目的:研究TRPM2在缺氧缺血性脑损伤新生大鼠脑皮层内的表达变化,以探讨其在缺氧缺血性脑损伤中的作用,并初步探讨参附注射液(SFI)干预治疗后对其影响及可能机制。方法:制备新生大鼠HIBD模型,将新生7日龄SD大鼠随机分为假手术组(S组)、模型组(HI组)、参附治疗组(SF组),HI组、SF组按术后观察时间点不同进一步分为6 h、12 h、1天、3天、5天、7天6个亚组,每组8只。处死时观察每只新生大鼠脑组织的大体形态;并用免疫组化和Western Blotting法检测各组病变侧脑组织TRPM2蛋白的表达变化。结果:①脑大体形态观察:模型组大鼠结扎侧半球脑组织受损严重,1天时苍白、水肿明显,体积明显大于对侧。S组大鼠大脑半球左右对称,未见任何病理变化。②Western blotting结果:HI组TRPM2蛋白的表达水平在各时间点均较S组明显升高(P<0.05)。TRPM2在HIBD后3天达到高峰,随后开始下降。SF组在1天、3天、5天、7天时TRPM2的水平均低于HI组(P<0.05),但高于S组(P<0.05)。③免疫组化染色结果:C组病变侧大脑皮层TRPM2阳性细胞数在HIBD后3天达到高峰,随后降低,SF组在HI后3天、5天、7天的相应时间点TRPM2阳性细胞数均低于HI组(P<0.05),但高于S组(P<0.05)。结论:①新生大鼠HIBD后病变侧大脑皮层TRPM2的表达水平明显升高,并具有时间差异性,表明其参与了HIBD的病理过程,可能在HIBD诱导的细胞凋亡中发挥重要作用。②参附注射液能够下调TRPM2的表达,从而起到对HIBD新生大鼠的保护作用。 Objective: To investigate the expression of TRPM2 in the cortex of neonatal rats with hypoxic-ischemic brain damage (HIBD) to explore the role of TRPM2 in hypoxic-ischemic brain damage (ICH) Its impact and possible mechanism. Methods: HIBD model was established in neonatal rats. The neonatal 7-day-old SD rats were randomly divided into sham operation group (S group), model group (HI group), Shenfu treatment group (SF group), HI group Postoperative observation of time points were further divided into 6 h, 12 h, 1 day, 3 days, 5 days, 7 days 6 subgroups, 8 in each group. At the time of sacrifice, the gross morphology of each neonatal rat brain was observed. The expression of TRPM2 protein in the lesion side of each group was detected by immunohistochemistry and Western Blotting. Results: ① Gross morphological observation: The brain tissue of rats in the model group was severely damaged in the ligation hemisphere, pale and edema appeared on the 1st day, and the volume was significantly larger than that on the contralateral side. Sympathetic hemispheres of rats in group S were symmetrical, and no pathological changes were observed. ② Western blotting results: The expression of TRPM2 protein in HI group was significantly higher than that in S group at each time point (P <0.05). TRPM2 peaked 3 days after HIBD and then began to decline. The levels of TRPM2 in SF group at 1 day, 3 days, 5 days and 7 days were lower than those in HI group (P <0.05), but higher than those in S group (P <0.05). ③ Immunohistochemical results: The number of TRPM2-positive cells in the cortex of the lesion in group C reached a peak at 3 days after HIBD, and then decreased. The number of TRPM2-positive cells in SF group at 3, 5 and 7 days after HI Lower than HI group (P <0.05), but higher than S group (P <0.05). Conclusion: ① The expression of TRPM2 in the ischemic cortex of neonatal rats with HIBD is significantly increased and has time difference, indicating that it is involved in the pathological process of HIBD and may play an important role in HIBD-induced apoptosis. ② Shenfu injection can downregulate the expression of TRPM2, which play a protective effect on HIBD neonatal rats.