PKC抑制剂灯盏花素对缺血/再灌流脑损害的作用研究

Experimental research of PKC inhibitor, erigeron breviscapus on the ischemic/reperfusional brain injury

目的蛋白激酶Ｃ（ＰＫＣ）与脑组织缺血性损伤有密切关系，且证明可调节一氧化氮（ＮＯ）合酶的活性。灯盏花素可抑制ＰＫＣ的活性，其对脑缺血／再灌流损伤的作用和机制需深入研究。方法采用线栓法制成大鼠大脑中动脉缺血／再灌流模型，对缺血脑组织ＮＯ含量、局部脑血流量（ｒＣＢＦ）、中性粒细胞髓过氧化物酶（ＭＰＯ）及脑梗塞体积进行测定。结果灯盏花素对缺血脑组织ＮＯ的产生无明显影响，但可明显改善缺血脑组织的ｒＣＢＦ和显著降低ＭＰＯ活性。结论ＰＫＣ抑制剂灯盏花素对脑缺血的保护作用与ＮＯ的变化无关，其主要是通过抑制ＰＫＣ、增加ｒＣＢＦ和降低缺血脑组织内中性粒细胞的粘附浸润而实现的。

AIM Protein kinase C (PKC) was considered to have an important role in the cerebral ischemic/reperfusional damage, and a regulating role to the nitric oxide synthase. The erigeron breviscapus can inhibite the PKC activity, but its role and machanism in the cerebral ischemia/reperfusion are needed to explore. METHODS The animal models of middle cerebral artery ischemia/reperfusion were established by suture method, the nitric oxide (NO) concentration, regional cerebral blood flow (rCBF), myeloperoxidase of leukocytes (MPO) and cerebral infarction volume were measured. RESULTS The erigeron breviscapus increased rCBF and decreased MPO activity, and had no effect on the changes of NO in the focal ischemic brain tissues. CONCLUSION The PKC inhibitor erigeron breviscapus can improve rCBF and prevent the adhesion and infiltration of leukocytes into ischemic brain tissue, which was not concerned with the change of NO concentration, and suggested it may really have a protective effect on ischemic brain tissue.