谢晓佳, 曹锐, 刘清国, 黄粤, 朱宏勋, 赵世同, 赵静怡. 电针太冲穴及曲池穴拮抗应激性高血压前期大鼠胸主动脉外膜重构的机制研究[J]. 实用临床医药杂志, 2022, 26(14): 1-6. DOI: 10.7619/jcmp.20220629
引用本文: 谢晓佳, 曹锐, 刘清国, 黄粤, 朱宏勋, 赵世同, 赵静怡. 电针太冲穴及曲池穴拮抗应激性高血压前期大鼠胸主动脉外膜重构的机制研究[J]. 实用临床医药杂志, 2022, 26(14): 1-6. DOI: 10.7619/jcmp.20220629
XIE Xiaojia, CAO Rui, LIU Qingguo, HUANG Yue, ZHU Hongxun, ZHAO Shitong, ZHAO Jingyi. Mechanism of electroacupuncture at Taichong and Quchi points in antagonizing adventitia remodeling of thoracic aorta in stress-induced prehypertension rats[J]. Journal of Clinical Medicine in Practice, 2022, 26(14): 1-6. DOI: 10.7619/jcmp.20220629
Citation: XIE Xiaojia, CAO Rui, LIU Qingguo, HUANG Yue, ZHU Hongxun, ZHAO Shitong, ZHAO Jingyi. Mechanism of electroacupuncture at Taichong and Quchi points in antagonizing adventitia remodeling of thoracic aorta in stress-induced prehypertension rats[J]. Journal of Clinical Medicine in Practice, 2022, 26(14): 1-6. DOI: 10.7619/jcmp.20220629

电针太冲穴及曲池穴拮抗应激性高血压前期大鼠胸主动脉外膜重构的机制研究

Mechanism of electroacupuncture at Taichong and Quchi points in antagonizing adventitia remodeling of thoracic aorta in stress-induced prehypertension rats

  • 摘要:
    目的 探讨电针太冲穴、曲池穴拮抗应激性高血压前期大鼠(SIPR)胸主动脉外膜重构的机制。
    方法 应用足底电击结合噪声刺激的方法制备SIPR模型。电针组选取太冲穴、曲池穴进行干预,并在不同时间点测量空白组、模型组和电针组大鼠血压值,观察动物行为学的改变。干预14 d结束后取材,采用苏木素-伊红染色(HE染色)及Masson染色观察胸主动脉病理变化;采用逆转录-聚合酶链反应(RT-PCR)检测胸主动脉转化生长因子β1TGF-β1)、白细胞介素-6(IL-6)、Smad3、白细胞介素-10(IL-10)的mRNA表达;采用Western blot法检测胸主动脉Smad7、α-平滑肌激动蛋白(α-SMA)、Ⅰ型及Ⅲ型胶原蛋白表达。
    结果 模型组大鼠血压升高且血管外膜损伤明显;电针组大鼠血压下降且外膜损伤较轻。与空白组相比,模型组TGF-β1IL-6IL-10Smad3的mRNA表达升高,差异有统计学意义(P<0.05或P<0.01)。与模型组相比,电针组TGF-β1Smad3IL-6的mRNA表达下降,IL-10 mRNA表达升高,差异有统计学意义(P<0.05或P<0.01)。与空白组相比,模型组大鼠Ⅰ型、Ⅲ型胶原蛋白及α-SMA蛋白表达升高,Smad7蛋白表达下降,差异有统计学意义(P<0.05或P<0.01)。与模型组相比,电针组Ⅰ型、Ⅲ型胶原蛋白及α-SMA蛋白表达下降,Smad7蛋白表达升高,差异有统计学意义(P<0.05或P<0.01)。
    结论 电针太冲穴、曲池穴可显著降低SIPR血压并能有效预防血管外膜重构,其机制可能与调控TGF-β1/Smads信号通路并减轻炎症反应有关。

     

    Abstract:
    Objective To investigate the mechanism of electroacupuncture at Taichong and Quchi points in antagonizing adventitia remodeling of thoracic aorta in stress-induced prehypertension rats (SIPR).
    Methods Foot shock combined with noise stimulation was used to prepare SIPR model. In the electroacupuncture group, Taichong point and Quchi point were selected for intervention, and the blood pressure values of rats in the blank group, model group and electroacupuncture group were measured at different time points, and the change of animal behavior was observed. At the end of 14 d intervention, the samples were taken and the thoracic aortic lesions were detected by hematoxylin eosin staining (HE staining) and Masson staining; reverse transcription polymerase chain reaction (RT-PCR) was used to detect the mRNA expressions of transforming growth factor β1(TGF-β1), interleukin-6(IL-6), Smad3 and interleukin-10(IL-10) in thoracic aorta; western blot was used to detect expressions of Smad7, α-smooth muscle activator protein (α-SMA), and typeⅠ and Ⅲ collagen.
    Results In the model group, the blood pressure increased and the vascular adventitia was damaged obviously; in the electroacupuncture group, the blood pressure decreased but the adventitia was slightly damaged. Compared with blank group, the mRNA expressions of TGF-β1, IL-6, IL-10 and Smad3 increased significantly in model group (P<0.05 or P<0.01). Compared with the model group, the mRNA expressions of TGF-β1, Smad3 and IL-6 decreased significantly in the electroacupuncture group, while the expression of IL-10 mRNA increased significantly (P<0.05 or P<0.01). Compared with the blank group, expressions of type Ⅰand Ⅲ collagen and α-SMA protein increased significantly, and expression of Smad7 protein decreased significantly (P<0.05 or P<0.01). Compared with the model group, expressions of type Ⅰand Ⅲ collagen and α-SMA protein decreased significantly, and expression of Smad7 protein increased significantly (P<0.05 or P<0.01).
    Conclusion Electroacupuncture at Taichong and Quchi points can significantly reduce blood pressure in SIPR and effectively prevent vascular adventitia remodeling, and its mechanism may be related to the regulation of TGF-β1/Smads signaling pathway and alleviation of inflammatory response.

     

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