补阳还五汤对急性脑缺血大鼠血清CD63和CD62P因子表达的影响

Influence of Buyang Huanwu Decoction on expressions of CD63 and CD62P in rat with acute cerebral ischemia

目的探讨补阳还五汤(黄芪,当归尾,赤芍,地龙、桃仁、红花、川芎)对急性脑缺血大鼠血清溶酶体颗粒糖蛋白63(CD63)和血小板α颗粒膜糖蛋白140(CD62P)细胞因子的影响。方法采用大脑中动脉线栓法建立大鼠急性局灶性脑缺血模型。将SPF级SD雄性大鼠100只随机均分为假手术组和模型组(生理盐水),氯吡格雷组[6.75 mg/(kg·d)],补阳还五汤高[26 g/(kg·d)]、低剂量组[6.5 g/(kg·d)]。连续给药14 d后观察和比较各组大鼠神经功能评分、脑梗死面积和血清CD63和CD62P水平变化情况。结果与模型组相比,氯吡格雷组、补阳还五汤高剂量组均能显著降低动物的神经功能评分(P<0.01)、增加体质量(P<0.05,P<0.01)和减少脑梗死面积(P<0.01和P<0.05)。酶联免疫法结果显示,模型组大鼠血清CD63、CD62P均较假手术组升高,补阳还五汤高、低剂量组与模型组比较,均能降低CD63和CD62P水平,差异有显著性(P<0.01和P<0.05),尤以高剂量组较为明显。结论补阳还五汤可能下调CD63、CD62P因子表达,减轻急性脑缺血模型大鼠的神经功能损伤和减少脑梗死面积。

AIM To investigate the influence of Buyang Huanwu Decoction（ BHD）（ Astragali Radix,the roots of Angelicae sinensis Radix,Paeoniae Radix rubra,Pheretima,Persicae Semen,Carthami Flos,Chuanxiong Rhizoma） on the expressions of CD63 and CD62 P in rat with acute cerebral ischemia. METHODS The acute focal cerebral ischemia models were established by middle cerebral artery occlution. The specific pathogen free SD rats were randomly and equally divided into sham operation and model（ distilled water）, Clopidogrel[6. 75 mg/（ kg·d） ]and high-dose [26 g/（ kg·d） ],low-dose [6. 5 g/（ kg·d） ]BHD groups. After consecutive administration for 14 d,the observation and comparison were made of the neurological score,cerebral infarction area and serum levels of CD63 and CD62 P. RESULTS Compared with the model group,Clopidogrel group and high-dose BHD group could significantly increase the weight（ P〈0. 05,P〈0. 01）,reduce the neurological score（ P〈0. 01） and decreased the cerebral infarction area of rats（ P〈0. 01,P〈0. 05）. ELISA results showed that rat serum CD63 and CD62 P in the model group were elevated in contrast to the sham operation group.Compared with the model group,the levels of CD63 and CD62 P in high-dose and low-dose BHD groups were lower（ P〈0. 01,P〈0. 05）,especially in the high-dose BHD group. CONCLUSION Buyang Huanwu Decoction can reduce cerebral ischemic damage and decreases the cerebral infarction area in rat with acute focal cerebral ischemia. Its mechanism may be associated with down-regulating the levels of CD63 and CD62 P.