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目的探索姜黄素改善急性肺栓塞(APE)的作用机制。方法采用自体血栓法复制APE动物模型,72只SD大鼠按体重随机分为正常组、假手术组、模型组、姜黄素组各18只,姜黄素组于手术前1天和40min,造模后6、24、72h给予姜黄素100mg/kg灌胃1次,其余3组在同一时间灌胃等量生理盐水。分别在造模后6、24、72h,随机取6只大鼠肺组织和血清,Western Blot法检测肺组织大鼠细胞外调节蛋白激酶(ERK)、三磷酸肌醇激酶(PI3K)、蛋白激酶B(Akt),ELISA法测定血清脑钠肽(BNP)、肌钙蛋白T(TnT)和D-二聚体(D-Dimer)。结果与正常组同时间点比较,模型组、姜黄素组在3个时间点ERK、PI3K、Akt差异均有统计学意义(P<0.01)。与模型组同时间点比较,仅姜黄素组的肺组织ERK在造模后24h时差异无统计学意义(P>0.05),其余各时间点姜黄素组大鼠肺组织ERK、PI3K、Akt均显著下降(P<0.01)。与正常组同时间点比较,模型组BNP、TnT和D-Dimer在3个时间点均显著升高(P<0.01);与模型组同时间点比较,姜黄素组的血清BNP、TnT和D-Dimer均显著下降(P<0.05或P<0.01)。结论姜黄素能降低APE大鼠的肺组织ERK、PI3K、Akt及血清BNP、TnT和D-Dimer水平,可能是姜黄素改善APE大鼠预后的机制之一。
Objective To explore the mechanism of curcumin in improving acute pulmonary embolism (APE). Methods The animal models of APE were duplicated by autologous thrombosis method. Seventy-two SD rats were randomly divided into normal group, sham-operation group, model group and curcumin group, and curcumin group, After 6,24,72h given curcumin 100mg / kg gavage 1, the remaining three groups were given the same amount of saline at the same time. The lung tissues and serum of 6 rats were randomly selected at 6, 24, and 72 h after model establishment. The expression of ERK, PI3K and protein kinases Serum brain natriuretic peptide (BNP), troponin T (TnT) and D-dimer were measured by ELISA. Results Compared with the normal group, ERK, PI3K and Akt in the model group and the curcumin group were significantly different at 3 time points (P <0.01). Compared with the model group at the same time point, there was no significant difference in the expression of ERK in the curcumin group only 24h after modeling (P> 0.05), while the levels of ERK, PI3K and Akt in the curcumin group Significantly decreased (P <0.01). Compared with the normal group, BNP, TnT and D-Dimer in the model group were significantly increased at 3 time points (P <0.01). Compared with the model group at the same time points, serum BNP, TnT and D -Dimer significantly decreased (P <0.05 or P <0.01). Conclusion Curcumin can reduce the levels of ERK, PI3K, Akt, BNP, TnT and D-Dimer in the lung tissue of APE rats and may be one of the mechanisms by which curcumin improves the prognosis of APE rats.