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Protective effect of baicalin against pulmonary arterial hypertension vascular remodeling through regulation of TNF‐α signaling pathway

机译:黄芩苷对肺动脉高压血管改造通过调节TNF-α信号通路的保护作用

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摘要

Pulmonary arterial hypertension (PAH) is a progressive cardiovascular disease with high mortality. However, there were no efficient medical drugs for PAH to enormously improve the survival and quality of life measures. The present study aimed to explore the protective effect of baicalin against experimental PAH in vivo and vitro. All the experimental rats received intraperitoneal injection of monocrotaline (MCT) to induce PAH model. Baicalin was given by intragastric administration from 2 days after MCT injection. Forty animals were randomly divided into four groups: Control, MCT, saline‐, and baicalin‐treated groups (n = 10 in each). Post‐operation, hemodynamic data, and index of right ventricular hypertrophy (RVHI) were recorded to evaluate the inhibition of baicalin on MCT‐induced PAH. Furthermore, pulmonary artery smooth muscle cells (PASMCs) model induced by tumor necrosis factor‐α (TNF‐α) was used to observe the inhibition of vascular cells proliferation in vitro. The results demonstrated that baicalin significantly attenuated MCT‐induced right ventricular systolic pressure (RVSP), the index of right ventricular hypertrophy, and vessel wall thickness; inhibit inflammatory and cell proliferation induced by MCT or TNF‐α, respectively. In addition, we found that baicalin might protect against experimental PAH via regulating the TNF‐α/BMPR2 signaling pathway.
机译:肺动脉高压(PAH)是一种高死亡率的渐进心血管疾病。然而,PAH没有有效的医疗药物,以极大地提高生存措施的生存和质量。本研究旨在探讨黄芩苷对体内体外实验PAH的保护作用。所有实验大鼠均接受腹腔注射偏菌碱(MCT)以诱导PAH模型。在MCT注射后2天通过胃内给药给予黄芩苷。将四十只动物随机分为四组:对照,MCT,盐水和黄芩苷治疗组(每组N = 10)。记录后操作后,血流动力学数据和右心室肥大(RVHI)指数,以评估黄芩苷对MCT诱导的PAH的抑制作用。此外,肿瘤坏死因子-α(TNF-α)诱导的肺动脉平滑肌细胞(PASMCS)模型用于观察体外血管细胞增殖的抑制。结果表明,黄芩苷显着减弱了MCT诱导的右心室收缩压(RVSP),右心室肥大指数和血管壁厚;分别抑制MCT或TNF-α诱导的炎症和细胞增殖。此外,我们发现,通过调节TNF-α/ BMPR2信号传导途径,BACICALIN可以防止实验性PAH。

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