Metabolic (Met) syndrome is characterized by hypertension, insulin resistance and dyslipidaemia with high risk of cardiovascular disease. Endoplasmic reticulum (ER) stress is a key contributor in the pathogenesis of Met syndrome. The current study investigates the effect of Tauroursodeoxycholate (TUDCA), an ER stress inhibitor, on Met syndrome-induced cardiovascular complications and the possible underlying signalling mechanisms. Met syndrome was induced in rats, which were then treated with TUDCA. Body weight, blood pressure, glucose tolerance and insulin tolerance tests were performed. ER stress, survival and oxidative stress markers were measured in heart and aorta tissue. The results showed that TUDCA improved metabolic parameters in rats with Met syndrome. Treatment mitigated the Met syndrome-induced cardiovascular complications through upregulating survival markers and downregulating ER and oxidative stress markers. These results highlight the protective effect of ER stress inhibition as a potential target in the management of cardiovascular complications associated with Met syndrome.

中文翻译：

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内质网应激的抑制改善了代谢综合征大鼠模型中的心血管损伤。

代谢（Met）综合征的特征是高血压，胰岛素抵抗和血脂异常，具有心血管疾病的高风险。内质网应激是Met综合征发病机制的关键因素。目前的研究调查了内质网应激抑制剂牛磺去氧胆酸盐（TUDCA）对Met综合征引起的心血管并发症及可能的潜在信号传导机制的影响。在大鼠中诱发Met综合征，然后用TUDCA治疗。进行了体重，血压，葡萄糖耐量和胰岛素耐量测试。在心脏和主动脉组织中测量ER应力，存活率和氧化应激标志物。结果表明，TUDCA改善了Met综合征大鼠的代谢参数。通过上调生存指标，下调ER和氧化应激指标，治疗减轻了Met综合征引起的心血管并发症。这些结果突出了ER应激抑制的保护作用，将其作为治疗与Met综合征相关的心血管并发症的潜在靶标。