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目的:探讨醒脑静注射液治疗新生儿缺氧缺血性脑损伤的机制。方法:建立新生儿缺氧缺血性损伤新生大鼠模型,将动物随机分为3组:假手术组、模型组和醒脑静组,每组24只。在不同时间点,收集各组脑组织,采用干湿质量法测定大鼠脑组织含水量,通过染色质免疫共沉淀及实时荧光定量PCR检测和比较各组脑组织HIF-1α在VEGF基因启动子的结合水平,以及VEGF启动子组蛋白H3第27位赖氨酸三甲基化(H3K27me3)和组蛋白H3赖氨酸4三甲基化(H3K4me3)的富集水平。结果:在各时间点,醒脑静治疗组HIF-1α结合在VEGF启动子上的水平较模型组均显著提高(P<0.05);醒脑静组VEGF启动子上H3K27me3富集水平较模型组显著降低(P<0.05),而H3K4me3富集水平显著升高(P<0.05)。结论:醒脑静注射液治疗HIBD的机制可能与促进HIF-1α结合到VEGF启动子上,促进VEGF的表达,同时改变VEGF启动子上H3K27me3和H3K4me3富集水平有关。
Objective: To investigate the mechanism of Xingnaojing Injection in treating neonatal hypoxic-ischemic brain damage. Methods: Newborn hypoxic-ischemic injury neonatal rat model was established. The animals were randomly divided into 3 groups: sham operation group, model group and Xingnaojing group, 24 rats in each group. At different time points, the brain tissue of each group was collected, the water content of brain tissue was determined by the method of wet and dry mass, the expression of HIF-1α in the brain tissue of each group was detected by the method of chromatin immunoprecipitation and real-time fluorescence quantitative PCR. And the level of enrichment of lysine trimethylated (H3K27me3) at position 27 of histone H3 of the VEGF promoter and histone H3 lysine 4 trimethylation (H3K4me3). Results: At each time point, the level of HIF-1α binding to VEGF promoter in Xingnaojing group was significantly higher than that in model group (P <0.05). The concentration of H3K27me3 in Xingnaojing group was higher than that in model group (P <0.05), while the enrichment level of H3K4me3 was significantly increased (P <0.05). Conclusion: The mechanism of Xingnaojing Injection in treating HIBD may be related to promoting the binding of HIF-1α to VEGF promoter, promoting the expression of VEGF and altering the level of H3K27me3 and H3K4me3 enrichment in VEGF promoter.