动物造模,脑缺血再灌注损伤 z-bio 2022-06-29 235

　　Objective: To investigate the neurotherapeutic effect and mechanism of IL-6/STAT3/miR-21 in pine bark extract on cerebral ischemia-reperfusion injury in mice.

　　Methods: 120 KM mice were randomly divided into normal control group, sham operation group, 14 d and 28 d model group, 14 d and 28 d treatment group, 20 mice in each group. Cerebral ischemia-reperfusion injury model; the treatment group was given pine bark extract proanthocyanidins by gavage 7 days before sacrifice, and the control group and the sham-operated group were given the same amount of normal saline by gavage. The differences in learning and memory abilities, histopathological changes in the hippocampus, and the expression levels of interleukin-6, STAT3, p-STAT3 protein and miR-21 were detected in each group.

　　Results: At the same time, the learning and memory ability of the mice in the node treatment group was stronger than that in the model group; the arrangement of Nissl bodies in the treatment group was disordered, and part of the cells were irregular in shape and the cytoplasmic coloration was relatively light, but better than that in the model group; the 28-day model The expression level of IL-6 in the group was lower than that in the 14-day model group, and the IL-6 in the hippocampus of the treatment group was significantly lower than that of the model group at the same time point; there was no significant difference in the total protein content of STAT3 in the hippocampus between the groups (P>0.05). , the p-STAT3 content of the treatment group was lower than that of the model group at the same time point; the expression of miR-21 in the hippocampus of the treatment group at 14 and 28 days was lower than that of the model group at the same time point, and decreased with time.

　　Conclusion: Pine bark extract proanthocyanidins can effectively inhibit IL-6, significantly reduce the phosphorylation level of STAT3, and finally reduce the expression of miR-21, thereby reducing cerebral ischemia-reperfusion brain injury in mice.