Objective: To investigate the effects and the underlying molecular mechanisms of curcumin on pulmonary artery smooth muscle cells in rat model with chronic obstructive pulmonary disease (COPD). Methods: A total of 75 male Wistar rats were randomly divided into control group (group CN), model group (group M), low-dose curcumin group (group CL), medium-dose curcumin group (group CM) and high-dose curcumin group (group CH). HE staining was used to observe the morphology of pulmonary artery. Proliferating cell nuclear antigen (PCNA), apoptosis-related protein Bcl-2 and Bax were detected by immunohistochemical staining. TUNEL kit was used to analyze the effects of curcumin on apoptosis of smooth muscle cells, and the protein expressions of SOCS-3/JAK2/STAT pathway in lung tissues were determined by western blot. Results: Right ventricular systolic pressure (RVSP) and right ventricular hypertrophy index (RVMI) in group M were significantly higher than those in group CN, group CH and group CM (all P<0.05). HE staining and TUNEL kit test showed that the number of pulmonary artery smooth muscle cells had a significant increase in group M, while the pulmonary artery tube became thin, and the smooth muscle cells shrinked in group CM and group CH. Immunohistochemistry showed that PCNA and Bcl-2 in group M were significantly higher than those in group CN (all P<0.05), while Bax expression was significantly lower than that in group CN (P<0.05). PCNA in group CM and group CH were significantly lower than that in group M (all P<0.05), while Bax expression was significantly higher than that in group M (P<0.05). Western blot showed that SOCS-3 protein was significantly decreased in group M, while the p-JAK2, p-STAT1, p-STAT3 were significantly increased (all P<0.05). Compared with group M, SOCS-3 protein in group CM and group CH were significantly increased (all P<0.05), while the p-JAK2, p-STAT3 were significantly reduced (all P<0.05). Conclusion: Curcumin could promote the apoptosis of smooth muscle cells in rats with COPD, and improve the mean pulmonary artery pressure and RVMI through stimulating SOCS-3/JAK2/STAT signaling pathway.
目的: 探讨姜黄素对慢性阻塞性肺疾病（COPD）模型大鼠肺动脉平滑肌细胞的作用及其分子生物学机制。
方法: 将75只雄性Wistar大鼠随机分为正常对照组，模型对照组，姜黄素小剂量组、中剂量组和大剂量组，采用HE染色法观察肺动脉管组织学形态，免疫组织化学染色检测增殖细胞核抗原（PCNA）、凋亡相关蛋白Bcl-2、Bax，TUNEL法检测姜黄素对平滑肌细胞凋亡的影响，蛋白质印迹法检测肺组织SOCS-3/JAK2/STAT通路相关蛋白表达情况。
结果: 模型对照组右心室收缩压（RVSP）、右心室肥大指数（RVMI）均高于正常对照组（均 P < 0.05），姜黄素大剂量组和中剂量组RVSP、RVMI均低于模型对照组（均 P < 0.05）；模型对照组肺动脉管增厚、平滑肌细胞数量显著增多，而姜黄素中剂量组和大剂量组肺动脉管变薄、平滑肌细胞固缩、变形；模型对照组PCNA、Bcl-2相对表达量高于正常对照组（均 P < 0.05），Bax相对表达量低于正常对照组（ P < 0.05）；姜黄素中剂量组和大剂量组PCNA相对表达量低于模型对照组（均 P < 0.05），Bax相对表达量高于模型对照组（均 P < 0.05）；模型对照组SOCS-3蛋白减少、而磷酸化JAK2、STAT1、STAT3增多，姜黄素中剂量组和大剂量组SOCS-3蛋白增多，磷酸化JAK2、RVMI STAT3减少。
结论: 姜黄素可促进COPD大鼠平滑肌细胞凋亡，改善平均肺动脉压以及RVMI，这一作用可能与刺激SOCS-3/JAK2/STAT信号途径有关。