋白的表达有关。

英文摘要：

AIM： To investigate the effect of gap junction in ischemic post-conditioning on cerebral ischemic-reperfusion injury in rats. METHODS： Sixty adult male SD rats were ran- domly divided into sham group, I/R group, IPO group, I/R＋CBX group and IPO＋CBX group. Thread occlusion method was used to make MCAO model. Neurological scores of rat were evaluated by Longa score. Infarct volume of brain tissue was measured by TTC staining. Histopathology of cerebral tissue was detected by HE staining. The expressions of Cx43 and PKC protein were detected by Western Blot. RESULTS： In I/R group, neurological deficit scores decreased, cerebral infarction area in- creased and histopathology changed significant- ly, while similar changes did not found in sham group. IPO has protective effect on I/R injury.Similarly, CBX increased the protection of IPO on I/R injury obviously. Results of Western Blot showed, in I/R group, Cx43 protein in- creased significantly and PKC decreased com- pared to the sham group （P〈0.01）. Mean- while, in IPO group Cx43 protein decreased ex- tremely and PKC increased compared to I/R group. Similarly, in IPO＋CBX group Cx43 pro- tein decreased significantly and PKC increased compared to IPO group. CONCLUSION： IPO has protective effect on I/R injury through the gap junction, which may be associated with the change of PKC protein.