【Animal Experiment】-The protective effect and mechanism of pine bark extract on cerebral ischemia-reperfusion injury in mice

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

  Method: 120 KM mice were randomly divided into normal control group, sham operation group, 14-day and 28-day model group, 14-day and 28-day treatment group, 20 mice in each group, using bilateral common carotid artery clamp method. Blood reperfusion injury model; the treatment group received oral proanthocyanidins extracted from pine bark 7 days before administration, and the control group and the sham operation group were given the same amount of normal saline. Give water by tube feeding. In each group of mice, learning and memory ability, hippocampal histopathological changes, and differences in the expression levels of interleukin-6, STAT3, p-STAT3 protein and miR-21 were detected.

  Result: At the same time, the learning and memory abilities of the mice in the treatment group were better than those in the model group. The Nissl bodies in the treatment group were randomly arranged, some cells were irregular in shape, and the cytoplasm was lighter, but better than the model group; at the same time point in the 28d model group, the expression level of IL-6 was lower than the 14-day model group, and the hippocampus of the treatment group IL-6 was significantly lower than the model group; the total STAT3 protein content of hippocampus was between each group. The difference was not statistically significant (P\→0.05), but the p-STAT3 content of the simultaneous treatment group was lower than that of the model group, and on the 14th and 28th day of treatment, the miR- in the hippocampus of the treatment group was lower. At the same time point, the expression of 21 was lower than that of the model group, and decreased over time.

  Conclusion: Pine bark extract proanthocyanidins effectively inhibit IL-6 and significantly reduce the phosphorylation level of STAT3, and ultimately reduce the expression of miR-21, which leads to cerebral ischemia and reduces brain damage in reperfusion mice.