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目的:研究大鼠脑缺血再灌注(I/R)损伤中miR-30a的功能及其作用机制。方法:血管内栓线法制备大鼠大脑中动脉阻塞(MCAO)模型，实时荧光定量PCR(qRT-PCR)检测脑组织中miR-30a的表达变化；大鼠侧脑室注射miR-30a慢病毒后，2，3，5-氯化三苯基四氮唑(TTC)染色法检测大鼠脑梗死面积，Bederson法检测大鼠神经功能缺损程度，酶联免疫吸附法(ELISA)检测脑组织3-硝基酪氨酸(3-NT)和一氧化氮(NO)浓度，Western blot检测脑组织kelch样环氧氯丙烷相关蛋白-1(Keap1)、核因子E2相关因子(Nrf-2)和1型血红素氧合酶(HO-1)蛋白水平。双荧光素酶报告实验检测miR-30a与Keap1的靶向关系。结果:与假手术组比，脑I/R后miR-30a的表达呈时间依赖性下调。而miR-30a过表达可在病理水平减小大脑梗死组织面积，功能水平降低神经功能缺损程度，分子水平降低脑组织3-NT、NO、Keap1水平，增强Nrf2和HO-1表达。而双荧光素酶报告实验也显示miR-30a可与Keap1 mRNA靶向结合。结论:MCAO大鼠脑组织中miR-30a的表达下调，并且miR-30a可通过靶向Keap1缓解大鼠脑I/R损伤。“,”Objective:To study the function and mechanism of miR-30a in rat cerebral ischemia-reperfusion (I/R) injury.Methods:The middle cerebral artery occlusion (MCAO) model was established by intravascular suture method, and the expression of miR-30a in brain tissue was detected by real-time quantitative polymerase chain reaction (qRT-PCR). After intracerebroventricular injection of miR-30a lentivirus, the infarct area was detected by 2, 3, 5-triphenyltetrazole chloride (TTC) staining, the neurological deficit was detected by Bederson method, and the concentration of neurotrophin-3 (3-NT) and nitric oxide (NO) in brain tissue was detected by enzyme-linked immunosorbent assay (ELISA). The protein levels of kelch like ECH associated protein 1 (Keap1), NF-E2-related factor 2 (Nrf-2) and hemeoxygenase-1 (HO-1) in brain tissue were detected by Western blot. Double luciferase reporter assay was used to detect the targeting relationship between miR-30a and Keap1.Results:Compared with sham operation group, the expression of miR-30a was down-regulated in a time-dependent manner after I/R. The overexpression of miR-30a can reduce the area of cerebral infarction tissue at the pathological level, the degree of neurological impairment at the functional level, the 3-NT, NO and Keap1 at the molecular level, and enhance the expression of Nrf2 and HO-1. The dual luciferase reporter assay also showed that miR-30a could bind to Keap1 mRNA.Conclusions:The expression of miR-30a was down-regulated in MCAO rat brain tissue, and miR-30a could attenuate cerebral I/R injury in rats by targeting Keap1.