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目的 探讨灯盏花素对慢性低氧大鼠PKC信号途径的影响。方法 将SD大鼠分为 :对照组 (A) ,低氧组 (B) ,低氧 +灯盏花素组 (C) ,低氧时间为 4wk。采用透射电镜、放射活性测定法、免疫组化等方法研究灯盏花素对慢性低氧大鼠肺动脉平均压 (mPAP)、左右心室重量比 (RV/LV +S)、肺细小动脉管壁面积 /管总面积 (WA/TA)、中膜平滑肌细胞核密度 (SMC)、肺细小动脉超微结构、肺组织PKC活性、肺细小动脉管壁PKC的影响。结果 (1)B组mPAP、RV/LV +S明显高于A组 (P <0 0 1) ,C组mPAP、RV/LV +S明显低于B组 (P <0 0 1) ;(2 )光镜下B组WA/TA、SMC明显高于A组 (P <0 0 1) ,C组WA/TA、SMC明显低于B组 (P <0 0 1) ;电镜显示B组肺动脉中膜平滑肌细胞增生 ,胶原纤维丰富 ;C组肺动脉中膜平滑肌细胞、胶原纤维较B组明显减少 ;(3)B组肺组织PKC总活性 (PKCt)、胞膜PKC活性(PKCm)、胞质PKC活性 (PKCc)及胞膜PKC活性 (PKCm)占PKC总活性 (PKCt)的百分比明显高于A组 (P <0 0 1) ,C组PKCt、PKCm、PKCc及PKCm占PKCt的百分比明显低于B组 (P <0 0 1) ;(4 )免疫组化显示B组肺细小动脉 (直径约10 0～ 2 0 0 μm)PKC含量明显高于A组 (P <0 0 1) ,C组较B组明显为低 (P <0 0 1)。结论 灯盏花素抑制PKC信号途径可能是其抑制慢性低氧
Objective To investigate the effect of breviscapine on PKC signaling pathway in chronic hypoxia rats. Methods SD rats were divided into control group (A), hypoxia group (B), hypoxia + breviscapine group (C), hypoxia time was 4wk. The effects of breviscapine on pulmonary arterial pressure (mPAP), left ventricle weight ratio (RV / LV + S), pulmonary arteriole wall area / area in chronic hypoxic rats were studied by transmission electron microscopy, radioactivity assay and immunohistochemistry. (WA / TA), SMC, ultrastructure of pulmonary arterioles, PKC activity in lung tissue and PKC in pulmonary arterioles. Results (1) The mPAP and RV / LV + S in group B were significantly higher than those in group A (P <0.01), and the levels of mPAP and RV / LV + S in group C were significantly lower than those in group B The WA / TA and SMC in group B were significantly higher than those in group A (P <0.01), and the WA / TA and SMC in group C were significantly lower than those in group B (P <0.01) (3) The PKCt, PKCm, PKCm of lung tissue in group B were significantly lower than that in group B (P <0.05) The percentages of PKCc, PKCc and PKCt in group C were significantly higher than those in group A (P <0.01). The percentage of PKCt, PKCm, PKCc and PKCm in group C was significantly lower than that in group C (P <0.01). (4) Immunohistochemistry showed that the content of PKC in pulmonary arterioles (diameter about 100 ~ 200 μm) in group B was significantly higher than that in group A (P <0.01), and in group C Which was significantly lower than that in group B (P <0.01). Conclusion Breviscapine inhibits PKC signaling pathway may be its inhibition of chronic hypoxia