Ischemic stroke is the primary cause of disability and mortality worldwide. Ischemia/reperfusion (I/R)-induced microcirculatory dysfunction and organ injury generally occur after ischemic stroke. Several studies have shown that intermedin (IMD) has a regulating function on cerebral microcirculation and blood-brain barrier via relaxing cerebral vessels and improving the local blood supply after cerebral ischemia. However, a unified conclusion has not been reached, and the underlying mechanism remains unclear. To observe and analyze the changes of cerebral microcirculation perfusion of cerebral IRI by IMD post-treatment in the rats and further explore the mechanism underlying the beneficial effect of IMD on cerebral IRI. Thirty-nine rats were divided into three groups: sham, I/R, and I/R + IMD groups. After IMD ischemia post-treatment, the rat cerebral infarction rate and the degree of neurological deficit were evaluated by TTC staining and neurological function score; the changes in the amount of cerebral microcirculation implantation on the injured side of the rats were observed by laser Doppler; the pathological changes and cell ultrastructure of rat cortex and hippocampus were observed by HE staining and transmission electron microscopy; the neuron apoptosis in the rat cortex and hippocampus was detected by TUNEL staining and immunohistochemical staining. Impaired neurological function, abnormal cortical/hippocampal neuron morphology, and the proportion of cerebral infarction were significantly improved in the IMD group compared with the I/R group, which suggested a possible neuroprotective role of IMD. IMD treatment also increased the average perfusion of cerebral surface microcirculation in rats by astonished 42.7 times. Finally, IMD administration decreased the caspase-3- and Bax-positive cell numbers and apoptotic cell ratio. IMD has a significant protective effect on neuronal damage caused by cerebral I/R in rats by improving cerebral microcirculation and inhibiting apoptosis.

缺血性中风是全世界致残和死亡的主要原因。缺血/再灌注 (I/R) 诱导的微循环功能障碍和器官损伤通常发生在缺血性中风后。多项研究表明，intermedin（IMD）通过舒张脑血管，改善脑缺血后局部血供，对脑微循环和血脑屏障具有调节作用。然而，尚未得出统一结论，其潜在机制尚不清楚。观察分析IMD后处理大鼠脑IRI脑微循环灌注的变化，进一步探讨IMD对脑IRI有益作用的机制。三十九只大鼠分为三组：假手术组、I/R组和I/R+IMD组。IMD缺血后处理后，采用TTC染色和神经功能评分评估大鼠脑梗死发生率和神经功能缺损程度；激光多普勒观察大鼠伤侧脑微循环植入量的变化；HE染色和透射电镜观察大鼠皮层和海马的病理变化和细胞超微结构；TUNEL染色和免疫组化染色检测大鼠皮层和海马神经元凋亡。与I/R组相比，IMD组神经功能受损、皮层/海马神经元形态异常、脑梗死比例明显改善，提示IMD可能具有神经保护作用。IMD治疗还使大鼠脑表面微循环的平均灌注增加了惊人的42.7倍。最后，IMD 给药降低了 caspase-3 和 Bax 阳性细胞数量和凋亡细胞比率。IMD通过改善脑微循环、抑制细胞凋亡对大鼠脑I/R引起的神经元损伤具有显着的保护作用。