HSG、Wnt/Ca^(2+)信号通路参与COPD相关性肺动脉高压血管重塑的研究  

Study on the involvement of HSG and Wnt/Ca^(2+)signaling pathways in vascular remodeling of COPD-related pulmonary hypertension

作　　者：吴闽付 陶金艳 宋国林 葛正行 李波 罗克佩 严眉 Wu Minfu;Tao Jinyan;Song Guolin;Ge Zhengxing;Li Bo;Luo Kepei;Yan Mei(Department of Emergency,the Second Affiliated Hospital of Guizhou University of Traditional Chinese Medicine,and the Center for Research on Chinese and Western Medicine in Critical Illness of Guizhou University of Traditional Chinese Medicine.Guiyang 550002,Guizhou,China;Yunyan District People's Hospital,Guiyang 550004,Guizhou,China)

机构地区：[1]贵州中医药大学第二附属医院急诊科,贵州中医药大学中西医危重症研究中心,贵州贵阳550002 [2]贵阳市云岩区人民医院,贵州贵阳550004

出　　处：《贵州医药》2025年第2期177-180,共4页Guizhou Medical Journal

基　　金：贵州省卫生健康委科学技术基金项目(gzwkj2023-128)。

摘　　要：目的本研究旨在通过动物实验探讨COPD相关性肺动脉高压肺动脉平滑肌细胞增值过程HSG基因及Wnt/Ca^(2+)途径作用。方法运用模拟COPD相关性肺动脉高压发病过程及机制构建PH模型,随后对正常组及模型组大鼠肺动脉平滑肌细胞进行定向培养,并运用RT-PCR、WB技术检测平滑肌细胞中HSG、Wnt5a基因及蛋白表达量,分析并探讨其可能存在的作用。结果与正常组大鼠相比,模型组大鼠肺动脉存在典型肺动脉高压病理表现,且其平滑肌细胞中HSG基因表达为(0.59±0.23),低于正常组平滑肌细胞的(1.00±0.00)(P<0.05);而Wnt5a基因表达量为(4.19±2.06),较正常组的(1.00±0.00)增加(P<0.05);模型组大鼠平滑肌细胞中HSG蛋白表达为(0.38±0.14),明显低于正常组的(0.93±0.10)(P<0.05);Wnt5a蛋白表达量为(0.67±0.09),明显高于正常组的(0.24±0.04)(P<0.05)。结论(1)本实验采取的造模方案有效,且可靠;(2)HSG及Wnt/Ca^(2+)途径均有可能参与了COPD相关性肺动脉高压平滑肌细胞的增生过程。Objective To investigate the roles of the HSG gene and the Wnt/Ca^(2+)pathway in the proliferation of pulmonary artery smooth muscle cells(PASMCs)associated with COPD-related pulmonary hypertension through animal experiments.Methods A pulmonary hypertension(PH)model was established by simulating the onset process and mechanisms of COPD-related pulmonary hypertension.Subsequently,PASMCs from both the normal group and the model group were cultured in a targeted manner.RT-PCR and Western Blotting(WB)techniques were used to detect the gene and protein expression levels of HSG and Wnt5a in PASMCs,and their potential roles were analyzed and discussed.Results Compared with the normal group,the model group rats exhibited typical pathological manifestations of pulmonary hypertension in their pulmonary arteries.The expression of the HSG gene in PASMCs of the model group was(0.59±0.23),which was lower than that in the normal group(1.00±0.00),and there were statistically significant differences(P<0.05).The expression of the Wnt5a gene was(4.19±2.06),which was higher than that in the normal group(1.00±0.00),there also were statistically significant differences(P<0.05).The protein expression of HSG in PASMCs of the model group was(0.38±0.14),significantly lower than that in the normal group(0.93±0.10),there were statistically significant differences(P<0.05).The protein expression of Wnt5a was(0.67±0.09),significantly higher than that in the normal group(0.24±0.04),there also were statistically significant differences(P<0.05).Conclusion The modeling approach adopted in this experiment is effective and reliable.Both the HSG gene and the Wnt/Ca^(2+)pathway may be involved in the proliferation of PASMCs associated with COPD-related pulmonary hypertension.

关 键 词：COPD相关肺动脉高压 HSG基因 Wnt/Ca 2+信号通路 平滑肌细胞 

分 类 号：R563.9[医药卫生—呼吸系统]