Abstract：
The primary and initial manifestations of hypertension encompass arterial hypoelasticity and histiocyte senescence. Oxidative stress plays a pivotal role in the progression of senescence. Elevated intracellular oxidative stress levels will directly induce cell damage, disrupt normal physiological signal transduction, which can cause mitochondrial dysfunction to accelerate the process of senescence. Alizarin, an anthraquinone active ingredient isolated from Rubia cordifolia L., has a variety of pharmacological effects, including antioxidant, anti-inflammatory and anti-platelet. Nevertheless, its potential in lowering blood pressure (BP) and mitigating hypertension-induced vascular senescence remains uncertain. In this study, we used spontaneously hypertensive rats (SHR) and human umbilical vein endothelial cells (HUVECs) to establish a model of vascular senescence in hypertension. Our aim was to elucidate the mechanisms underpinning the vascular protective effects of Alizarin. By assessing systolic blood pressure (SBP) and diastolic blood pressure (DBP), H&E staining, SA-β-Gal staining, vascular function, oxidative stress levels, calcium ion concentration and mitochondrial membrane potential, we found that Alizarin not only restored SBP and increased endothelium-dependent relaxation (EDR) in SHR, but also inhibited oxidative stress-induced mitochondrial damage and significantly delayed the vascular senescence effect in hypertension, and the mechanism may be related to the activation of VEGFR2/eNOS signaling pathway.
摘要：
高血压的主要和最初表现包括动脉弹性不足和组织细胞衰老。氧化应激在衰老进程中起关键作用。细胞内氧化应激水平升高会直接诱导细胞损伤,破坏正常的生理信号转导，这可能导致线粒体功能障碍加速衰老过程。茜素,从茜草中分离出的蒽醌活性成分，具有多种药理作用，包括抗氧化剂，抗炎和抗血小板。然而，其在降低血压(BP)和缓解高血压诱导的血管衰老方面的潜力仍不确定.在这项研究中,用自发性高血压大鼠(SHR)和人脐静脉内皮细胞(HUVECs)建立高血压血管衰老模型。我们的目的是阐明支撑茜素血管保护作用的机制。通过评估收缩压（SBP）和舒张压（DBP），H&E染色,SA-β-Gal染色,血管功能,氧化应激水平，钙离子浓度和线粒体膜电位，我们发现，在SHR中，茜素不仅恢复SBP和增加内皮依赖性舒张（EDR），同时还能抑制氧化应激诱导的线粒体损伤,显著延缓高血压血管衰老效应,其机制可能与VEGFR2/eNOS信号通路的激活有关。
