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目的 :探讨蛋白激酶C(PKC)在慢性低氧大鼠肺动脉重构中的作用。方法 :采用透射电镜、放射活性测定法、免疫组化、图像分析等方法综合进行评价。结果 :①肺动脉平均压 (mPAP)、右心室重量比 (RV LV +S)显著高于对照组 (P <0 .0 1) ;②光镜下肺细小动脉管壁面积 管总面积 (WA TA)、肺细小动脉中膜平滑肌细胞核密度 (SMC)显著高于对照组 (P <0 .0 1) ;电镜显示肺动脉中膜平滑肌细胞增生 ,胶原纤维较对照组明显为多 ;③肺组织PKC总活性(PKCt)、胞膜PKC活性 (PKCm)、胞浆PKC活性 (PKCc)及PKCm PKCt的百分比显著高于对照组 (P <0 .0 1) ;④免疫组化显示肺细小动脉 (直径约 10 0～ 2 0 0 μm)PKC含量、Ⅰ型胶原含量显著高于对照组 (P <0 .0 1) ,Ⅲ型胶原组间无明显差异 (P >0 .0 5 ) ;⑤肺组织PKCt、PKCm、PKCm PKCt和肺动脉管壁PKC的表达与肺细小动脉中膜平滑肌细胞核密度 (SMC)、肺动脉管壁Ⅰ型胶原的表达均呈正相关。结论 :PKC参与慢性低氧肺动脉平滑肌细胞增殖、管壁胶原表达的调控 ,从而参与了低氧性肺动脉重构的过程
Objective: To investigate the role of protein kinase C (PKC) in pulmonary artery remodeling in rats with chronic hypoxia. Methods: Transmission electron microscopy, radioactivity assay, immunohistochemistry, image analysis and other methods were comprehensively evaluated. Results: ① The mean pulmonary arterial pressure (mPAP) and right ventricular mass ratio (RV LV + S) were significantly higher than those of the control group (P0.01) ), And the SMC of pulmonary arterioles was significantly higher than that of the control group (P <0.01). Electron microscopy showed that pulmonary artery smooth muscle cells proliferated and collagen fibers were significantly more than those of the control group. ③PKC The percentage of PKCt, PKCm, PKCc and PKCm of PKCm were significantly higher than that of the control group (P <0.01) .④Immunohistochemistry showed that the diameter of pulmonary arterioles PKC content and collagen type Ⅰ were significantly higher than those in the control group (P <0.01). There was no significant difference between the three groups (P> 0.05) , PKCm, PKCm PKCt and pulmonary artery wall PKC expression were positively correlated with the SMC of pulmonary arterioles and the expression of type Ⅰ collagen in pulmonary artery wall. CONCLUSION: PKC is involved in the proliferation and the expression of collagen in the wall of chronic hypoxic pulmonary artery smooth muscle cells, which is involved in the process of hypoxic pulmonary remodeling