彭潇，方世记，郑丽云，邱伟文

    (1.温州医科大学附属第五医院 神经内科，浙江 丽水 323000；2.温州医科大学附属第五医院 介入科，浙江 丽水 323000；3.温州医科大学附属第六医院 神经内科，浙江 丽水 323000)

    丹酚酸A对大鼠脑缺血再灌注后细胞凋亡的保护作用及其机制

    彭潇1，方世记2，郑丽云1，邱伟文3

    (1.温州医科大学附属第五医院 神经内科，浙江 丽水 323000；2.温州医科大学附属第五医院 介入科，浙江 丽水 323000；3.温州医科大学附属第六医院 神经内科，浙江 丽水 323000)

    目的：探讨丹酚酸A(Sal A)对大鼠脑缺血再灌注后细胞凋亡的保护作用及其机制。方法：采用线拴法构建大脑中动脉缺血再灌注(MCA-IR)模型。将正常SD大鼠随机分为假手术组(对照组)、MCA-IR模型组(MCA-IR组)、Sal A+MCA-IR组(Sal A组)；Sal A组于建模前1周每日腹腔注射1.0、2.5、5.0 mg/kg Sal A。于再灌注后24 h取梗死脑组织用TUNEL法检测脑细胞凋亡，Western blot检测磷酸化Akt(p-Akt)和Akt的表达，免疫组织化学法检测海马区胞浆型磷脂酶A2(cPLA2)的表达。结果：Sal A组海马CA1区细胞凋亡率和MDA含量较MCA-IR组降低，而SOD量较MCA-IR组显著增加(P<0.05)，MCA-IR组海马区p-Akt表达较对照组显著下降(P<0.05)，而cPLA2较对照组显著增高(P<0.05)，1.0、2.5、5.0 mg/kg Sal A预处理后，MCA-IR模型大鼠海马区cPLA2表达显著降低(P<0.05)，而p-Akt表达显著增加(P<0.05)。结论：Sal A降低缺血再灌注损伤后细胞凋亡，起到损伤保护作用，其机制与其降低cPLA2表达，激活Akt信号通路有关。

    丹酚酸A；细胞凋亡；蛋白激酶B；脑缺血再灌注；大鼠

    Abstract: Objective:To investigate the protective effect of salvianolic acid A (Sal A) against apoptosis in cerebral ischemia-reperfusion model and its mechanism.Methods:SD rats were randomly divided into sham operation group (sham group), middle cerebral artery ischemia reperfusion model (MCA-IR) group (MCA-IR group), Sal A pretreatment and MCA-IR group (Sal A+MCA-IR group). MCA-IR was established in MCA-IR group and Sal A+MCA-IR group in which rats were pre-treated with 1.0, 2.5, 5.0 mg/kg Sal A via intraperitoneal injection daily for 1 week. The artery were reperfused for 24 h and rats were sacrificed. TUNEL was used to assayed the cell apoptosis, immunohistochemistry was implied to test the expression of cPLA2 and Western blot was undergone to analyzed p-Akt and total Akt. Immunohistochemistry was used to analyze the expression of cPLA2.Results:The apoptosis rate and MDA level in Sal A+MCA-IR group was lower, but SOD was higher than that in MCA-IR group (P<0.05). The expression of p-Akt in Hippocampus of MCA-IR model decreased, while the expression of cPLA2 increased significantly compared with control group. 1.0, 2.5, 5.0 mg/kg Sal A pretreatment reversed the decrease of p-Akt and increase of cPLA2.Conclusion:Sal A inhibits the apoptosis through decreasing the expression of cPLA2 and activating Akt pathway signaling in MCA-IR model. ......