石决牡蛎汤通过p38MAPK通路改善自发性高血压大鼠血管重构的机制研究

来源 :广州中医药大学学报 | 被引量 : 0次 | 上传用户:tlljs
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【目的】探讨石决牡蛎汤通过p38丝裂原活化蛋白激酶(p38MAPK)信号通路改善自发性高血压大鼠(SHR)血管重构的作用。【方法】将40只16周龄自发性高血压大鼠随机分为模型对照组,石决牡蛎汤高、中、低剂量组,卡托普利组,每组8只;将8只Wistar-Kyoto大鼠设为正常对照组。治疗8周后,采用苏木精—伊红(HE)染色法观察胸主动脉形态,光镜下采用计算机图像分析系统测量血管内膜中层厚度(IMT)、管腔直径(LD),酶联免疫吸附法(ELISA)测定血清中内皮素-1(ET-1)水平,硝酸还原酶法测定血清中一氧化氮(NO)水平,免疫组织化学法检测磷酸化p38MAPK(p-p38MAPK)在胸主动脉组织中的表达水平。【结果】与模型对照组比较,石决牡蛎汤中、高剂量组及卡托普利组收缩压和舒张压、ET-1水平均显著降低,NO水平增高,中药高剂量组及卡托普利组IMT、IMT/LD值显著降低,差异均有统计学意义(P<0.05)。免疫组织化学结果显示,石决牡蛎汤中、高剂量组及卡托普利组能较显著抑制p-p38MAPK在胸主动脉的表达。【结论】石决牡蛎汤可能通过抑制p38MAPK信号通路、调节ET/NO系统改善自发性高血压大鼠血管重构。 【Objective】 To investigate the effect of Shi Decoction oyster soup on vascular remodeling in spontaneously hypertensive rats (SHR) via the p38 mitogen activated protein kinase (p38 MAPK) signaling pathway. 【Methods】 Forty eight-week-old spontaneously hypertensive rats were randomly divided into model control group, Shi Jie Oyster Decoction high, medium and low dose group, captopril group, 8 rats in each group. Eight Wistar- Kyoto rats were set as normal control group. After 8 weeks of treatment, the shape of thoracic aorta was observed by hematoxylin-eosin (HE) staining. The thickness of medial intima (IMT), lumen diameter (LD) Serum levels of endothelin-1 (ET-1) were measured by enzyme-linked immunosorbent assay (ELISA), nitric oxide (NO) levels were measured by nitrate reductase method, phosphorylated p38MAPK Aortic tissue expression levels. 【Results】 Compared with the model control group, systolic and diastolic blood pressure, ET-1 levels and the level of NO in Shidiazhu Oyster Decoction medium and high dose groups and Captopril group were significantly increased The IMT and IMT / LD values ​​in the Lee group were significantly decreased (P <0.05). Immunohistochemical results showed that stone decoction oyster soup, high-dose group and captopril group can significantly inhibit the expression of p-p38MAPK in the thoracic aorta. 【Conclusion】 Shi decoction oyster soup may improve vascular remodeling in spontaneously hypertensive rats by inhibiting the p38 MAPK signaling pathway and regulating ET / NO system.
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